Genome complexity: epigenetics

Sorting out the true meaning of epigenetics on top of existing regulatory mechanisms for gene expression:-http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3645541/#!po=7.14286

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Direct epigentic modifications immediately inherited:-"Although the Science paper is based on heritability over just seven generations, other results with the Arabidopsis strains show that epigenetic traits are stably inherited for at least 20 generations. Johannes: 'Such stable traits can be of interest to plant breeders. Apart from variations in the gene sequence, epigenetic variation may contribute to commercially interesting traits.' - 
"The epigenetic markers may also affect evolution, independent of DNA sequence. 'They cause variation on which natural selection can act', Johannes explains. As such, traits caused by epigenetic variation may make an independent contribution to changes in a species. 'Our findings were made using inbred strains, but we also have evidence that we can find some of the same epigenetic QTLs in wild populations of this species as well.' This suggests it is not just a laboratory artefact but something that plays a role in nature."-
http://www.sciencedaily.com/releases/2014/02/140211094159.htm

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Stress in parents can make changes in behaviors in offspring mice:-http://www.the-scientist.com//?articles.view/articleNo/39695/title/Traces-of-Trauma-in-Sperm-RNA/

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A new highly technical review article:-"Speculative Conclusions about an Epigenetic Interface between Experience and Genome Change
 
"Mobile DNA and other NGE [non-genetic engineering] functions are the key agents for adaptively significant changes in genome organization and DNA sequences. The data reviewed and tabulated above establish the importance of RNA-directed chromatin formatting in the regulation and operation of mobile elements, viruses and DNA repair functions. In addition, there is a remarkable correlation between the life history events that activate NGE functions to destabilize genomes and those that lead to alteration of chromatin states and DNA methylation patterns.
 
"The preceding observations lead to the plausible hypothesis that epigenetic regulation serves as a key interface between organismal life history and the agents that restructure genomic DNA. This hypothesis is supported by the limited number of cases where empirical observations have established direct molecular connections between NGE functions and components of the epigenetic control system: histones, nucleosomes, and chromatin reformatting complexes."-
 
"If, as I expect, further research bolsters the epigenome-NGE correlations and connections documented above, then we need to ask: what components(s) of the epigenetic control apparatus communicate information about experience to NGE operators? We do not know the answer to this fundamental question. However, the data reported in Table 4 indicate that ncRNAs are good candidates for key intermediates in the experience-genome signal transduction process. If this is so, then ncRNAs are logical molecular targets for modulating genome change toward potentially adaptive outcomes. Let us hope that research aimed at examining this proposal deepens our understanding of how life history impacts both epigenetic and genome change operations (Tables 2...4), whether or not my speculation ultimately proves to be correct."-http://journal.frontiersin.org/Journal/10.3389/fgene.2014.00087/full

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Newborn's DNA is changed by maternal diet in Gambia. More epigenetic mechanisms:-http://www.nature.com/ncomms/2014/140429/ncomms4746/full/ncomms4746.html-"We here report a prospective study that replicates the season of conception effects on epigenotype and extends the findings to additional human MEs. We further show that DNA methylation is predictably influenced by periconceptional maternal plasma biomarker concentrations of key micronutrients involved in one-carbon metabolism. This represents a demonstration in humans that a mother's nutritional status at the time of conception can influence her child's epigenome, with likely lifelong implications."

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Rapid changes in lizards moved to a new island:-http://www.livescience.com/1-image-day.html?cmpid=557681-"Observed changes in head morphology were caused by adaptation to a different food source. According to Irschick, lizards on the barren island of Pod Kopiste were well-suited to catching mobile prey, feasting mainly on insects. Life on Pod Mrcaru, where they had never lived before, offered them an abundant supply of plant foods, including the leaves and stems from native shrubs. Analysis of the stomach contents of lizards on Pod Mrcaru showed that their diet included up to two-thirds plants, depending on the season, a large increase over the population of Pod Kopiste.
 
"As a result, individuals on Pod Mrcaru have heads that are longer, wider and taller than those on Pod Kopiste, which translates into a big increase in bite force," says Irschick. "Because plants are tough and fibrous, high bite forces allow the lizards to crop smaller pieces from plants, which can help them break down the indigestible cell walls."
 
"Examination of the lizard's digestive tracts revealed something even more surprising. Eating more plants caused the development of new structures called cecal valves, designed to slow the passage of food by creating fermentation chambers in the gut, where microbes can break down the difficult to digest portion of plants. Cecal valves, which were found in hatchlings, juveniles and adults on Pod Mrcaru, have never been reported for this species, including the source population on Pod Kopiste.
 
"These structures actually occur in less than 1 percent of all known species of scaled reptiles," says Irschick. "Our data shows that evolution of novel structures can occur on extremely short time scales. Cecal valve evolution probably went hand-in-hand with a novel association between the lizards on Pod Mrcaru and microorganisms called nematodes that break down cellulose, which were found in their hindguts."

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How a small number of genes can make a complex human:-There are a finite number of genes in the genome, and changing which of those gets turned on or off gives you a certain level of complexity, Calarco said. What alternative splicing does is add another layer of complexity, allowing an organism to diversify a cell type even more  we think this contributes a great deal to an organism's ability to diversify its cellular function and cellular architecture.-http://news.harvard.edu/gazette/story/2014/08/neurons-at-work/-This may explain some of the innovations

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Another study showing an actual complex mechanism of making proteins using alternative splicing:-"Gene expression involves transcription of DNA to messenger RNA (mRNA) followed by translation of mRNA into proteins. Although each gene is coded to produce a single corresponding protein, a mechanism known as alternative splicing makes it possible for mRNA to be translated into any number of different proteins. Each mRNA transcript consists of numerous protein-coding 'exon' segments separated by non-coding 'intron' segments. Alternative splicing is a regulated process in which splicing proteins selectively target different combinations of exons to produce a variety of possible proteins."-http://medicalxpress.com/news/2014-10-pairs-proteins-collaborate-splice-rnas.html

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This is an example of the type of DNA change that Shapiro has proposed:

https://www.sciencedaily.com/releases/2016/11/161115111720.htm

"Researchers at the University of Oxford have demonstrated that the diets of organisms can affect the DNA sequences of their genes.

In a study on two groups of parasites, the team detected differences in DNA sequences that could be attributed to the composition of their food.

"Study co-author Dr Steven Kelly, from Oxford's Department of Plant Sciences, said: 'Organisms construct their DNA using building blocks they get from food. Our hypothesis was that the composition of this food could alter an organism's DNA. For example, could a vegetarian panda have predictable genetic differences from a meat-eating polar bear?

"'To test this hypothesis, we picked simple groups of parasites to use as a model system. These parasites share a common ancestor but have evolved to infect different hosts and eat very different foods.

"'We found that different levels of nitrogen in a parasite's diet contributed to changes in its DNA. Specifically, parasites with low-nitrogen, high-sugar diets had DNA sequences that used less nitrogen than parasites with nitrogen-rich, high-protein diets.'

"The study involved groups of eukaryotic parasites (Kinetoplastida) and bacterial parasites (Mollicutes) that infect different plant or animal hosts.

"The results, based on novel mathematical models developed by the researchers, reveal a previously hidden relationship between cellular metabolism and evolution. They provide new insights into how DNA sequences can be influenced by adaptation to different diets.

***

"'It has been unclear why very closely related organisms can look so different in their genetic makeup. By bringing together two fundamental aspects of biology -- metabolism and genetics -- we have advanced our understanding of this area.

"'It's a difficult question to answer, because there are so many factors that can influence the DNA sequence of an organism. But our study explains a very high percentage of these differences and provides evidence that we really are what we eat."

Comment: this is an exact instance of what Shapiro has shown. Necessary adaptation to environmental challenges, no change in species.

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We still don't know how this is done, exact reproduction of body form and type:-http://www.the-scientist.com//?articles.view/articleNo/40860/title/Precisely-Placed/

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Using stickleback fish, rapid changes are followed. Both freshwater and saltwater are used. One adaptation took only ten years:-http://phys.org/news/2014-09-fish-teeth-reveals-regulatory-dna.html

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How epigenetic modifications are passed to next generations is now being found:-"After DNA replication and division, cells generally remember which of their genes should be active and which repressedbut how? A study in worms published today (September 18) in Science reveals that part of the mechanism involves divvying up modified histonesmolecular tags that label active or repressed genesbetween daughter chromosomes at replication. Researchers from the University of California, Santa Cruz and Indiana University, Bloomington, found that although the tags in each chromosome are reduced as a result of division, subsequent recruitment of histone-modifying enzymes reestablishes the full tag quota, thus preserving the memory of modifications for the next round of division.
 
They show very elegantly using their system that modified histones can be inherited through multiple rounds of cell division and can be passed on . . . to the next generation, said Shiv Grewal, an epigenetics and chromatin researcher at the National Cancer Institute who was not involved in the work. That's quite remarkable."-
http://www.the-scientist.com//?articles.view/articleNo/41050/title/Heritable-Histones/-Histones are the molecules around which DNA is wrapped.

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This gene seems to have led to bilateral organisms with three layers of cells from the simple two-layered organisms that preceded them:-http://phys.org/news/2014-09-genetic-evolution-bilateral-animals.html-Of course this gene provides a phenotype change, but not the future development of many complex organ systems.

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Humans engineer stem cells' genome to produce specific tissue, in this case gut lining, and guess what, the cells produce what is expected. Thus we see how tightly controlled is the product of the genome:-http://www.sciencedaily.com/releases/2014/10/141019151800.htm-That is not the point of the paper, but it also makes the point that we can make life only from life. It is a closed system.

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How to read DNA. It is complex:-"Remarkably, the team found that the reading patterns for enhancer and gene messages are highly similar in many respects, sharing a common architecture. "Our data suggests that the same basic reading process is happening at genes and these non-genic regulatory elements," explains Siepel. "This points to a unified model for how DNA transcription is initiated throughout the genome."-"Working together, the biochemists from Lis's laboratory and the computer jockeys from Siepel's group carefully compared the patterns at enhancers and genes, combining their own data with vast public data sets from the NIH's Encyclopedia of DNA Elements (ENCODE) project. "By many different measures, we found that the patterns of transcription initiation are essentially the same at enhancers and genes," says Siepel. "Most RNA messages are rapidly targeted for destruction, but the messages at genes that are read in the right direction - those destined to be a protein - are spared from destruction." The team was able to devise a model to mathematically explain the difference between stable and unstable transcripts, offering insight into what defines a gene. According to Siepel, "Our analysis shows that the 'code' for stability is, in large part, written in the DNA, at enhancers and genes alike.""-http://medicalxpress.com/news/2014-11-dna-insight-genes-evolve.html

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Controlled in part by telomere length. Telomeres cap chromosomes and shorten with age of the cell, limiting gene expression control:-"Specifically, the team showed that when a telomere is long, the endcap can form a loop with the chromosome that brings the telomere close to genes previously considered too far away to be regulated by telomere length. Once the telomere and the distant genes on the same chromosome are close to each other, the telomere can generally switch those genes off.-"Conversely, when telomeres are short, the chromosome does not form a loop and the telomere can no longer influence whether target genes are switched on or off.-"The researchers were able to identify three genes whose expression patterns are altered by telomere length but believe this number is the just the tip of the iceberg.-"'We have developed the concept that telomere shortening could be used as a timing mechanism to respond to physiological changes in very long-lived organisms, such as humans, to optimize fitness in an age-appropriate fashion," said Dr. Wright.'"-http://medicalxpress.com/news/2014-11-scientists-uncover-mechanism-cells-impacting.html

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Researchers are surprised that gene expression in mice and humans differ.That is why we are human and they are mice:-http://www.the-scientist.com//?articles.view/articleNo/41453/title/Species-Specific/-Same genes, different results. In their minds is it a threat to common descent?

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Up to 60% of RNA transcripts edited! This is an IM fully at work, but note, the squid is still the squid, no massive changes to a new body type, just modifications to fit the changing environment. This is the sentience beloved by dhw, and autonomous within limited parameters of transient adaptive change. Full mutational change to a new form? No. Semiautonomous adaptation under full response control within the animals DNA. I say under full adaptive control, automatic responses controlled by DNA coding, because squids stay squids. No obvious evolution. My belief is that with a marked environmental permanent change, the squid will change body form somewhat. A recent study I read in the past two days stated that environment drives evolution and I accept that as a major valid point. Can't think of where I read it.-"Now a new study published in eLife by Dr. Eli Eisenberg of Tel Aviv University's Department of Physics and Sagol School of Neuroscience, in collaboration with Dr. Joshua J. Rosenthal of the University of Puerto Rico, showcases the first example of an animal editing its own genetic makeup on-the-fly to modify most of its proteins, enabling adjustments to its immediate surroundings. The research, conducted in part by TAU graduate student Shahar Alon, explored RNA editing in the Doryteuthis pealeii squid.-"We have demonstrated that RNA editing is a major player in genetic information processing rather than an exception to the rule," said Dr. Eisenberg. "By showing that the squid's RNA-editing dramatically reshaped its entire proteome -- the entire set of proteins expressed by a genome, cell, tissue, or organism at a certain time -- we proved that an organism's self-editing of mRNA is a critical evolutionary and adaptive force." This demonstration, he said, may have implications for human diseases as well.-"It was astonishing to find that 60 percent of the squid RNA transcripts were edited. The fruit fly, for the sake of comparison, is thought to edit only 3% of its makeup," said Dr. Eisenberg. "Why do squid edit to such an extent? One theory is that they have an extremely complex nervous system, exhibiting behavioral sophistication unusual for invertebrates. They may also utilize this mechanism to respond to changing temperatures and other environmental parameters."-http://www.sciencedaily.com/releases/2015/02/150212114327.htm

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DAVID: Up to 60% of RNA transcripts edited! This is an IM fully at work, but note, the squid is still the squid, no massive changes to a new body type, just modifications to fit the changing environment. This is the sentience beloved by dhw, and autonomous within limited parameters of transient adaptive change. Full mutational change to a new form? No. Semiautonomous adaptation under full response control within the animals DNA. -http://www.sciencedaily.com/releases/2015/02/150212114327.htm-Of course the squid is still the squid, because this is adaptation and not innovation. The whole point of the discussion concerning an inventive mechanism is that NOBODY knows how innovations have come about, and so we are looking for an explanation. Since we do know that there is a mechanism which enables organisms to change themselves, it is not unreasonable to hypothesize that the same mechanism under certain conditions might also be able to invent. If you accept common descent, you have to accept that innovations must have taken place within individual organisms and been passed on to subsequent generations. And so we go back to the alternatives: 1) they did it themselves; 2) God dabbled or preprogrammed every single innovation; 3) all the innovations were beneficial strokes of luck.

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> dhw: Of course the squid is still the squid, because this is adaptation and not innovation. The whole point of the discussion concerning an inventive mechanism is that NOBODY knows how innovations have come about, and so we are looking for an explanation. Since we do know that there is a mechanism which enables organisms to change themselves, it is not unreasonable to hypothesize that the same mechanism under certain conditions might also be able to invent. If you accept common descent, you have to accept that innovations must have taken place within individual organisms and been passed on to subsequent generations. And so we go back to the alternatives: 1) they did it themselves; 2) God dabbled or preprogrammed every single innovation; 3) all the innovations were beneficial strokes of luck.-My choices are luck cannot do it, so 1 % 2 are the only ones left for me. Then I look at 1 and revert to the idea that much of the progress of evolution is preprogrammed. It is easiest to stop at 'God did it'.

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The epigenetic survey of how cells modify DNAS to become specialized cells:-http://www.sciencedaily.com/releases/2015/02/150218092046.htm-Look at the diagram to see the different sites at work.-"Much like mapping the human genome laid the foundations for understanding the genetic basis of human health, new maps of the human epigenome may further unravel the complex links between DNA and disease. The epigenome is part of the machinery that helps direct how genes are turned off and on in different types of cells.-"Researchers supported by the National Institutes of Health Common Fund's Roadmap Epigenomics Program have mapped the epigenomes of more than 100 types of cells and tissues, providing new insight into which parts of the genome are used to make a particular type of cell. The data, available to the biomedical research community, can be found at the National Center for Biotechnology Information website-
"Almost all human cells have identical genomes that contain instructions on how to make the many different cells and tissues in the body. During the development of different types of cells, regulatory proteins turn genes on and off and, in doing so, establish a layer of chemical signatures that make up the epigenome of each cell. In the Roadmap Epigenomics Program, researchers compared these epigenomic signatures and established their differences across a variety of cell types. The resulting information can help us understand how changes to the genome and epigenome can lead to conditions such as Alzheimer's disease, cancer, asthma, and fetal growth abnormalities."

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Spell-checking actively protects DNA in cell production, but not completely. Mutations result:-"Ben Lehner and his team had previously described that somatic mutations are much more likely in some parts of the human genome, thus damaging genes that may cause cancer. In a new paper published on 23rd February in Nature, they show that this is because genetic mistakes are better repaired in some parts of the genome than in others. This variation was generated by a particular DNA repair mechanism called "mismatch repair" - a sort of a spellchecker that helps fix the errors in the genome after copying. Lehner and Supek show that the efficiency of this 'DNA spellchecker' varies depending on the region of the genome, with some parts of chromosomes getting more attention than others.-"The work presented by Lehner and Supek sheds new light on a process that was unexplored - what makes some parts of the human genome more vulnerable to damage? "We found that regions with genes switched on had lower mutation rates. This is not because less mistakes are happening in these regions but because the mechanism to repair them is more efficient", explains Ben Lehner, group leader, ICREA and AXA professor of risk prediction in age-related diseases at the EMBL-CRG Systems Biology unit in Barcelona. The 'mismatch repair' cellular machinery is extremely accurate when copying important regions containing genes that are key for cell functioning, but becomes more relaxed when copying less important parts. In other words, there appears to be a limited capacity for DNA repair in our cells, which is directed where it matters most."-http://medicalxpress.com/news/2015-02-dna-spellchecker-genes-equally-mutate.html

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In four days, Bacteria without flagella (due to gene deletion) recovered them by substitution within their genes:-http://www.the-scientist.com//?articles.view/articleNo/42284/title/Evolutionary-Rewiring/-This is a fascinating set of evolution experiments, wrote evolutionary biologist Richard Lenski of Michigan State University in an e-mail to The Scientist. Their experiments show how a biological functionin this case, flagellar motility in Pseudomonas fluorescenscan re-evolve after the deletion of a seemingly critical gene. The bacteria regained motility not by reacquiring the lost gene . . . but instead by mutations in other genes that put their products to new uses.-"There was another shock to come: each bacterial strain that regained its swimming abilityfirst slow, then fastdid so via essentially the same evolutionary process. The team sequenced the genomes of different slow- and fast-swimming strains and discovered that all of the slow swimmers had mutations in genes that would directly or indirectly increase expression of a nitrogen regulatory protein called NtrC. Furthermore, all of the fast swimmers had mutations in the gene for NtrC itself.-"NtrC shares 30 percent amino acid identity with FleQ, suggesting the proteins may be able to minimally cross-react with each other's target genes. Sure enough, the researchers determined that the initial mutations, which ramped up NtrC levels, enabled a minor upregulation of FleQ's target genes. The second mutations to NtrC itself then improved the protein's interaction with the FleQ targets, boosting their expression, and the bacteria's ability to swim.-"The results highlight the importance of gene duplication in evolution, said Hughes, and the ability of the resulting diverged proteins to moonlight in roles aside from their main function. Indeed, said Jeff Barrick of the University of Texas in Austin who was not involved in the work, such cross-talk gives organisms greater robustness, allowing them to restore a function even though they are missing a genetic part.-"But while the re-evolved flagella enabled the bacteria to access food supplies at the farthest reaches of the Petri dish, the ability came at a price. The bacteria that became much better at swimming were much worse at nitrogen regulation, said Johnson. However, she added, sometimes the advantage can be so great that it's worth paying that cost because otherwise you die."-This shows the value of gene duplication, but also the price of loss of function in nitrogen control. This is not an IM, because nothing is new, but it is built-in epigenetic protection controls. I interpret this as a built-in life-protection process in bacteria, another layer of genome complexity.-Another view of the study:-"Remarkably, this happened because the mutants had rewired a cellular switch, which normally controls nitrogen levels in the cell, to activate the flagellum. This allowed the bacteria to move to new food sources and avoid starvation.-"To understand how this had happened biologists at the University of York, compared which genes were being activated in bacteria before and after evolution. Professor Brockhurst said: "Bacteria use lots of genetic switches to turn their genes on and off. Each genetic switch controls a different set of genes.-"Amazingly, we found that just a single tiny change to one of these genetic switches was enough to convert it from being a switch that would normally turn on the genes for using nitrogen into a switch that now turns on the genes to build the flagella. The result is that the bacterium had, in effect, evolved a way to hotwire its motor practically overnight." -"Dr Tiffany Taylor, of the University of Reading and lead author of the study, added: "But the hotwiring comes at a cost. The replacement key is a molecule borrowed from a system which regulates nitrogen levels. The mutant bacteria can now move, but it can't regulate nitrogen properly, which can build up and become toxic. Of course, it's an evolutionary price worth paying when the alternative is certain death."-"These results suggest that new functions can evolve far quicker and much more easily than anyone previously expected. Dr Louise Johnson, an evolutionary biologist at the University of Reading, said: "Evolution has been described as a process of 'tinkering', but this work shows that evolution can be remarkably repeatable. When the situation is desperate, life finds a way.'"-
 Read more at: http://phys.org/news/2015-02-bacteria-hotwire-genes-faulty-motor.html#jCp

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Children and grandchildren of Holocaust survivors have lower levels of stress hormones:-http://www.scientificamerican.com/article/descendants-of-holocaust-survivors-have-altered-stress-hormones/?WT.mc_id=SA_EVO_20150309-"It is not completely clear why survivors produce less cortisol, but Yehuda's team recently found that survivors also have low levels of an enzyme that breaks down cortisol. The adaptation makes sense: reducing enzyme activity keeps more free cortisol in the body, which allows the liver and kidneys to maximize stores of glucose and metabolic fuelsan optimal response to prolonged starvation and other threats. The younger the survivors were during World War II, the less of the enzyme they have as adults. This finding echoes the results of many other human epigenetic studies that show that the effects of certain experiences during childhood and adolescence are especially enduring in individuals and sometimes even across generations (right).-"Most recently, a new study looked at the descendants of the Holocaust survivors. Like their parents, many have low levels of cortisol, particularly if their mothers had PTSD. Yet unlike their parents, they have higher than normal levels of the cortisol-busting enzyme. Yehuda and her colleagues theorize that this adaptation happened in utero. The enzyme is usually present in high levels in the placenta to protect the fetus from the mother's circulating cortisol. If pregnant survivors had low levels of the enzyme in the placenta, a greater amount of cortisol could make its way to the fetus, which would then develop high levels of the enzyme to protect itself.-"Epigenetic changes often serve to biologically prepare offspring for an environment similar to that of the parents, Yehuda explains. In this case, however, the needs of the fetus seem to have trumped that goal. With low levels of cortisol and high levels of the enzyme that breaks it down, many descendants of Holocaust survivors would be ill adapted to survive starvation themselves. In fact, that stress hormone profile might make them more susceptible to PTSD (below, yellow); previous studies have indeed suggested that the offspring of Holocaust survivors are more vulnerable to the effects of stress and are more likely to experience symptoms of PTSD. These descendants may also be at risk for age-related metabolic syndromes, including obesity, hypertension and insulin resistance, particularly in an environment of plenty."

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Protect the ends of chromosomes in aging. Also may modify gene expression:-http://www.the-scientist.com/?articles.view/articleNo/42253/title/Rethinking-Telomeres/-"Telomeres are DNA repeats at the ends of chromosomes that protect genetic material from degradation. Because DNA polymerase cannot fully replicate the ends of chromosomes, telomeres shorten each time a cell divides. Telomeres also prevent the ends of chromosomes from fusing to one another by recruiting protective protein caps.-"New work led by Jerry W. Shay and Woodring Wright of the University of Texas Southwestern Medical Center in Dallas demonstrates that telomeres are more than just buffer zones. The team found that as chromosomes fold within the nucleus, telomeres come into contact with faraway genes and alter their expression. As telomeres shorten, which happens with aging, chromosome looping and gene-expression patterns change.-"'I'm delighted with this evidence that the [telomere] sequence may actually be doing some regulation and that the decrease of the sequence in some cells may drastically affect the way they are behaving, says Mary-Lou Pardue, who studies telomeres at MIT and was not involved in the research. She points out that telomeres are longer and have a more complex sequence than should be necessary to simply protect the chromosome ends.-"Previous work had shown that genes near telomeres are repressed. Shay says that he and his colleagues began to suspect that telomeres were regulating more than just nearby genes when they found that the expression of a gene called ISG15 increased as the telomeres of its chromosomes shortened, even while genes closer to the ends of the chromosomes remained unaffected."

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Trying to follow how DNA is copied and errors appear. Again reality starts at a quantum level:-"Watson and Crick had originally hypothesized that the bases could nudge hydrogens out of the way to allow mis-matched connections. Aided by the NMR technique, Kimsey provided the first direct evidence for just such an atomic rearrangement in a DNA duplex. He also showed that a similar phenomenon occurs in RNA, the chemical cousin of DNA.-"This tiny movement, or "quantum jitter," takes such an enormous amount of energy that bases are successful at accomplishing the feat only once out of every 10,000 or so attempts. Even then, they can only hold their new shape for a very short period of time50 to 200 microsecondsbefore the hydrogens pop back into their original position.-"The researchers looked back at previous biological studies and found that these rare alternative states appeared in the DNA about as often as the polymerase machinery's copying errors.-"'This is a remarkable study that illuminates a fundamental mechanism responsible for the random mutations that drive evolution and contribute to cancer," said Bert Vogelstein, M.D., a cancer researcher at Johns Hopkins University School of Medicine who was not involved in this research."-
 Read more at: http://phys.org/news/2015-03-quantum-jitters-basis-evolution-cancer.html#jCp

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It turns out WE are not entirely US. Horizontal gene transfers are found:-"A number of genes, including the ABO blood group gene, were confirmed as having been acquired by vertebrates through HGT. The majority of the other genes were related to enzymes involved in metabolism.-"In humans, they confirmed 17 previously-reported genes acquired from HGT, and identified 128 additional foreign genes in the human genome that have not previously been reported.-"Some of those genes were involved in lipid metabolism, including the breakdown of fatty acids and the formation of glycolipids. Others were involved in immune responses, including the inflammatory response, immune cell signalling, and antimicrobial responses, while further gene categories include amino-acid metabolism, protein modification and antioxidant activities.-"The team were able to identify the likely class of organisms the transferred genes came from. Bacteria and protists, another class of microorganisms, were the most common donors in all species studied. They also identified HGT from viruses, which was responsible for up to 50 more foreign genes in primates."-http://www.sciencedaily.com/releases/2015/03/150312123319.htm

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It is a very important property:-http://www.sciencedaily.com/releases/2015/03/150316160712.htm-"We discovered this interesting physics of DNA that its sequence determines the flexibility and thus the stability of the DNA package inside the cell," said Gutgsell Professor of Physics Taekjip Ha, who is a member of the Carl R. Woese Institute for Genomic Biology at the University of Illinois. "This is actually very elementary DNA physics. Many people thought we should have known this many decades ago, but there are still surprises in the physics of DNA."-"The DNA is packaged into chromosomes, which resemble beaded bracelets. The string of DNA is coiled around beads, called histones, to create nucleosomes. These nucleosomes are braided together into beaded strings that are intricately woven into chromosomes.-"Scientists knew the DNA could be uncoiled from the nucleosome, but it was assumed that the two ends were symmetric, meaning uncoiling the DNA would be like untying a shoe. University of Illinois researchers found that the DNA is actually very asymmetric, like the string wrapped around a yoyo. Pulling on one end of DNA will simply tighten the coil while pulling on the other will cause it to uncoil like a yoyo.-"The physics of this nucleosome packaging is determined by the DNA's sequence, which makes the strand of DNA flexible enough to satisfy two conflicting principles: it has to be stable enough to compact DNA, but dynamic enough so the strand can be uncoiled and read to make proteins.-"'There are many good studies that show that if you change the sequence of the gene, then it will affect other things. Different proteins may be created because they require certain sequences for binding and so on," said Ha. "But no one had really thought about sequence changes having an effect on DNA physics, which in turn cause changes in the biology."-"Ha's research has shown that it is easier for the cell's protein-making machinery to read from the "weak" end of the nucleosome that uncoils more easily. They believe that genetic mutations related to diseases, like cancer, alter the stability of the nucleosome."-Not a simple double helix. All by chance of course.

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"Marc Bühler and his team at the Friedrich Miescher Institute for Biomedical Research (FMI) have elucidated the mechanism underlying small RNA-mediated gene silencing, thus solving a mystery which has been puzzling the research community for over a decade. Their findings, published today in Nature, have great potential for applications in various fields." - Read more at: http://phys.org/news/2015-03-genes-permanently-silenced-small-rnas.html#jCp-"As the scientists report in Nature today, a group of proteins known as the Paf1 complex (Paf1C) - itself part of the RNA polymerase complex - prevents small RNA molecules from silencing sections of the genome. When Paf1C was mutated in yeast, RNA fragments could be used to shut down targeted genome regions. This effect is robust and long-lasting. Bühler says: "In our experiments, we showed that gene silencing is also maintained in the next generation, even when the original RNA molecule is no longer present. So what we've discovered is a wholly epigenetic mechanism: we can alter gene expression across generations - and thus influence cell development - without directly changing the DNA sequence.'"

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Opinion of Denis Noble:-http://www.dpag.ox.ac.uk/team/group-leaders/denis-noble-
Noble D.-"The 'Modern Synthesis' (Neo-Darwinism) is a mid-20th century gene-centric view of evolution, based on random mutations accumulating to produce gradual change through natural selection. Any role of physiological function in influencing genetic inheritance was excluded. The organism became a mere carrier of the real objects of selection, its genes. We now know that genetic change is far from random and often not gradual. Molecular genetics and genome sequencing have deconstructed this unnecessarily restrictive view of evolution in a way that reintroduces physiological function and interactions with the environment as factors influencing the speed and nature of inherited change. Acquired characteristics can be inherited, and in a few but growing number of cases that inheritance has now been shown to be robust for many generations. The 21st century can look forward to a new synthesis that will reintegrate physiology with evolutionary biology. "

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DAVID: Opinion of Denis Noble:- http://www.dpag.ox.ac.uk/team/group-leaders/denis-noble
 
 
 Noble D.
 
"The 'Modern Synthesis' (Neo-Darwinism) is a mid-20th century gene-centric view of evolution, based on random mutations accumulating to produce gradual change through natural selection. Any role of physiological function in influencing genetic inheritance was excluded. The organism became a mere carrier of the real objects of selection, its genes. We now know that genetic change is far from random and often not gradual. Molecular genetics and genome sequencing have deconstructed this unnecessarily restrictive view of evolution in a way that reintroduces physiological function and interactions with the environment as factors influencing the speed and nature of inherited change. Acquired characteristics can be inherited, and in a few but growing number of cases that inheritance has now been shown to be robust for many generations. The 21st century can look forward to a new synthesis that will reintegrate physiology with evolutionary biology. "-Thank you for this. Good to see random mutations on the way out. Physiological functions and interactions with the environment, plus the inheritance of acquired characteristics, suggest to me that evolutionists are heading towards the truly amazing conclusion that there is an autonomous inventive mechanism at work, which enables individual organisms not only to adapt but also to innovate. Haven't we heard that before somewhere?

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The spools around which DNA wraps can control gene expression and pass it on to subsequent generations:-http://www.sciencedaily.com/releases/2015/04/150402161751.htm-Part of a possible IM?-"Scientists studied proteins found in cells, known as histones, which are not part of the genetic code, but act as spools around which DNA is wound. Histones are known to control whether or not genes are switched on.-"Researchers found that naturally occurring changes to these proteins, which affect how they control genes, can be sustained from one generation to the next and so influence which traits are passed on.-"The finding demonstrates for the first time that DNA is not solely responsible for how characteristics are inherited. It paves the way for research into how and when this method of inheritance occurs in nature, and if it is linked to particular traits or health conditions.-"It may also inform research into whether changes to the histone proteins that are caused by environmental conditions -- such as stress or diet -- can influence the function of genes passed on to offspring.-"The research confirms a long-held expectation among scientists that genes could be controlled across generations by such changes. However, it remains to be seen how common the process is, researchers say."

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By tagging a protein cell knows it needs to be disposed of:-http://www.the-scientist.com//?articles.view/articleNo/42663/title/Cellular-Garbage-Disposal-Illuminated/-"Aaron Ciechanover, Avram Hershko, and Irwin Rose, the researchers who discovered the process in the 1980s, shared the 2004 Nobel Prize in Chemistry for their work on ubiquitin-mediated protein degradation. But the molecular particulars of the process remained murky until last week. Kirschner and his colleagues found that an enzyme called APC/C adds ubiquitins to proteins headed for the rubbish heap in an iterative fashion, through processive affinity amplification. They also found that the proteosome singles out ubiquitin-tagged proteins for degradation by recognizing distributed arrays of short ubiquitins chains, with the configuration of those chains determining how the protein passes through specific channels in the proteosome. Previous models posited that proteins tagged with tetraubiquitins were the only ones slated for degradation.-"'Both studies substantially enrich our knowledge of ubiquitination and degradation, reveal new properties of APC/C and the proteasome, and challenge established concepts about the ubiquitin-proteasome system, wrote David Komander, a researcher at the Medical Research Council Laboratory of Molecular Biology in the U.K. in a commentary in Science."-Note all done by molecular activity, managed by the genome.

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Our immune system must differentiate between 'good' and 'bad' bacteria:-
"An international research team led by Weill Cornell Medical College investigators has discovered an answer to why the human immune system ignores roughly 100 trillion beneficial bacteria that populate the gastrointestinal tract. The findings, published April 23 in the journal Science, advance investigators' understanding of how humans maintain a healthy gastrointestinal tract, and may provoke new ways to treat inflammatory bowel diseaseincluding Crohn's disease and ulcerative colitiswhose origins have been mysterious and treatment difficult.
 
"The investigators studied T cellscritical components of the adaptive immune systemwhich have the capacity to recognize, eliminate and remember foreign microbes that invade our bodies. T cells are named after the thymus, an organ where they develop and are taught not to attack normal human tissues and organs, leaving them free to target and eradicate disease-causing foreign invaders. One question that had puzzled scientists until now is how these cells learn to ignore beneficial bacteria in the intestine that are also foreign, but not harmful.-"In the study, the research team discovered that once they leave the thymus, T cells are again educated in the gastrointestinal tract, or gut, to leave beneficial bacteria alone. This dual education strategy is vital to supporting healthy immune function, the investigators say. -http://medicalxpress.com/news/2015-04-immune-cells-beneficial-bacteria.html

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Transcription speeds up and slows down. The study shows how little we understand about a very complex system of copying:-"Once upon a time, scientists thought RNA polymerasethe molecule that kicks off protein synthesis by transcribing DNA into RNAworked like a wind-up toy: Set it down at a start site in our DNA and it would whir steadily along, reeling off an RNA copy, until it reached the stop site-"'It's more like a high-performance sports car," said Stirling Churchman, assistant professor of genetics at Harvard Medical School. "It has to speed up, slow down and deal with obstacles in its path."-"First, Churchman found evidence that RNA polymerase really does change speed sharply in our cells. Other researchers had suspected this but had only been able to study it in simplified, modified systems outside the cell.-"For example, Churchman and her team saw RNA polymerase slow down right before it reached particular obstacles called transcription factorsproteins that help RNA polymerase do its job.-"Di Iulio discovered that RNA polymerase slowed down when it encountered DNA that would later become part of the final protein. (Many parts of the RNA copy produced during transcription get cut out, and the remaining bits get pieced back together before a protein is made.) No one had seen that before, Churchman said.-"'The RNA polymerase was somehow detecting it was on DNA that would be retained," said Churchman. "We saw this characteristic pattern of pauses like speed bumps before and after these DNA segments. We don't know yet why they're there or what's causing them.'-"Churchman wouldn't have been able to see the speed bumps with a lower-resolution tool because they happened so sharply, spiking and plunging within ten nucleotides.-"Third, Churchman's team saw evidence of convergent transcription, a scenario where a second RNA polymerase "sports car" started further down the gene and drove toward the beginning, potentially leading to two polymerases colliding head-on.-"Other researchers had seen this at specific places along the genome. The work of Churchman's group indicated that it happens in as many as 25 percent of genes.-"Churchman also determined that convergent transcription tends to happen in less-expressed genes.-"In short, the findings indicate that there's a lot going on, said Churchman.-"'There isn't just the decision to turn a gene on or off; there are all these other control valves during the creation of RNA," she said. "Ultimately, it emphasizes the simplicity of our current views of how transcription occurs.'-"The study only scratches the surface of what NET-seq can help Churchman and others learn about gene transcription, she said. But every little bit helps."-
 Read more at: http://phys.org/news/2015-04-rna-machinery-genomic-obstacle.html#jCp

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New markers found in algae, C. elegans, and fruit fly:-http://www.the-scientist.com//?articles.view/articleNo/42858/title/New-Epigenetic-Mark-Found-on-Metazoan-DNA/-"The epigenetic mark of DNA methylation, once thought to be rare if not nonexistent in worms and flies, occurs throughout the genomes of these organisms and in algae on the base adenine, not the cytosine known to be modified in mammals, according to a trio of papers published today (April 30) in Cell.-"The results are mysterious and exciting, said Josep Casadesús of the University of Seville, Spain, who was not involved in the work. The secret of these three Cell papers is that now there are technologies that can detect very low levels [of methylation] that were impossible to detect with the old methods.-"In bacteria, 6mA marks the template strand during DNA replication, enabling a cell to spot errors and regulate the cell cycle. The modification also helps differentiate bacterial DNA from viral genomic material, which lacks methylation. In eukaryotes, by contrast, methylated cytosine (5mC) is involved in development and DNA base repair. Because the mark is present on the DNA, it can be transferred both during DNA replication and even, potentially, from generation to generation. However, 5mC is not present in the roundworm C. elegans and only exists at low levels in Drosophila, so it was thought that DNA methylation was unimportant in these organisms."-I'm not surprised. I think there are rules and patterns all through the overall pattern of DNA development and controls. Research is just scratching the surface as new techniques are developed. We have a lot more to learn.

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How do epigenetic markers arise in evolution? No one knows. Cornelius Hunter points out the fallacies in Darwinian thinking:-http://darwins-god.blogspot.com/2015/05/chuan-he-evolution-created-epigenetics.html-"Under evolution, the protein machines that attach the epigenetic markers must have fortuitously evolved from random mutations. But placing markers would not have helped if they were not in the right place, and in response to the right environmental signals. In fact, such protein machines could easily wreak havoc if they weren't working just right.-" But even given all that, such a marvel would do no good. That is because a tiny methyl group, or any other epigenetic marker, must be interpreted by other molecular machines. In other words, there must also have evolved the machines needed to recognize and perform the appropriate regulatory actions, as indicated by the given marker.-" Evolution requires an enormous sequence of random mutations to occur before fitness improvements could be realized."-An absolutely logical set of reasons why random mutation cannot work. So we are back to an IM or direct guidance. And I must insist with this set of reasons the IM must have guidance.

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This is a must read with care and full understanding. It is a description of the inventive mechanism imbedded in gene networks. It describes patterns and suggests laws covering the drive to complexity that seems to be the force behind evolvability.-There are nuggets below, but it must be fully digested. It reeks of design, but the author can't say that. Darwinists would pounce.-http://nautil.us/issue/20/creativity/the-strange-inevitability-of-evolution-"Ah, but isn't all this wonder simply the product of the blind fumbling of Darwinian evolution, that mindless machine which takes random variation and sieves it by natural selection? Well, not quite. You don't have to be a benighted creationist, nor even a believer in divine providence, to argue that Darwin's astonishing theory doesn't fully explain why nature is so marvelously, endlessly inventive. Darwin's theory surely is the most important intellectual achievement of his time, perhaps of all time, says evolutionary biologist Andreas Wagner of the University of Zurich. But the biggest mystery about evolution eluded his theory. And he couldn't even get close to solving it.-"What Wagner is talking about is how evolution innovates: as he puts it, how the living world creates. Natural selection supplies an incredibly powerful way of pruning variation into effective solutions to the challenges of the environment. But it can't explain where all that variation came from. As the biologist Hugo de Vries wrote in 1905, natural selection may explain the survival of the fittest, but it cannot explain the arrival of the fittest. Over the past several years, Wagner and a handful of others have been starting to understand the origins of evolutionary innovation. Thanks to their findings so far, we can now see not only how Darwinian evolution works but why it works: what makes it possible.-***-"The trouble is that traits don't in general map so neatly onto genes: They arise from interactions between many genes that regulate one another's activity in complex networks, or gene circuits. No matter, you might think: Evolution has plenty of time, and it will find the good gene circuits eventually. But the math says otherwise.-***
"In all these cases the questions are the same, and point to, as Wagner puts it, a dirty secret behind the success of the so-called modern synthesis of Darwinian evolutionary theory and genetics. How does evolution find workable solutions when it lacks the means to explore even a small fraction of the options? And how does evolution find its way from an existing solution to a viable new onehow does it create? The answer is, at least in part, a simple one: It's easier than it looks. But only because the landscape that the evolutionary process explores has a remarkable structure, and one that neither Darwin nor his successors who merged Darwinism with genetics had anticipated.-***-"Yet the question that remains is: Why does the space of evolutionary options have this essential, robust structure? We simply don't know why genotype networks are interwoven the way they are, admits Wagner. Jesse Bloom of the Fred Hutchinson Cancer Research Center in Seattle, a specialist on protein evolution, suggests that perhaps that question is back to front: One could posit that evolution is only able to work effectively if this property exists, and so the things that ended up evolving have this property, he says. But he admits that this would be hard to prove.-***-"These ideas suggest that evolvability and openness to innovation are features not just of life but of information itself. That is a view long championed by Schuster's sometime collaborator, Nobel laureate chemist Manfred Eigen, who insists that Darwinian evolution is not merely the organizing principle of biology but a law of physics, an inevitable result of how information is organized in complex systems. And if that's right, it would seem that the appearance of life was not a fantastic fluke but almost a mathematical inevitability."

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In my humble opinion, this is much like the big bang in that it only regresses the question one step back. You have this huge chemical probability space, but where did the organization and fine tuning for that probability space come from. Having a solid, flexible foundation is every bit as much evidence of preplanning as it is the opposite.

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What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.

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Tony: In my humble opinion, this is much like the big bang in that it only regresses the question one step back. You have this huge chemical probability space, but where did the organization and fine tuning for that probability space come from. Having a solid, flexible foundation is every bit as much evidence of preplanning as it is the opposite.-At least the Darwin folks notice something is wrong with the whole idea of innovation.

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A complex article about a protein that helps control cell division and can modify gene expression:-http://phys.org/news/2015-05-protein-cement-stabilizes-crossroad-chromosomes.html-"A new study by researchers at the Perelman School of Medicine at the University of Pennsylvania published in Science this week describes how the centromere is stabilized during replication. DNA in the nucleus is packaged into protein/DNA complexes called nucleosomes. As it turns out, the centromere is distinguished not only by its DNA sequence but also by a special type of nucleosome, which includes a protein called CENP-A.-"Their findings also address the question of the stability of CENP-A molecules at centromeres. Under normal conditions CENP-A binds centromeres and effectively never lets go. Indeed, when the authors tracked where proteins "reside" in live cells, they found that, unlike traditional nucleosomes that package the DNA throughout the rest of the chromosome, CENP-A-containing nucleosomes apparently never dissociate after newly generated CENP-A protein is first delivered to the centromere during a short time window following cell division. "The CENP-A is basically cemented at the centromere of origin," Black explains. But in cells lacking CENP-C, CENP-A dissociates readily, suggesting that CENP-C binding to CENP-A is what imparts that stability. -"Investigators have known for the past 20 years that part of chromosome inheritance is controlled by epigenetics, implicating the protein spools around which DNA is wound as the driving force, rather than what is encoded in the DNA sequence itself. Those spools are built of histone proteins, and chemical changes to these spool proteins can either loosen or tighten their interaction with DNA. This, in turn, alters a gene's expression up or down. In the case of the centromere, it marks the site where spindle fibers attach independently of the underlying DNA sequence.-"Black notes that these data suggest a model of epigenetic biology distinct from the traditional view of nucleosomes as static scaffolds on which key functional molecules assemble. Instead, the team's data suggest that histone variants and post-translational modifications, which change the biological properties of nucleosomes through changes in shape (by adding or removing enzyme docking sites) make nucleosomes active participants in cell division and gene expression.-"This mode of nucleosome regulation and stabilization may well be common to other epigenetic processes, Black adds. Indeed, he says the results suggest that other histone variants and histone post-translational modifications may serve a similar function as the example at the centromere with CENP-A and CENP-C, for instance in the regulation of gene expression.-"'I don't know how widely this occurs," he says, "but I'd be very surprised if this was the only place in nature that had evolved to take advantage of the fact that the shape of nucleosomes can be regulated by protein-binding events.'"-
 Read more at: http://phys.org/news/2015-05-protein-cement-stabilizes-crossroad-chromosomes.html#jCp

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Yes they do, and they always have, including Darwin himself! Unlike his followers, though, Darwin was at least humble and honest enough to admit it.

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What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.

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DAVID: This is a must read with care and full understanding. It is a description of the inventive mechanism imbedded in gene networks. It describes patterns and suggests laws covering the drive to complexity that seems to be the force behind evolvability.
There are nuggets below, but it must be fully digested. It reeks of design, but the author can't say that. Darwinists would pounce.-http://nautil.us/issue/20/creativity/the-strange-inevitability-of-evolution-It also reeks of autonomy, unless you think your God directs every change, or preprogrammed every innovation 3.7 billion years ago. However, there is one more quote I would like to comment on, as I do not quite understand it but suspect that it slightly distorts the picture:
 
The structure of these combinatorial landscapes of biomolecules then enables nature to make bold and creative innovations rather than being forever consigned to making incremental variations on what already exists. Evolution need only take a random walk along a web of neutral (or at least almost neutral) mutations, that, without impairing the fitness of an organism, surrounds it with very different neighbors: innovative solutions to selective pressures that are there for the taking when the circumstances compel it. Through this neutral drift, organisms can reach locations in phase space which would not have been accessible by strictly adaptive mutation from their original starting position.-Perhaps you could explain what they mean by a random walk along a web of neutral mutations.
 
To make the process clearer, I would say it is not some strange force called nature that innovates, but individual organisms themselves that combine (combinatorial landscapes). And evolution does not take a random walk, but individual organisms themselves respond inventively as well as adaptively to random changes in the environment. Nor do circumstances necessarily compel innovation, as bacteria have remained bacteria since it all began: innovations are not motivated solely by the need to survive, but also by the desire to improve. And finally, to go back to autonomy, we should never forget that in 99% of cases, the inventive/adaptive mechanism fails. Once again, if your God designed it in the first place, he either preprogrammed the failure, intervened to engineer it, or left organisms to fend for themselves (= autonomy).-Thank you for this article. Definitely very important!

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> dhw: Perhaps you could explain what they mean by a random walk along a web of neutral mutations.-This comes from the field of mathematical approaches to finding innovation through mutation. A random walk is literally just that, wandering around through a lovely landscape, not knowing exactly what you are looking for or what to find and how to use it. There are formulas based on how many proteins there are of certain types, and figuring odds. What the writer is saying is that there are patterns of protein forms that make the search easier, according to computer research. Note it comes back to patterns in planning from the beginning. To me pre-planning. 
> 
> dhw: To make the process clearer, I would say it is not some strange force called nature that innovates, but individual organisms themselves that combine (combinatorial landscapes). And evolution does not take a random walk, but individual organisms themselves respond inventively as well as adaptively to random changes in the environment.-I see here you are making your own interpretation and disagreeing with the author. You have that right. I do it all the time. You are accepting epigenetics, which I think was pre-planned to help organisms do exactly what you describe.-> dhw: Nor do circumstances necessarily compel innovation, as bacteria have remained bacteria since it all began: innovations are not motivated solely by the need to survive, but also by the desire to improve.-Be careful, 'desire to improve' smells of teleology. How do bacteria even conceive of improving themselves? -> dhw: And finally, to go back to autonomy, we should never forget that in 99% of cases, the inventive/adaptive mechanism fails. Once again, if your God designed it in the first place, he either preprogrammed the failure, intervened to engineer it, or left organisms to fend for themselves (= autonomy).-But yet there are humans living all around you, despite your complaint. You should be grateful worked so well to give you your experience of life.
> 
> Thank you for this article. Definitely very important!-Thank you. It is very important. We have no idea how innovation works. Darwin didn't know and his guess is obviously wrong.

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Another extremely important article about the feed-back control loops in the genome, and the finding of an orchestrating gene the helps control the whole process. This is the type of complexity I predicted in my S vs. R book would be found, and would demand that a God-controlled evolution is the only reasonable conclusion, if one accepts evolution as having occurred: -http://darwins-god.blogspot.com/2015/05/nfgfr1-protein-that-regulates-regulators.html-"This week new research out of SUNY Buffalo continues to make this story even more devastating for evolution. The research involves a gene, containing 24 exons, that codes for a special protein known as the nuclear Fibroblast Growth Factor Receptor-1, or nFGFR1.-"The nFGFR1 protein plays an important gene regulation role during embryonic development. In this role, nFGFR1 does not regulate the production of proteins that do something in the cell, such as synthesizing a chemical or metabolizing food. Instead, nFGFR1 regulates the regulatory proteins.-"In other words, the nFGFR1 protein represents a higher level of gene regulation. The expression of genes is influenced by regulatory proteins, and the expression of the regulatory proteins is influenced by yet other proteins, such as nFGFR1. This is yet another unequivocal refutation of evolutionary theory."-***
"We've known that the human body has almost 30,000 genes that must be controlled by thousands of transcription factors that bind to those genes, yet we didn't understand how the activities of genes were coordinated so that they properly develop into an organism.-"Now we think we have discovered what may be the most important player, which organizes this cacophony of genes into a symphony of biological development with logical pathways and circuits.-"We found that this protein works as a kind of orchestration factor,' preferably targeting certain gene promoters and enhancers. The idea that a single protein could bind thousands of genes and then organize them into a hierarchy, that was unknown. Nobody predicted it."-Nobody except those who were thinking past the Darwinian block to rational thought about the process of evolution.-http://www.sciencedaily.com/releases/2015/05/150508110526.htm-"One of developmental biology's most perplexing questions concerns what signals transform masses of undifferentiated cells into tremendously complex organisms, a process called ontogeny.-"New research by University at Buffalo scientists, published in PLOS ONE, provides evidence that it all begins with a single "master" growth factor receptor that regulates the entire genome."

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dhw: Perhaps you could explain what they mean by a random walk along a web of neutral mutations.
Thank you for your explanation, which I shan't reproduce. A random walk doesn't sound much like pre-planning to me, and I still don't see how neutral mutations can lead to innovations, but perhaps we should leave it at that.-dhw: To make the process clearer, I would say it is not some strange force called nature that innovates, but individual organisms themselves that combine (combinatorial landscapes). And evolution does not take a random walk, but individual organisms themselves respond inventively as well as adaptively to random changes in the environment.
DAVID: I see here you are making your own interpretation and disagreeing with the author. You have that right. I do it all the time. You are accepting epigenetics, which I think was pre-planned to help organisms do exactly what you describe.-People often forget that every innovation has to take place within individual organisms, and that is hard to imagine. If we reject random mutations, innovation implies a mind, but life, Nature and evolution are not terms we normally associate with a mind. Your answer is God, but many experts say that organisms also have some sort of mind. The question then is whether the ability to respond inventively to environmental change comes from outside the organism (God) or inside. 
 
dhw: Nor do circumstances necessarily compel innovation, as bacteria have remained bacteria since it all began: innovations are not motivated solely by the need to survive, but also by the desire to improve.
DAVID: Be careful, 'desire to improve' smells of teleology. How do bacteria even conceive of improving themselves?-Most of them obviously don't, but they can conceive of defending and adapting themselves. The experts you disapprove of tell us that even such minuscule organisms are individual. It's not unimaginable that all innovations are brought about by certain individual organisms having a greater degree of awareness than others - just as individual humans vary enormously in their degree of intelligence, inventiveness etc. By coincidence, today's Sunday Times reviews a new book by a biochemist named Nick Lane: THE VITAL QUESTION: -For two billion years, earth was populated by busy but boring bacteria and archaea, single-cell life forms known as prokaryotes [...] An archaea and a bacteria, against all the odds, mingled in a process known as endosymbiosis, and started a whole new process from which eukaryotes - cells with nuclei - emerged. -God preprogramming these two little critters? God dabbling? Sheer luck? Two autonomous little explorers deciding to experiment? We should remember that every single innovation afterwards entails a similar process of "mingling", or perhaps we should call it cooperating.
 
dhw: And finally, to go back to autonomy, we should never forget that in 99% of cases, the inventive/adaptive mechanism fails. Once again, if your God designed it in the first place, he either preprogrammed the failure, intervened to engineer it, or left organisms to fend for themselves (= autonomy).
DAVID: But yet there are humans living all around you, despite your complaint. You should be grateful worked so well to give you your experience of life.-My post is not a complaint. I am merely pointing out that your insistence on pre-planning runs into difficulty when you are confronted with the 99% of apparent failures. As for gratitude, yes indeed, I cherish my experience of life. That does not mean I have to believe in divine pre-planning and/or dabbling.

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dhw: Perhaps you could explain what they mean by a random walk along a web of neutral mutations.
> Thank you for your explanation, which I shan't reproduce. A random walk doesn't sound much like pre-planning to me, and I still don't see how neutral mutations can lead to innovations, but perhaps we should leave it at that.-But that is exactly the point. What you can't see about 'neutral mutations' no one else can either, so the point of the article that the 'innovation process' is a big black box is correct.
> 
> dhw: If we reject random mutations, innovation implies a mind, but life, Nature and evolution are not terms we normally associate with a mind. Your answer is God, but many experts say that organisms also have some sort of mind. The question then is whether the ability to respond inventively to environmental change comes from outside the organism (God) or inside.-How did it develop inside without planning?- 
> dhw: It's not unimaginable that all innovations are brought about by certain individual organisms having a greater degree of awareness than others - just as individual humans vary enormously in their degree of intelligence, inventiveness etc.-I wouldn't ever compare bacteria to human variation in mental ability.-
> dhw: By coincidence, today's Sunday Times reviews a new book by a biochemist named Nick Lane: THE VITAL QUESTION: 
> 
> For two billion years, earth was populated by busy but boring bacteria and archaea, single-cell life forms known as prokaryotes [...] An archaea and a bacteria, against all the odds, mingled in a process known as endosymbiosis, and started a whole new process from which eukaryotes - cells with nuclei - emerged.-And this week an article on just that subject, finding eukaryote genes in Archaea:-"In this weeks' edition of Nature, researchers from Uppsala University in Sweden, along with collaborators from the universities in Bergen (Norway) and Vienna (Austria) report the discovery of a new group of Archaea, the Lokiarchaeota (or 'Loki' for short), and identify it to be a missing link in the origin of eukaryotes.-"'By studying its genome, we found that Loki represents an intermediate form in-between the simple cells of microbes, and the complex cell types of eukaryotes", says Thijs Ettema.- "'Loki formed a well-supported group with the eukaryotes in our analyses", says Lionel Guy, one of the senior scientists involved in the study from Uppsala University.-"'In addition, we found that Loki shares many genes uniquely with eukaryotes, suggesting that cellular complexity emerged in an early stage in the evolution of eukaryotes", says Anja Spang, researcher at Department of Cell and Molecular Biology , Uppsala University, and one of the lead-authors of the study.-"The name Lokiarchaeota is derived from the hostile environment close to where it was found, Loki's Castle, a hydrothermal vent system located on the Mid-Atlantic Ridge between Greenland and Norway at a depth of 2,352 meters.-"Hydrothermal vents are volcanic systems located at the ocean floor. The site where Loki is heavily influenced by volcanic activity, but actually quite low in temperature", says Steffen Jørgensen from the University of Bergen in Norway, who was involved in taking the samples where Loki was found." - Read more at: http://phys.org/news/2015-05-link-evolution-complex-cells.html#jCp-Also: http://www.sci-tech-today.com/story.xhtml?story_id=0220026MHQU8
> 
> dhw: God preprogramming these two little critters? God dabbling? Sheer luck? Two autonomous little explorers deciding to experiment? We should remember that every single innovation afterwards entails a similar process of "mingling", or perhaps we should call it cooperating.-Well, we all know the current theory of mitochondria starting out as being engulfed energy organisms.-
> dhw: My post is not a complaint. I am merely pointing out that your insistence on pre-planning runs into difficulty when you are confronted with the 99% of apparent failures.-How do you know the 99% failure rate was not planned? That is your human view of poor planning, just like the funny-looking retina objections.

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dhw: If we reject random mutations, innovation implies a mind, but life, Nature and evolution are not terms we normally associate with a mind. Your answer is God, but many experts say that organisms also have some sort of mind. The question then is whether the ability to respond inventively to environmental change comes from outside the organism (God) or inside.
DAVID: How did it develop inside without planning?-I have conceded over and over again that the inventive mechanism may have been designed by your God. The theistic evolutionary issue between us in all these discussions is whether your God preplanned or dabbled every innovation, or whether the mechanism is autonomous. In discussing this, we need always to bear in mind that innovations take place within individual organisms, and it is misleading - as the article does and you sometimes do - to talk of life/Nature/evolution being inventive.-dhw: It's not unimaginable that all innovations are brought about by certain individual organisms having a greater degree of awareness than others - just as individual humans vary enormously in their degree of intelligence, inventiveness etc.

DAVID: I wouldn't ever compare bacteria to human variation in mental ability.-The usual objection, to which I must give the usual reply: nobody is saying that bacterial intelligence is the same as human intelligence. The point here is that since innovations take place within individual organisms, and even the smallest individual organisms are said to differ from one another (just as we do), it is possible that some are cleverer than others. That may explain why, when conditions change, some die, some adapt, and a few innovate.
 
dhw: By coincidence, today's Sunday Times reviews a new book by a biochemist named Nick Lane: THE VITAL QUESTION: 
For two billion years, earth was populated by busy but boring bacteria and archaea, single-cell life forms known as prokaryotes [...] An archaea and a bacteria, against all the odds, mingled in a process known as endosymbiosis, and started a whole new process from which eukaryotes - cells with nuclei - emerged.-DAVID: And this week an article on just that subject, finding eukaryote genes in Archaea:-Thank you. Perhaps the jigsaw is gradually coming together.-dhw: My post is not a complaint. I am merely pointing out that your insistence on pre-planning runs into difficulty when you are confronted with the 99% of apparent failures.
DAVID: How do you know the 99% failure rate was not planned? That is your human view of poor planning, just like the funny-looking retina objections.-I'm not talking about poor planning. I'm pointing out that you yourself have great difficulty reconciling a 99% extinction rate, plus countless weird and wonderful creatures and lifestyles (which according to you are too complex to have resulted from anything other than divine preprogramming or dabbling) with your insistence that all of them serve or served the purpose of producing humans. But I quite understand how necessary it is for you to launch diversionary attacks.

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> dhw: I have conceded over and over again that the inventive mechanism may have been designed by your God. ... In discussing this, we need always to bear in mind that innovations take place within individual organisms, and it is misleading - as the article does and you sometimes do - to talk of life/Nature/evolution being inventive.-The increasing complexity from early to recent evolution is inventiveness conducted by living organisms. You are quibbling. The recent review article I presented showed that we have no idea how innovation occurs.-
> dhw: The point here is that since innovations take place within individual organisms, and even the smallest individual organisms are said to differ from one another (just as we do), it is possible that some are cleverer than others. That may explain why, when conditions change, some die, some adapt, and a few innovate.-Agreed but we don't know how.-> 
> dhw: I'm not talking about poor planning. I'm pointing out that you yourself have great difficulty reconciling a 99% extinction rate, plus countless weird and wonderful creatures and lifestyles... with your insistence that all of them serve or served the purpose of producing humans. But I quite understand how necessary it is for you to launch diversionary attacks.-Not diversionary. Once again, if God did it and I don't understand why or how, that does not mean one should not be able to accept that God worked through an evolutionary process. My problem is I cannot read His mind as He plans His goals, nor can anyone else.

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In thale cress, slow enough over generations for natural selection to act, but much faster than sequence mutation. Epigenetics is methylation, not base change, with additions and subtractions over time.-http://www.the-scientist.com//?articles.view/articleNo/42948/title/Estimating-Epigenetic-Mutation-Rates/-"Methylation on the DNA base cytosine can regulate the expression of genes and transposable elements in organisms including the model plant A. thaliana, in which 14 percent of the cytosines are methylated. While some methylation marks are maintained from generation to generation in A. thaliana, others are rapidly acquired or lost over time.-"To understand if these methylation changes can be subject to natural selection, researchers from the University of Groningen in the Netherlands, the University of Georgia, and the University of Minnesota mapped cytosine methylation at single-base resolution over as many as 32 generations of three different lines of the plant. The scientists then designed a model to estimate how quickly methylation at a particular location was gained or lost between generations and fit the model to their experimental data on the known locations of the methylated cytosines. They found that methylation changes are common throughout the genome. Some regions were more likely to lose methylation than to gain it, while others, such as transposable elements, were as much as 30 times more likely to gain methylation than lose it.-'Epigenetic mutations are about 100,000 times more likely than DNA sequence mutations, study coauthor Frank Johannes of Groningen said in a statement. Importantly, however, the epigenetic mutation rate is still low enough to be subject to natural selection, the authors wrote in their paper."

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dhw: In discussing this, we need always to bear in mind that innovations take place within individual organisms, and it is misleading - as the article does and you sometimes do - to talk of life/Nature/evolution being inventive.
DAVID: The increasing complexity from early to recent evolution is inventiveness conducted by living organisms. You are quibbling. The recent review article I presented showed that we have no idea how innovation occurs.-Of course we have no idea. That's why we come up with hypotheses. My IM hypothesis depends on the inventive mechanism within individual organisms, as you have agreed, and not on the inventiveness of Nature, which is a blanket concept that ignores individuality.-dhw: The point here is that since innovations take place within individual organisms, and even the smallest individual organisms are said to differ from one another (just as we do), it is possible that some are cleverer than others. That may explain why, when conditions change, some die, some adapt, and a few innovate.-DAVID: Agreed but we don't know how.-Your agreement is music to my ears.-dhw: I'm not talking about poor planning. I'm pointing out that you yourself have great difficulty reconciling a 99% extinction rate, plus countless weird and wonderful creatures and lifestyles... with your insistence that all of them serve or served the purpose of producing humans. But I quite understand how necessary it is for you to launch diversionary attacks.
DAVID: Not diversionary. Once again, if God did it and I don't understand why or how, that does not mean one should not be able to accept that God worked through an evolutionary process. My problem is I cannot read His mind as He plans His goals, nor can anyone else.-We both accept the evolutionary process, and I accept the possibility that your God may have started it all, but you DO try to read his mind.His goal, you say, was to produce humans; he did it by preprogramming or by dabbling, to which you have added an inventive mechanism that must also be preprogrammed or dabbled with, because it is not autonomous. So long as you put forward such hypotheses, it seems to me fair enough to examine their reasonableness in the light of what we can observe. You are more than happy to do so when confronted with the hypothesis of the autonomous inventive mechanism!

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DAVID: Not diversionary. Once again, if God did it and I don't understand why or how, that does not mean one should not be able to accept that God worked through an evolutionary process. My problem is I cannot read His mind as He plans His goals, nor can anyone else.
> 
> dhw: We both accept the evolutionary process, and I accept the possibility that your God may have started it all, but you DO try to read his mind.His goal, you say, was to produce humans;...... So long as you put forward such hypotheses, it seems to me fair enough to examine their reasonableness in the light of what we can observe. You are more than happy to do so when confronted with the hypothesis of the autonomous inventive mechanism!-I just look at the astounding result of evolution, us, and that guides my thinking. I have no idea why we should be the result of a natural process. And my thought processes are not one-dimensional. You know all the reasons I think there is a planning mind, the major one being I can not imagine an inorganic universe inventing consciousness. It already had to exist in a prior period.

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The Earth has four seasons, and gene expression for inflammation varies with the season all over the world:-http://www.the-scientist.com//?articles.view/articleNo/42959/title/Seasonal-Genes/-"The results indicate sort of a molecular signature of the seasons in humans, said Ghislain Breton, who studies circadian rhythms at the University of Texas at Houston, but was not involved in the work.-"In immune cells of the blood, the expression of genes that promote inflammation tends to rise in the winter and dip in the summer, the teamled by investigators at the University of Cambridgefound. The researchers hypothesized that these and other seasonal gene-expression patterns may help explain the seasonality of diseases, from infectious maladies like the flu to chronic conditions such as heart disease.-'We now know that all immune cell types have their own circadian clocks, as is the case for virtually all other organs and cell types in the body,' -***-"An outstanding question is whether expression levels of pro-inflammatory genes rise in the winter as an offensive measure against pathogens or as a response to heightened pathogen exposure.That's the chicken and egg' argument, said Todd."

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dhw: We both accept the evolutionary process, and I accept the possibility that your God may have started it all, but you DO try to read his mind. The goal, you say, was to produce humans; he did it by preprogramming or by dabbling, to which you have added an inventive mechanism that must also be preprogrammed or dabbled with, because it is not autonomous. So long as you put forward such hypotheses, it seems to me fair enough to examine their reasonableness in the light of what we can observe. You are more than happy to do so when confronted with the hypothesis of the autonomous inventive mechanism! -DAVID: I just look at the astounding result of evolution, us, and that guides my thinking. I have no idea why we should be the result of a natural process. And my thought processes are not one-dimensional. You know all the reasons I think there is a planning mind, the major one being I can not imagine an inorganic universe inventing consciousness. It already had to exist in a prior period.-I have the same problem as you, but have equal difficulty imagining a universal consciousness inventing itself, or simply being there without ever beginning, not to mention preprogramming or specially creating the weaverbird's nest when all it wants to do is create us.

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Only 3.3% of proteins match:-"In all they found a whopping 3.3% of the Lokiarchaeota proteins to be similar to eukaryotic proteins.-" That leads the evolutionists to declare that today's Lokiarchaeota shares a common ancestry with eukaryotes. From a scientific perspective that is not merely an unsupported conclusion, it is contradictory to a mountain of empirical evidence."-http://darwins-god.blogspot.com/2015/05/evolutionists-overreach-on-eukaryote.html-Here is a dissenting paper:-"In the grand schema of evolution, a mythical prokaryote to eukaryote cellular transition allegedly gave rise to the diversity of eukaryotic life (eukaryogenesis). One of the key problems with this idea is the fact that the prokaryotic world itself is divided into two apparent domains (bacteria and archaea) and eukarya share similarities to both domains of prokaryotes while also exhibiting many major innovative features found in neither. In this article, we briefly review the current landscape of the controversy and show how the key molecular features surrounding DNA replication, transcription, and translation are fundamentally distinct in eukarya despite superficial similarities to prokaryotes, particularly archaea. These selected discontinuous molecular chasms highlight the impossibility for eukarya having evolved from archaea. In a separate paper, we will address alleged similarities between eukarya and bacteria."-https://answersingenesis.org/biology/microbiology/information-processing-differences-between-archaea-and-eukarya/-And the same problem with descent from bacteria:-"Because bacteria, archaea, and eukarya contain unique mosaics of genetic features and biochemical similarities, it has been notoriously difficult for evolutionists to infer the molecular biological properties of a first or last eukaryotic common ancestor. Eukarya share similarities to both domains of prokaryotes (Bacteria and Archaea) while also exhibiting many innovative molecular features found in neither. Nevertheless, evolutionists postulate that some sort of mythical bacterial-archaeal precursor gave rise to the first eukaryotic cell. In a previous report, we showed that a vast chasm exists between archaea and eukarya in regard to basic molecular machines involved in DNA replication, RNA transcription, and protein translation. The differences in information processing mechanisms and systems are even greater between bacteria and eukarya, which we elaborate upon in this report. Based on differences in lineage-specific essential gene sets and in the vital molecular machines between bacteria and eukarya, we continue to demonstrate that the same unbridgeable evolutionary chasms existfurther invalidating the myth of eukaryogenesis."-https://answersingenesis.org/biology/microbiology/information-processing-differences-between-bacteria-and-eukarya/- Conclusion: We still have no idea how eukaryotes appeared.

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As predicted the human genome is way more complex than simply coding three letters for one amino acid:-http://www.uncommondescent.com/intelligent-design/guest-post-part-1-of-2-qualitative-complex-and-specified-information-within-genes-an-introduction/-"We all know that mutations in DNA can result in a different amino acid appearing in a protein. For example the DNA triplet codon if read as CTT would be translated to the amino acid Leucine (L; obviously via the mRNA intermediate). However, if there was a mutation from the C to the G, the frame would read GTT and this would be translated into a Valine (V). As we all further know, we can have deleterious, neutral, and beneficial mutations (in a given context). Additionally, a mutation in the third letter of the DNA triplet codon is often redundant at the level of the amino acid because of the redundant nature of the genetic code (perfectly optimised many would say). Obviously then, removal of or insertion of a new DNA base will have a much greater impact on the sequence (as you will shift the reading frame) and therefore is usually deleterious.-"Now I would make a request that I am not attacked for over-simplifying this concept, but to talk very simply about evolutionary change, mutations will occur at random in certain positions in the DNA sequence and this may be inherited (germline mutations) with a consequence of either deleterious, neutral or beneficial, with most thought to be near-neutral.-"There remains a question though that has fascinated me for a while, and led me to look at some examples of this. What if we discovered other layers of code within the same gene? What would be the impact of a mutation on this other code, relative to the foremost code? How much would this then limit the availability of more than one code to co-evolve, realistically?-***-"Now with the advance of proteomics and our ability to detect peptides and map the human proteome, a lot of information has come to light. In particular, it is apparent we are missing a lot of proteins found in cells but not annotated as genes in our databases. Surprisingly, for quite some time the field has held to the dogma of one gene, one Open Reading Frame (ORF) - and potentially many different proteins due to alternative splicing events, for example. Yet recent studies mapping the human proteome (A draft map of the human proteome. Kim et al. 2014. Nature. 509, 575-581) have yielded many MS spectra that cannot be assigned to annotated genes in the human genome.-***-" In this sense, Kim et al.`s study strongly supports the existence of the alternative proteome. Clearly, the alternative proteins detected by Kim et al. and by our team are the proverbial tip of the iceberg. A full map of the human proteome is thus still years away, and will require several important changes in our current thinking concerning the proteome and the concept that each mature mRNA only codes for one protein. "

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This was a truly amazing article. There is so much in it to pick from that it is hard to know where to start. One point that really piqued my interest is in the comment responses where there is a link to a study showing that the age of the gene is irrelevant. Even 'young' genes are absolutely necessary for life.

--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.

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Tony: This was a truly amazing article. There is so much in it to pick from that it is hard to know where to start. One point that really piqued my interest is in the comment responses where there is a link to a study showing that the age of the gene is irrelevant. Even 'young' genes are absolutely necessary for life.-My point has always been how much complexity do you need before one recognizes it has to have been designed? With all the interlocking parts, it cannot be done one step at a time.

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Tony: This was a truly amazing article. There is so much in it to pick from that it is hard to know where to start. One point that really piqued my interest is in the comment responses where there is a link to a study showing that the age of the gene is irrelevant. Even 'young' genes are absolutely necessary for life.
> 
> David: My point has always been how much complexity do you need before one recognizes it has to have been designed? With all the interlocking parts, it cannot be done one step at a time.-And I certainly agree with that. Interestingly, if you say "it cannot be done one step at a time", that precludes most definitions of evolution, and certainly precludes common descent.

--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.

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> > David: My point has always been how much complexity do you need before one recognizes it has to have been designed? With all the interlocking parts, it cannot be done one step at a time.
> 
> Tony: And I certainly agree with that. Interestingly, if you say "it cannot be done one step at a time", that precludes most definitions of evolution, and certainly precludes common descent.-Unless you choose my choice of theories: God guided an evolutionary process of His invention. The patterns of phonotype and the patterns of genes means to me He set up patterns to be used and the process followed very naturally. There are so many instants of apparent saltation that step-by-step is only Darwin's thought, with no proof. And now epigenetic research brings back Lamarkism. I view Darwin theory of evolution as dead.

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Trying to estimate human mutation rates by comparing genomes results in very uncertain estimates of rates. This puts the estimates of when ancestors branched off in great doubt:-http://www.nature.com/news/dna-mutation-clock-proves-tough-to-set-1.17079-"A slower molecular clock worked well to harmonize genetic and archaeological estimates for dates of key events in human evolution, such as migrations out of Africa and around the rest of the world1. But calculations using the slow clock gave nonsensical results when extended further back in time  positing, for example, that the most recent common ancestor of apes and monkeys could have encountered dinosaurs. Reluctant to abandon the older numbers completely, many researchers have started hedging their bets in papers, presenting multiple dates for evolutionary events depending on whether mutation is assumed to be fast, slow or somewhere in between.-"Last year, population geneticist David Reich of Harvard Medical School in Boston, Massachusetts, and his colleagues compared the genome of a 45,000-year-old human from Siberia with genomes of modern humans and came up with the lower mutation rate2. Yet just before the Leipzig meeting, which Reich co-organized with Kay Prüfer of the Max Planck Institute for Evolutionary Anthropology, his team published a preprint article3 that calculated an intermediate mutation rate by looking at differences between paired stretches of chromosomes in modern individuals (which, like two separate individuals' DNA, must ultimately trace back to a common ancestor). Reich is at a loss to explain the discrepancy. The fact that the clock is so uncertain is very problematic for us, he says. It means that the dates we get out of genetics are really quite embarrassingly bad and uncertain.'

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DNA is tightly wound making repair difficult on the side next to the histone:-http://phys.org/news/2015-07-mechanism-dna.html-"The dense packing allows DNA molecule with a length of about two meters to fit into a microscopic cell nucleus, but it makes significant surfaces of the DNA inaccessible for the repair enzymesthe proteins that manage the "repair" of damaged DNA regions. The damage of the DNA, if not repaired, leads to accumulation of mutations, cell death, and to the development of various diseases, including neurodegenerative, e.g. Alzheimer's disease.-***-"Scientists know quite a lot about the mechanism of the repair. It is known that for the synthesis of a protein, information written in the genetic code, which could be imagined as the manual for its assembly where triples of nucleotides match certain amino acids, should be taken out of the nucleus into the cytoplasm of the cell.-"Thin and long strand of the DNA is packed in the nucleus and can tear at the exit to the outside. Moreover, it cannot be sacrificed as the cell's nuclear DNA is is only present in two copies. Therefore, when it is necessary to synthesize specific protein, small region of DNA is unwound, the two strands are disconnected, and the information on the protein structure with one of the DNA strands is written in form of RNA, single-stranded molecule. The mRNA molecule, which serves as the template for making a protein, is synthesized by the principle of complementarity: each nucleotide pair corresponds to another one.-***-"During the transcription of information (its rewriting into RNA) the RNA polymerase enzyme "rides" on the DNA chain, and stops when it finds the break. Like a proofreader of a text, RNA polymerase after it is stalled, triggers a cascade of reactions, resulting in the repair enzymes fixing the damaged area. At the same time, the RNA polymerase cannot detect discontinuities present in the other DNA strand.-"'We have shown, not yet in the cell, but in vitro, that the repair of breaks in the other DNA chain, which is "hidden" in the nucleosome, is still possible. According to our hypothesis, it occurs due to the formation of special small DNA loops in the nucleosome, although normally DNA wounds around the histone "spool" very tightly",says Vasily M. Studitsky,"The loops form when the DNA is coiled back on nucleosome together with polymerase. RNA polymerase can "crawl" along the DNA loops nearly as well as on histone-free DNA regions, but when it stops near locations of the DNA breaks, it "panics", triggering the cascade of reactions to start DNA "repairs".-"During the experiment, special sites, where single-stranded breaks can be introduced by adding specific enzymes in a test tube, were inserted into the DNA. Then a single nucleosome transcribed by a single RNA molecule was studied. In this model system, which was developed in 2002 by the same group of scientists, histones were assembled on the molecule with an accuracy within one nucleotide. Having specially introduced breaks at precise locations on the DNA, the researchers examined the impact of breaks on the progression of the RNA polymerase. It turned out that only in nucleosomes, rather than in the histone-free DNA, the enzyme stopped, when the break was present in the other DNA strand. Wherein it did not stop before the break, but immediately after it. It was difficult enough to understand the mechanism that allows it to notice the damage at the "back" of RNA polymerase, as if it had "eyes on the back of the head", although, obviously, it does not have neither one nor the other.-"The analysis of breaks in different positions allowed to hypothesize that stalling of RNA polymerase is caused by the formation of the loop, which blocks movement of the enzyme. The findings open up a new direction for the work on the subject of DNA repair."

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Complex pathways that modify simple DNA coding and allow very precise responses to stimuli. Such high complexity requires planning to be developed:-http://www.sciencedaily.com/releases/2015/07/150731103659.htm-"Messenger (mRNA) molecules are a key component of protein biosynthesis. They are first transcribed as a "working copy" of the DNA and then translated into protein molecules. RNA-binding proteins such as RC3H1 (also known as ROQUIN) regulate the degradation of the mRNA molecules and thus prevent the production of specific proteins. Researchers at the Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC) have now shown that ROQUIN binds several thousand mRNA molecules. They demonstrated that ROQUIN also influences the gene regulator NF-kappaB, a key mediator of cellular inflammation and stress responses, in a new article published in Nature Communications.-"RC3H1/ROQUIN has already been described in previous studies as an RNA-binding protein that influences the stability of various mRNAs. Until now, however, it was unclear how ROQUIN recognizes mRNAs and how many mRNAs are regulated by ROQUIN. Dr. Yasuhiro Murakawa and Dr. Markus Landthaler of the Berlin Institute for Medical Systems Biology (BIMSB) of the MDC, in collaboration with the MDC research groups led by Professor Udo Heinemann, Dr. Stefan Kempa, Professor Claus Scheidereit, Dr. Jana Wolf and others, showed that ROQUIN binds to more than 3,800 different mRNAs, and they identified more than 16,000 sites to which the protein binds. Thus, ROQUIN appears to have greater influence on the regulation of gene expression than previously thought. In addition, the researchers identified the RNA recognition sequences of ROQUIN, thus providing insight into where protein-RNA interactions take place.-"ROQUIN preferentially binds mRNAs generated in response to DNA damage but also in the context of inflammatory responses. Many of the affected mRNAs encode for proteins, which in turn influence the activity of genes and thus regulate the production of other proteins. According to the researchers, ROQUIN contributes to the fine-tuning of the regulatory mechanisms.-"One of the target transcripts of ROQUIN is the mRNA coding for the protein A20 (also known as TNFAIP3). A20 serves as feedback control of the IkappaBalpha-kinase complex (IKK) that regulates the activation of the gene regulator NF-kappaB. The IKK/NF-kappaB pathway regulates the expression of a number of genes and is one of the key mediators in inflammatory and cellular stress responses, e.g. induced by DNA damage.-"To prevent the sustained activation of the IKK/NF-kappaB pathway, this signaling pathway itself induces the increased expression of proteins such as A20, accompanied by decreased IKK/NF-kappaB activation. By regulating the decay of the mRNA for A20, ROQUIN thus indirectly modulates the activity of the IKK/NF-kappaB pathway."

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An enzyme method is shown to repair DNA double-stranded breaks. This invokes the issue of irreducible complexity. How does evolution set up a repair mechanism before such mistakes occur? And if the mistakes are lethal as well they could be, this requires the repair mechanism to be on board at the same time the DNA is developed:-http://medicalxpress.com/news/2015-08-reveals-insight-dna.html-"DNA double-strand breaks (DSBs) are the worst possible form of genetic malfunction that can cause cancer and resistance to therapy. New information published this week reveals more about why this occurs and how these breaks can be repaired. 
 
"Scientists at The University of Texas MD Anderson Cancer Center reported their findings about the role of the enzyme fumarase in DNA repair in the Aug. 3, 2015 issue of Nature Cell Biology.-"'Our study showed that the enzymatic activity of the metabolic enzyme fumarase and its product, fumarate, are critical elements of the DNA damage response and that fumarase deficiency promotes tumor growth due to impairment of DNA repair," said Zhimin Lu, M.D., Ph.D., professor of Neuro-Oncology.-"Lu's team demonstrated that fumarase accomplishes this through a process critical for gene regulation and expression known as histone methylation. Many cancers are thought to result from misregulated histone methylation.-"Another crucial component of the DNA repair process is DNA-PK, a protein kinase that governs DNA damage response, helping to assure genetic stability. The researchers defined how DNA-PK and fumarase interact to increase histone methylation, allowing for DNA repair and restoration of healthy cells.-"'We know that histone methylation regulates DNA repair, but the mechanisms underlying this repair has not been fully understood," he said. "Our research revealed a 'feedback' mechanism that underlies DNA-PK regulation by chromatin-associated fumarase and the function of this fumarase in regulating histone methylation and DNA repair."-"This chain-of-event repair process occurs at the DSB regions and initiates a DNA damage "fix" by joining the tail ends of the double strand breaks."

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The genetic information must be preserved during mitosis. The mechanism is now found condensing the information into the nucleus:-http://phys.org/news/2015-08-scientists-key-proteins-segregate-vital.html-"Now, new research from The Wistar Institute has identified an interaction between proteins that provides a pivotal role in organizing chromosomes so that vital genetic information gets passed on safely.-"To understand how dividing cells protect and faithfully segregate genes that have been transcribed, researchers focused on a protein complex found in human cells called condensin. This set of proteins helps compact more than 20,000 protein-coding genes in the human genome into something that can fit inside the nucleus of each of our cells.-"Previously, Noma's lab showed that many genes are connected to centromeres. Centromeres are sites where two chromatids - copies of newly replicated chromosomes - are positioned to be properly split up during mitosis. Condensin mediates the clustering of RNA polymerase III-transcribed genes (abbreviated Pol III genes) and Pol II-transcribed "housekeeping" genes that are necessary for every cell to function properly. However, scientists did not know exactly how the condensin was being recruited to aid in this process.-"In this study, Noma and his colleagues identified the interactions of proteins that link condensin and mitosis. By studying mitosis in yeast, they were able to identify a subunit of condensin called Cnd2 that binds directly to a protein called the TATA box-binding protein (TBP). TBP is a general transcription factor required for every type of transcription. When Cnd2 binds to TBP, it recruits condensin onto Pol III genes and Pol II-transcribed housekeeping genes. When this happens, condensin tethers these genes to the centromeres so that when mitosis occurs, the genetic information remains protected and intact as the chromatins are split apart."-Comment: As usual highly complex molecular interactions control the process. Note the use of the word 'information'.

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In mammals one female chromosome is inactivated for proper genome function:-http://www.sciencedaily.com/releases/2015/08/150810110747.htm-"Nature ensures this does not happen: one of the X chromosomes is completely and permanently inactivated during a female's early development in the womb. The mechanism responsible for this inactivation is not yet fully understood. However, research into mice has shown that a ribonucleic acid (RNA) molecule called Xist plays a pivotal role in the process. Several hundred copies of this molecule attach themselves to one of the two X chromosomes. Scientists believe that these RNA molecules dock onto other molecules which then inactivate the chromosome.-***-"The scientists were thus able to isolate surviving stem cells and identify seven genes that are central to X inactivation. One of them is called Spen. Scientists were already aware that Spen produces a protein which allows it to bind with RNA and essentially prevents the genes from being read. In other experiments, ETH researchers were able to show that if a mouse cell lacks the Spen gene, the proteins responsible for altering chromosome structure are not able to accumulate as efficiently at the X chromosome.-***-"The genes for Xist and Spen are found in humans as well. Thus, as Wutz points out, this research offers us some insight into the human system -- at least at the theoretical level, as mouse genetics cannot be mapped directly to humans.-"A few years ago, a team of French researchers postulated that, in addition to Xist, humans also have another system which ensures that the single X chromosome in men and one of the two X chromosomes in women remain active. This activating system does not exist in mice. Due to the interplay of activating and inactivating factors, regulation of X chromosomes in humans might therefore be more complicated than originally thought. Geneticists wanting to understand these processes in detail still have plenty of work ahead of them."-Comment: Sexual reproduction allows for more variation in evolution, but created this problem and required this solution. Still looks planned to me.

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A very supportive new article:

https://aeon.co/essays/on-epigenetics-we-need-both-darwin-s-and-lamarck-s-theories?utm_...

"genetic mutation rates for complex organisms such as humans are dramatically lower than the frequency of change for a host of traits, from adjustments in metabolism to resistance to disease. The rapid emergence of trait variety is difficult to explain just through classic genetics and neo-Darwinian theory. To quote the prominent evolutionary biologist Jonathan B L Bard, who was paraphrasing T S Eliot: ‘Between the phenotype and genotype falls the shadow.’

***

"And the problems with Darwin’s theory extend out of evolutionary science into other areas of biology and biomedicine. For instance, if genetic inheritance determines our traits, then why do identical twins with the same genes generally have different types of diseases? ...How is it that hundreds of environmental contaminants can alter disease onset, but not DNA sequences? In evolution and biomedicine, the rates of phenotypic trait divergence is far more rapid than the rate of genetic variation and mutation – but why?

***

"At the start, Lamarck might have been pilloried as a religious heretic, but in modern times, it is the orthodoxy of science – and especially Darwin’s untouchable theory of evolution – that has caused his name to be treated as a joke. Yet by the end of his career, Darwin himself had come around; even without the benefit of molecular biology, he could see that random changes were not fast enough to support his theory in full.

"Lamarck’s – make sense. Indeed, although the vast majority of environmental factors cannot directly alter the molecular sequence of DNA, they do regulate a host of epigenetic mechanisms that regulate how DNA functions – turning the expression of genes up or down, or dictating how proteins, the products of our genes, are expressed in cells.

***

"All of these epigenetic mechanisms are critical and have unique roles in the molecular regulation of how DNA functions. The regulation of biology, it follows, will never involve a ‘genetic-only process’, nor an ‘epigenetic-only process’. Instead, the processes of epigenetics and genetics are completely integrated. One does not work without the other.

***

"Environmentally induced epigenetic transgenerational inheritance has now been observed in plants, insects, fish, birds, rodents, pigs and humans. It is, therefore, a highly conserved phenomenon. The epigenetic transgenerational inheritance of phenotypic trait variation and disease has been shown to occur across a span of at least 10 generations in most organisms, with the most extensive studies done in plants for hundreds of generations.

***

"Much as Lamarck suggested, changes in the environment literally alter our biology. And even in the absence of continued exposure, the altered biology, expressed as traits or in the form of disease, is transmitted from one generation to the next.
The environment plays an essential role in evolution. In a Darwinian sense, it determines which individuals and species will survive through the inexorable engine of natural selection. But a large number of environmental factors can also impact evolution and biology more directly, through epigenetic means: traits can shift through exposures to temperature and light or in response to nutritional parameters such as high fat or caloric restriction diets. A host of chemicals or toxins from plants and the general environment can impact phenotypic variation and health.

***

" Although the field of evolution is currently focused on neo-Darwinian genetic concepts, our findings suggest that epigenetics also has a role in the speciation and evolution of Darwin’s finches.

***

"Neo-Darwinian and neo-Lamarckian mechanisms both drive evolution, and they appear to be intertwined... Classic neo-Darwinian evolution involves genetic mutation and genetic variation as the main molecular mechanisms generating variation. Add to these mechanisms the phenomenon of environmental epigenetics, which directly increases trait variation, and you enhance the ability of the environment to mediate natural selection and evolution.

***

" embracing neo-Lamarckian ideas does nothing to challenge classic neo-Darwinian theory. The accepted sciences are essential and accurate, but part of a bigger, more nuanced story that expands our understanding and integrates all our observations into a cohesive whole. The unified theory explains how the environment can both act to directly influence phenotypic variation and directly facilitate natural selection,

***

"A unified theory of evolution should combine both neo-Lamarckian and neo-Darwinian aspects to expand our understanding of how environment impacts evolution. The contributions of Lamarck more than 200 years ago should not be discounted because of Darwin, but instead integrated to generate a more impactful and insightful theory. Likewise, genetics and epigenetics must not be seen as conflicting areas, but instead, integrated to provide a broader repertoire of molecular factors to explain how life is controlled."

Comment: Very supportive of Lamarck

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QUOTES: "At the start, Lamarck might have been pilloried as a religious heretic, but in modern times, it is the orthodoxy of science – and especially Darwin’s untouchable theory of evolution – that has caused his name to be treated as a joke. Yet by the end of his career, Darwin himself had come around; even without the benefit of molecular biology, he could see that random changes were not fast enough to support his theory in full.”
"A unified theory of evolution should combine both neo-Lamarckian and neo-Darwinian aspects to expand our understanding of how environment impacts evolution. The contributions of Lamarck more than 200 years ago should not be discounted because of Darwin, but instead integrated to generate a more impactful and insightful theory. Likewise, genetics and epigenetics must not be seen as conflicting areas, but instead, integrated to provide a broader repertoire of molecular factors to explain how life is controlled."

I couldn’t agree more. I did not know that Darwin had come round to Lamarckism. Good for him. It ties in neatly with his prophecy that fields of inquiry would be opened “on the direct action of external conditions”.

QUOTE: “Much as Lamarck suggested, changes in the environment literally alter our biology. And even in the absence of continued exposure, the altered biology, expressed as traits or in the form of disease, is transmitted from one generation to the next.”

Although of course far from conclusive, this supports the hypothesis that organisms have a mechanism that enables them not only to adapt to changing conditions, but also to exploit them by creating new “traits”: what I have called an autonomous inventive mechanism which, in the light of our discussion on the weaverbird, might also be called a designing intelligence.

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QUOTE: “Much as Lamarck suggested, changes in the environment literally alter our biology. And even in the absence of continued exposure, the altered biology, expressed as traits or in the form of disease, is transmitted from one generation to the next.”

dhw: Although of course far from conclusive, this supports the hypothesis that organisms have a mechanism that enables them not only to adapt to changing conditions, but also to exploit them by creating new “traits”: what I have called an autonomous inventive mechanism which, in the light of our discussion on the weaverbird, might also be called a designing intelligence.

And I've called epigenetic adaptations, not at a level of designed speciation, or intricate lifestyle design.

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A cave fish in Germany shows the adaptations that can occur in short periods. It is still the same species but changed:

https://www.newscientist.com/article/2126523-first-ever-cavefish-discovered-in-europe-e...

"The pale-coloured loach, shown above, is thought to have diverged from surface fish as glaciers from the last ice age receded some 16,000 to 20,000 years ago.

“'Our first genetic studies, plus knowledge of the geological history of the region, suggest the cave loach population is amazingly young, certainly not older than 20,000 years,” says Jasminca Behrmann-Godel at the University of Konstanz in Germany, who led the team that analysed the fish. “Despite this short time span, the fish show trademark adaptions to cave life compared with loaches from surface locations nearby, including a pale body colouration, much smaller eyes, plus larger nostrils and barbels.”

"It shows that adaptation to these subterranean habitats can be fast, and just a few thousand years might be enough for a fish to adapt to cave life, says Behrmann-Godel. “Cavefish could exist virtually everywhere in principle, and there’s no good reason to expect long evolution times for them to adapt to cave environments,” she says.

***

"knowledge of local geology enabled the birth of the new lineage to be dated. The cave system had been sealed for hundreds of thousands of years, but an opening called the Aach spring made it accessible when Alpine glaciers retreated northward around 16,000 to 20,000 years ago. This allowed surface loaches to enter the system for the first time, and they have followed their own evolutionary trajectory since.

"The cavefish’s eyes are about 10 per cent smaller than those of surface loaches, and their barbels are longer. They also lack scales. Most obviously, they have lost the dark brown blotches typical of surface loaches.

“'The barbels are enlarged in what seems to be a possible adaption to tactile sensing in the dark,” says Roi Holzman of Tel Aviv University in Israel, who studies how cavefish navigate. “In other cavefish species, barbels are also equipped with chemosensors to help them identify food in sediment, so these fish will need to be further studied to figure these mechanisms out.'”

Comment: this shows how rapidly epigenetic adaptations can occur to changes in environment. Reznick's guppies took only two years.

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QUOTE: "It shows that adaptation to these subterranean habitats can be fast, and just a few thousand years might be enough for a fish to adapt to cave life, says Behrmann-Godel. “Cavefish could exist virtually everywhere in principle, and there’s no good reason to expect long evolution times for them to adapt to cave environments,” she says.

DAVID’s comment: this shows how rapidly epigenetic adaptations can occur to changes in environment. Reznick's guppies took only two years.

A few thousand years is short in geological time, but I’d be surprised if cavefish took that long. The guppy example shows far greater rapidity! All this raises the whole question of the extent to which epigenetic changes (whether necessary or the result of exploration) may eventually lead to new species and even new organs. I’m thinking once more of the process that led from water-based to land-based life.

Not unrelated to this subject is the article you have given us (thank you for both articles) on plankton weaponry:

QUOTE: Now, new research finds that the tiny weapons of Nematodinium and related dinoflagellates are their own invention: Though the weapons look a lot like the stingers of jellyfish, the structures evolved independently, possibly because an arms race has developed in a plankton-eat-plankton world.

DAVID’s comment: A very simple animal has very complex weaponry. It is another example of convergence. I think this was not developed stepwise because of its complexity.

Of course I like the word “invention”. Even very simple organisms develop their own complex methods of survival. If your God did not preprogramme or personally dabble each of these weapons, and if they were not the product of chance mutations, we are left with the hypothesis that these simple animals invented them – which suggests an autonomous inventive intelligence (perhaps God-given). Interesting!

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dhw: Not unrelated to this subject is the article you have given us (thank you for both articles) on plankton weaponry:

QUOTE: Now, new research finds that the tiny weapons of Nematodinium and related dinoflagellates are their own invention: Though the weapons look a lot like the stingers of jellyfish, the structures evolved independently, possibly because an arms race has developed in a plankton-eat-plankton world.

DAVID’s comment: A very simple animal has very complex weaponry. It is another example of convergence. I think this was not developed stepwise because of its complexity.

dhw: Of course I like the word “invention”. Even very simple organisms develop their own complex methods of survival. If your God did not preprogramme or personally dabble each of these weapons, and if they were not the product of chance mutations, we are left with the hypothesis that these simple animals invented them – which suggests an autonomous inventive intelligence (perhaps God-given). Interesting!

A very simple organism inventing these highly complex weapons simply isn't going to happen. I stick with my comment. If these organisms need weapons of this magnitude for survival, it has to be a saltation.

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dhw: Not unrelated to this subject is the article you have given us (thank you for both articles) on plankton weaponry:

QUOTE: Now, new research finds that the tiny weapons of Nematodinium and related dinoflagellates are their own invention: Though the weapons look a lot like the stingers of jellyfish, the structures evolved independently, possibly because an arms race has developed in a plankton-eat-plankton world.

DAVID’s comment: A very simple animal has very complex weaponry. It is another example of convergence. I think this was not developed stepwise because of its complexity.

dhw: Of course I like the word “invention”. Even very simple organisms develop their own complex methods of survival. If your God did not preprogramme or personally dabble each of these weapons, and if they were not the product of chance mutations, we are left with the hypothesis that these simple animals invented them – which suggests an autonomous inventive intelligence (perhaps God-given). Interesting!

DAVID: A very simple organism inventing these highly complex weapons simply isn't going to happen. I stick with my comment. If these organisms need weapons of this magnitude for survival, it has to be a saltation.

A saltation simply means a jump – i.e. the invention arrived rapidly and not gradually. If organisms are capable of rapid adaptations, perhaps they are also capable of rapid innovations. Your comment, taken in conjunction with your other dogmas, means that your God either preprogrammed these different weapons 3.8 billion years ago or directly dabbled them in order to provide the energy to keep life going until he was able to achieve his only goal: to produce humans, which he could do without difficulty. And this makes sense to you?

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DAVID: A very simple organism inventing these highly complex weapons simply isn't going to happen. I stick with my comment. If these organisms need weapons of this magnitude for survival, it has to be a saltation.

dhw: A saltation simply means a jump – i.e. the invention arrived rapidly and not gradually. If organisms are capable of rapid adaptations, perhaps they are also capable of rapid innovations. Your comment, taken in conjunction with your other dogmas, means that your God either preprogrammed these different weapons 3.8 billion years ago or directly dabbled them in order to provide the energy to keep life going until he was able to achieve his only goal: to produce humans, which he could do without difficulty. And this makes sense to you?

Your proposal that organisms can jump with rapid adaptations is possible, but this can be through God's actions just as well. As for producing humans in 3.8 billion years, brings us to considering limits vs. God's choice of timing, nothing more. I believe He choose that length of time rather than He is limited. Perfect sense to me.

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dhw: A saltation simply means a jump – i.e. the invention arrived rapidly and not gradually. If organisms are capable of rapid adaptations, perhaps they are also capable of rapid innovations. Your comment, taken in conjunction with your other dogmas, means that your God either preprogrammed these different weapons 3.8 billion years ago or directly dabbled them in order to provide the energy to keep life going until he was able to achieve his only goal: to produce humans, which he could do without difficulty. And this makes sense to you?

DAVID: Your proposal that organisms can jump with rapid adaptations is possible, but this can be through God's actions just as well. As for producing humans in 3.8 billion years, brings us to considering limits vs. God's choice of timing, nothing more. I believe He choose that length of time rather than He is limited. Perfect sense to me.

There is no question that organisms do jump with rapid adaptations – we can witness that for ourselves with fish that adapt to pollution and with bacteria that seem able to adapt rapidly to any challenge thrown at them. It is innovation that is the problem. And yes, everything could be through God’s actions. He could be personally directing the behaviour of every individual organism on Earth including you and me. He can do whatever you want him to do.

I am aware that you have now rejected your own hypothesis that God might be limited. However, I’m afraid I can see no coherent logic in the hypothesis that God had only one purpose in life, namely to produce humans - which he could do “without any difficulty” - but chose first to specially design millions of other organisms and lifestyles and natural wonders (then get rid of 99% of them), such as the weaverbird’s nest and the monarch’s four-generational migration and the fly’s compound eye, in order to provide energy to keep life going until he produced the one organism he actually wanted to produce. (See “Purpose and design” for further discussion.)

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dhw: I am aware that you have now rejected your own hypothesis that God might be limited. However, I’m afraid I can see no coherent logic in the hypothesis that God had only one purpose in life, namely to produce humans - which he could do “without any difficulty” - but chose first to specially design millions of other organisms and lifestyles and natural wonders (then get rid of 99% of them), such as the weaverbird’s nest and the monarch’s four-generational migration and the fly’s compound eye, in order to provide energy to keep life going until he produced the one organism he actually wanted to produce.

The issue involved far more evidence than you list. One must look at the end product, the human being: the useful hands, the upright posture, the giant brain with its unexplained consciousness and capacity for complex planning,the rapid evolution when its brother organisms sat still. You either recognize the importance or you sluff it off. I see only purpose and directionality in the history. You are blinded by the side issue of natures wonders and the balance of nature which we agree only supplies energy so evolution can take a long time to reach the end point. Perhaps you should stick with your human chauvinism complaints as an excuse to avoid the obvious.

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dhw: I’m afraid I can see no coherent logic in the hypothesis that God had only one purpose in life, namely to produce humans - which he could do “without any difficulty” - but chose first to specially design millions of other organisms and lifestyles and natural wonders (then get rid of 99% of them), such as the weaverbird’s nest and the monarch’s four-generational migration and the fly’s compound eye, in order to provide energy to keep life going until he produced the one organism he actually wanted to produce.
DAVID: The issue involved far more evidence than you list. One must look at the end product, the human being: the useful hands, the upright posture, the giant brain with its unexplained consciousness and capacity for complex planning, the rapid evolution when its brother organisms sat still. You either recognize the importance or you sluff it off. I see only purpose and directionality in the history. You are blinded by the side issue of natures wonders and the balance of nature which we agree only supplies energy so evolution can take a long time to reach the end point. Perhaps you should stick with your human chauvinism complaints as an excuse to avoid the obvious.

You seem to have missed the point here, and yet grasped it on the “Purpose and design” thread! I have never denied the skills and the levels of consciousness that distinguish us from our fellow animals, and all my hypotheses allow for the possibility that your God has dabbled. The point at issue is not lack of purpose, but your dogmatic claim that humans were your God’s ONLY PURPOSE and “everything else” was related to that. I absolutely do not agree with the purpose you have assigned to the energy supply! Your God is apparently now saying to himself: “All I want to do is produce humans, which I can do without difficulty, but first I’ll design the weaverbird’s nest and lots and lots of other natural wonders, so that it will take me a long time to produce the only thing I really want to produce.” I’m sorry, but this sounds pretty silly to me.

BBella: So, by saying, "God showed the bird how to create it, probably by giving the bird a design to follow", it sounds as though you are pretty much saying God did send him to bird school! […]
David: I'm not sure about bird school. The design was more likely implanted into the bird's genome where it acted as an instinct.

So you’re not sure your God didn’t hold courses on nest-building, and presumably on butterfly migration, fishy camouflage, waspy parasitism etc. so that it would take a long time for him to produce humans. Until now, though, you have only offered preprogramming and dabbling, so the “more likely” explanation is that 3.8 billion years ago he said: “I only want to create humans, which I can do without any difficulty, but first I’ll preprogramme the weaverbird’s nest and lots and lots of other natural wonders so that it will take me longer to produce the only thing I want to produce.” You "see only purpose", and the purpose you see for all the natural wonders is for God to put off doing the one thing he wants to do! Fortunately, our discussions take a different turn under “Purpose and design”.

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dhw:The point at issue is not lack of purpose, but your dogmatic claim that humans were your God’s ONLY PURPOSE and “everything else” was related to that. I absolutely do not agree with the purpose you have assigned to the energy supply! Your God is apparently now saying to himself: “All I want to do is produce humans, which I can do without difficulty, but first I’ll design the weaverbird’s nest and lots and lots of other natural wonders, so that it will take me a long time to produce the only thing I really want to produce.” I’m sorry, but this sounds pretty silly to me.

What a convoluted interpretation: God's primary choice in creating humans may or may not have required a long time. It is entirely possible that God decided to take a while in getting there by slowly (in human terms) evolving humans. He might have been able to do it whenever He wanted, which appears to be Tony's view. This is why we have discussed pre-programming, dabbling , or limitations. We see the history, but when we plug in God's possible actions without Biblical interpretation we have no clear indisputable answer, and so we debate, each from a different viewpoint. I've deleted your further restatement of your comment as this answer suffices.

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dhw: The point at issue is not lack of purpose, but your dogmatic claim that humans were your God’s ONLY PURPOSE and “everything else” was related to that. I absolutely do not agree with the purpose you have assigned to the energy supply! Your God is apparently now saying to himself: “All I want to do is produce humans, which I can do without difficulty, but first I’ll design the weaverbird’s nest and lots and lots of other natural wonders, so that it will take me a long time to produce the only thing I really want to produce.” I’m sorry, but this sounds pretty silly to me.

DAVID: What a convoluted interpretation: God's primary choice in creating humans may or may not have required a long time. It is entirely possible that God decided to take a while in getting there by slowly (in human terms) evolving humans. He might have been able to do it whenever He wanted, which appears to be Tony's view. This is why we have discussed pre-programming, dabbling , or limitations. We see the history, but when we plug in God's possible actions without Biblical interpretation we have no clear indisputable answer, and so we debate, each from a different viewpoint. I've deleted your further restatement of your comment as this answer suffices.

I can only take each statement of yours as you make it. You wrote: "You are blinded by the side issue of natures wonders and the balance of nature which we agree only supplies energy so evolution can take a long time to reach the end point."
Nature’s wonders are not a side issue, they are part of THE issue under discussion. Until now your two dogmas have been that (a) God’s sole purpose (which you seem to equate with “end point”) was the production of humans, and (b) he personally designed all of Nature’s wonders. This creates a problem: why did he personally design all of Nature’s wonders if his sole purpose was to create humans? And yes indeed, you have floundered around with all the possibilities you have listed, but on Saturday 8 April you announced: “I explored, not vacillated, several avenues of thought. I’ve now concluded that God chose a lengthy evolutionary process. There was no delay.” This is confirmed by: "The balance of nature…only supplies energy so that evolution [as directed by your God] can take a long time to reach the end point" [humans]. You rejected limitations, so you are left with God choosing to design all the wonders so that it can take a long time for him to do the one thing he wants to do. You now seem to realize that this does not make sense, and so on Sunday 9 April you go back to a list of all the possibilities, there is no clear answer, and gone is Saturday’s decisive conclusion. Quite right too. This leaves us with the options discussed under “Purpose and design”, including what you have at last accepted as a possibility: God’s sole purpose may NOT have been to produce humans, and God may NOT have designed all the natural wonders. Why not leave it at that?

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dhw: I can only take each statement of yours as you make it. You wrote: "You are blinded by the side issue of natures wonders and the balance of nature which we agree only supplies energy so evolution can take a long time to reach the end point."
Nature’s wonders are not a side issue, they are part of THE issue under discussion. Until now your two dogmas have been that (a) God’s sole purpose (which you seem to equate with “end point”) was the production of humans, and (b) he personally designed all of Nature’s wonders. This creates a problem: why did he personally design all of Nature’s wonders if his sole purpose was to create humans?

And my answer is constant, balance of nature for energy supply.

dhw: And yes indeed, you have floundered around with all the possibilities you have listed, but on Saturday 8 April you announced: “I explored, not vacillated, several avenues of thought. I’ve now concluded that God chose a lengthy evolutionary process. There was no delay.” This is confirmed by: "The balance of nature…only supplies energy so that evolution [as directed by your God] can take a long time to reach the end point" [humans]. You rejected limitations, so you are left with God choosing to design all the wonders so that it can take a long time for him to do the one thing he wants to do.

I'm still fully in favor of the thesis that God chose a lengthy time, and arranged for a copious food supply.

dhw:You now seem to realize that this does not make sense, and so on Sunday 9 April you go back to a list of all the possibilities, there is no clear answer, and gone is Saturday’s decisive conclusion. Quite right too. This leaves us with the options discussed under “Purpose and design”, including what you have at last accepted as a possibility: God’s sole purpose may NOT have been to produce humans, and God may NOT have designed all the natural wonders. Why not leave it at that?

Because I do not accept that interpretation. My list was to show the various ways I have previously proposed to interpret God's actions in producing humans. I thought my intent in that review was clear. I also believe your theories are possible, but not probable. This is a fluid discussion.

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dhw: Nature’s wonders are not a side issue, they are part of THE issue under discussion. Until now your two dogmas have been that (a) God’s sole purpose (which you seem to equate with “end point”) was the production of humans, and (b) he personally designed all of Nature’s wonders. This creates a problem: why did he personally design all of Nature’s wonders if his sole purpose was to create humans?
DAVID: And my answer is constant, balance of nature for energy supply.

So once again you have God designing the weaverbird’s nest in order to supply energy so that life could continue until he produced humans. This is why I use the nest as my prime example. It doesn’t make sense.

dhw: You rejected limitations, so you are left with God choosing to design all the wonders so that it can take a long time for him to do the one thing he wants to do.
DAVID: I'm still fully in favor of the thesis that God chose a lengthy time, and arranged for a copious food supply.

If God exists, there can be no doubt that it took longer for him to produce humans than to produce dinosaurs, and that whatever system he used resulted in there being enough food for some species to survive. And so there is nothing controversial in what you have just written. The problem arises when you say that God’s sole purpose was to produce humans, and he chose to take a long time over doing so, and designed the weaverbird’s nest to provide energy while he was taking a long time to produce humans. THAT is what did not make sense to you earlier, and THAT is what has resulted in your different explanations which one day you regard as conclusions and the next day regard only as possibilities.

dhw:You now seem to realize that this does not make sense, and so on Sunday 9 April you go back to a list of all the possibilities, there is no clear answer, and gone is Saturday’s decisive conclusion. Quite right too. This leaves us with the options discussed under “Purpose and design”, including what you have at last accepted as a possibility: God’s sole purpose may NOT have been to produce humans, and God may NOT have designed all the natural wonders. Why not leave it at that?
DAVID: Because I do not accept that interpretation. My list was to show the various ways I have previously proposed to interpret God's actions in producing humans. I thought my intent in that review was clear. I also believe your theories are possible, but not probable. This is a fluid discussion.

I do not ask you to accept any interpretation. I am fully aware of all your attempts to explain the dichotomy between what have previously been your two dogmatic beliefs, and welcome the fact that you regard my different hypotheses as possible, which means you accept the possibility that one or both of your dogmatic beliefs may be wrong.

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DAVID: And my answer is constant, balance of nature for energy supply.

dhw: So once again you have God designing the weaverbird’s nest in order to supply energy so that life could continue until he produced humans. This is why I use the nest as my prime example. It doesn’t make sense.

You've backtracked. You've admitted food energy supply is needed for evolution to continue. The nest is part of a eco-niche. The bush of life is made up of hundreds/thousands of them.

DAVID: I'm still fully in favor of the thesis that God chose a lengthy time, and arranged for a copious food supply.

dhw: If God exists, there can be no doubt that it took longer for him to produce humans than to produce dinosaurs, and that whatever system he used resulted in there being enough food for some species to survive. And so there is nothing controversial in what you have just written. The problem arises when you say that God’s sole purpose was to produce humans, and he chose to take a long time over doing so, and designed the weaverbird’s nest to provide energy while he was taking a long time to produce humans. THAT is what did not make sense to you earlier, and THAT is what has resulted in your different explanations which one day you regard as conclusions and the next day regard only as possibilities.

Our discussion help me to study the history and formulate final conclusions. I may wander around, but I've gotten to a firm point: God chose a long time to evolve humans, perhaps because He felt some limitations (but we can't be sure). To supply energy for life in a prolonged process He created the full bush of life with all its odd lifestyles including strange nests. Tony's point that God provided the Natures wonders also for our enjoyment may apply.

DAVID: I also believe your theories are possible, but not probable. This is a fluid discussion.[/i]

dhw: I do not ask you to accept any interpretation. I am fully aware of all your attempts to explain the dichotomy between what have previously been your two dogmatic beliefs, and welcome the fact that you regard my different hypotheses as possible, which means you accept the possibility that one or both of your dogmatic beliefs may be wrong.

Since we have preferences not proven beliefs, of course one or all may be wrong.

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DAVID: And my answer is constant, balance of nature for energy supply.
dhw: So once again you have God designing the weaverbird’s nest in order to supply energy so that life could continue until he produced humans. This is why I use the nest as my prime example. It doesn’t make sense.
DAVID: You've backtracked. You've admitted food energy supply is needed for evolution to continue. The nest is part of a eco-niche. The bush of life is made up of hundreds/thousands of them.

There is no backtracking. The fact that food is needed for evolution to continue and that there are hundreds of thousands of eco-niches provides not the slightest support for your insistence that every eco-niche was created in order to keep life going until humans could be produced! That is the whole point of this discussion.

DAVID: Our discussion help me to study the history and formulate final conclusions. I may wander around, but I've gotten to a firm point: God chose a long time to evolve humans, perhaps because He felt some limitations (but we can't be sure). To supply energy for life in a prolonged process He created the full bush of life with all its odd lifestyles including strange nests. Tony's point that God provided the Natures wonders also for our enjoyment may apply.

If your God exists, and since humans took a relatively long time to appear, it is perfectly reasonable to assume that God knew what he was doing and took a relatively long time to produce humans. The whole question is why! It is the rigidity of your two basic premises (humans as the sole purpose, to which everything else is related) that leads to all the “wandering around”, and your firm point is as wishy-washy as ever: he chose to take a long time and you don’t know why, but perhaps he was forced to do so by limitations (the opposite of choice), or perhaps not. Why not accept the possibility that there was no “delay” because your God simply didn’t set out to produce humans and/or everything else was not related to that purpose? As for “our enjoyment”, do you honestly believe that Nature’s wonders only arrived after humans appeared? Why not accept the possibility that Nature’s wonders were not for OUR enjoyment but for your God’s?

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dhw: If your God exists, and since humans took a relatively long time to appear, it is perfectly reasonable to assume that God knew what he was doing and took a relatively long time to produce humans. The whole question is why! ... Why not accept the possibility that there was no “delay” because your God simply didn’t set out to produce humans and/or everything else was not related to that purpose? As for “our enjoyment”, do you honestly believe that Nature’s wonders only arrived after humans appeared? Why not accept the possibility that Nature’s wonders were not for OUR enjoyment but for your God’s?

Tony's response yesterday answers your question of 'why' by pointing out working through stages of development: Wednesday, April 12, 2017, 03:09. Enjoyment was also one of Tony's suggestions. When we arrived the wonders were there for our enjoyment. Pre-planning or just balance of nature for food supply?

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C. elegans can transfer avoidance for four generations, and then it disappears:

https://www.sciencedaily.com/releases/2019/06/190606150247.htm

"Princeton University researchers have discovered that learned behaviors can be inherited for multiple generations in C. elegans, transmitted from parent to progeny via eggs and sperm cells.

***

"'In their natural environment, worms come into contact with many different bacterial species. Some of these are nutritious food sources, while others will infect and kill them," said Murphy, a professor in Princeton's Department of Molecular Biology and the Lewis-Sigler Institute for Integrative Genomics. "Worms are initially attracted to the pathogen Pseudomonas aeruginosa, but upon infection, they learn to avoid it. Otherwise they will die within a few days."

***

"They found that when mother worms learned to avoid pathogenic P. aeruginosa, their progeny also knew to avoid the bacteria. The natural attraction of offspring to Pseudomonas was overridden even though they had never previously encountered the pathogen. Remarkably, this inherited aversive behavior lasted for four generations, but in the fifth generation the worms were once again attracted to Pseudomonas. In another surprise, the researchers observed that inheritance of learned avoidance was not universal for all pathogenic bacteria; although mother worms could learn to avoid the pathogenic bacterium Serratia marcescens, which is less abundant than Pseudomonas in C. elegans' environment, this aversion was not passed down to offspring. Intrigued, the researchers set out to explore what controls transmission of P. aeruginosa avoidance behavior across generations.

"The authors showed that C. elegans mothers must actually become ill from ingesting P. aeruginosa in order to transmit avoidance to future generations; exposure to odors emitted by the pathogen wasn't sufficient to provoke avoidance. Nonetheless, neuronal sensory pathways are important for inherited avoidance, because avoidance behavior in both mothers and their progeny was associated with upregulated expression of several neuronally-associated genes. Among these, elevated expression of the TGF-β ligand daf -7 in mothers was needed for progeny to inherit pathogen aversion. Moore and her colleagues found that daf-7 expression in a certain type of sensory neuron, ASI neurons, correlated strongly with inherited avoidance behavior.

"'The process of inheriting this learned avoidance [also] requires the activity of small RNAs called piRNA," Murphy said. piRNAs have been implicated in other transgenerational epigenetic inheritance pathways in C. elegans, where they're thought to silence gene expression and indirectly regulate DNA packing. The researchers found that the piRNA-associated protein PRG-1, while not necessary for C. elegans mothers to learn avoidance of P. aeruginosa, was required for increased daf-7 expression in progeny, and for their inherited avoidance behavior. Whether piRNAs and PRG-1 operate primarily in the mother, the progeny, or both to promote inheritance of avoidance behavior isn't yet known.

"Importantly, expression of daf-7 remains elevated in the ASI neurons of progeny for four generations, then returns to basal levels in the fifth generation, which is when the inherited avoidance behavior also disappears. As Murphy points out, although inheritance of avoidance behavior provides a survival advantage, it's also necessary for this avoidance behavior to eventually go away. That's because P. aeruginosa is only pathogenic at high temperatures; at lower temperatures, it's increasingly safe to eat, as are other Pseudomonas species. If the pathogenic threat is temporary, the eventual lapsing of inherited avoidance allows future generations to return to feasting on nutritious Pseudomonas.

"'Transgenerational learned pathogenic avoidance is mediated by TGF-beta and the Piwi/PRG-1 Argonaute pathway" by Rebecca S. Moore, Rachel Kaletsky, and Coleen T. Murphy appears in the June 13 issue of Cell."

Comment: a glimpse into the complex genomic processes that cause epigenetic modifications. So complex that design must have been used

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Epigenetic marks may last forever, changing the idea they were temporary:

https://phys.org/news/2020-01-fossil-upend-basic-tenet-evolutionary.html

"...a UC San Francisco-led research team has discovered the first conclusive evidence that selection may also occur at the level of the epigenome—a term that refers to an assortment of chemical "annotations" to the genome that determine whether, when and to what extent genes are activated—and has done so for tens of millions of years. This unprecedented finding subverts the widely accepted notion that over geologic timescales, natural selection acts exclusively on variation in the genome sequence.

***

"In a study published Jan. 16, 2020 in the journal Cell, the researchers show that Cryptococcus neoformans—a pathogenic yeast that infects people with weakened immune systems and is responsible for about 20 percent of all HIV/AIDS-related deaths—contains a particular epigenetic "mark" on its DNA sequence, which, based on their lab experiments and statistical models, should have disappeared from the species sometime during the age of the dinosaurs.

"But the study shows that this methylation mark—so named because it's created through a process that attaches a molecular tag called a methyl group to the genome—has managed to stick around for at least 50 million years—maybe as long as 150 million years—past its predicted expiration date. This amazing feat of evolutionary tenacity is made possible by an unusual enzyme and a hefty dose of natural selection.

"What we've seen is that methylation can undergo natural variation and can be selected for over million-year time scales to drive evolution," explained Hiten Madhani, MD, Ph.D., professor of biochemistry and biophysics at UCSF and senior author of the new study. "This is a previously unappreciated mode of evolution that's not based on changes in the organism's DNA sequence."

***

"In the new study, Madhani and his collaborators show that hundreds of millions of years ago, the ancestor of C. neoformans had two enzymes that controlled DNA methylation. One was what's known as a "de novo methyltransferase," which was responsible for adding methylation marks to "naked" DNA that had none. The other was a "maintenance methyltransferase" that functioned a bit like a molecular Xerox. This enzyme copied existing methylation marks, which had been put in place by the de novo methyltransferase, onto unmethylated DNA during DNA replication. And like every other species with an epigenome that includes methylation, the ancestor of C. neoformans had both types of methyltransferase.

"But then, sometime during the age of the dinosaurs, the ancestor of C. neoformans lost its de novo enzyme. Its descendants have been living without one since then, making C. neoformans and its closest relatives the only species alive today known to have DNA methylation without a de novo methyltransferase. "We didn't understand how methylation could still be in place since the Cretaceous period without a de novo enzyme," said Madhani.

***

"Asked why evolution would select for these particular marks, Madhani explained that "one of methylation's major functions is genome defense. In this case we think it's for silencing transposons."

"Transposons, also known as jumping genes, are stretches of DNA that are able to extract themselves from one part of the genome and insert themselves into another. If a transposon were to insert itself into the middle of a gene needed for survival, that gene may no longer function and the cell would die. Therefore, transposon-silencing methylation provides an obvious survival advantage, which is exactly what's needed to drive evolution."

comment: I don't how this happened, but Lamarck is alive and well. Epigenetics can definitely play a role in progressive evolution

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Experience in Jews who are descendants of the Holocaust victims. There are methylation changes and a difference in anxiety levels:-http://www.jewishworldreview.com/0615/jewish_guilt_genes.php3-"Researchers studying the children and grandchildren of Holocaust survivors have found that they have higher rates of post-traumatic stress after enduring car accidents, possibly due to modifications in their stress hormone system inherited from their survivor parents"-'Do uniquely Jewish experiences from the past  like the pogroms our great-grandparents escaped  affect the way we behave today? I think that's a valid question, Szyf says.-
"Do uniquely Jewish experiences from the past  like the pogroms our great-grandparents escaped  affect the way we behave today?'-'Jews that left Europe were highly self-selected for their survival skills and perseverance, he adds, which might have been due to their genetic tendencies rather than epigenetic changes.-"In the end, though, it may not matter whether inherited genes or inherited methylation of those genes or plain-old nurture plays the dominant role.-'Jews have always tended to lead lives that emphasized education, family structure and religious values, Szyf says. So it should come as no surprise that these values have been passed on."

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Chinese famine in the 1950's create high blood sugar in progeny for two generations:

http://medicalxpress.com/news/2016-12-famine-metabolism-successive.html

"The increased risk of hyperglycemia associated with prenatal exposure to famine is also passed down to the next generation, according to a new study of hundreds of families affected by widespread starvation in mid-20th Century China.

"Hyperglycemia is a high blood glucose level and a common sign of diabetes. The new study in the American Journal of Clinical Nutrition reports that hundreds of people who were gestated during a horrific famine that afflicted China between 1959 and 1961 had significantly elevated odds of both hyperglycemia and type 2 diabetes. Even more striking, however, was that their children also had significantly higher odds of hyperglycemia, even though the famine had long since passed when they were born.

***

"Among 983 people gestated during the famine years, 31.2 percent had hyperglycemia and 11.2 percent had type 2 diabetes. By comparison, among 1,085 people gestated just after the famine ended, the prevalence of hyperglycemia was 16.9 percent, and the prevalence of type 2 diabetes as 5.6 percent. Controlling for factors such as gender, smoking, physical activity, calorie consumption and body-mass index, the researchers calculated that in utero famine exposure was associated with 1.93-times higher odds of hyperglycemia and a 1.75 times greater chance of type 2 diabetes.

"The next generation sustained the significant risk of hyperglycemia when both parents had been famine-exposed. Overall in the second generation, hyperglycemia prevalence were 5.7 percent for 332 people with no famine-exposed parents, 10.0 percent for 251 people with famine-exposed fathers, 10.6 percent for 263 people with famine-exposed mothers, and 11.3 percent for the 337 people for whom both parents had famine exposure. Adjusting for all the same lifestyle factors, the offspring of two famine-exposed parents had 2.02 times the odds of hyperglycemia of people with no famine-exposed parents. The odds of hyperglycemia from one-parent exposure were also substantially elevated but not quite statistically significant.

"The odds of type 2 diabetes were not statistically significant after adjustment for multiple comparisons among the second generation, but co-corresponding author Dr. Sun Changhao, professor of nutrition and dean of the School of Public Health at Harbin, noted that these people were only in their 20s and 30s and could still be at increased risk as they age and that the research team will continue to follow up on these participants.

"Because the study only shows an association between metabolic changes and in utero famine exposure, it can't prove causality or the biological mechanism underlying a cause. But prior research on the effects of famine in humans and in laboratory animals suggest that famine does indeed cause such health risks, the study authors said.

"'It is indeed a remarkable finding that is consistent what with what one would have expected from prior findings from animal experiments," said lead author Jie Li, a Brown postdoctoral fellow."

Comment: It is an interesting finding, but the underlying mechanism is not fully explained. Probably epigenetic effects in the genome.

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Latest study of an enzyme:

https://medicalxpress.com/news/2022-03-advances-dna.html

"The fact that DNA can be repaired after it has been damaged is one of the great mysteries of medical science, but pathways involved in the repair process vary during different stages of the cell life cycle. In one of the repair pathways known as base excision repair (BER), the damaged material is removed, and a combination of proteins and enzymes work together to create DNA to fill in and then seal the gaps.

***

"In BER, an enzyme called polymerase beta (PolyB) fulfills two functions: It creates DNA, and it initiates a reaction to clean up the leftover "chemical junk." Through five years of study, Suo's team learned that by capturing PolyB when it is naturally cross-linked with DNA, the enzyme will create new genetic material at a speed 17 times faster than when the two are not cross-linked. This suggests that the two functions of PolyB are interlocked, not independent, during BER.

'The research improves the understanding of cellular genomic stability, drug efficacy and resistance associated with chemotherapy.

***

"This research examined naturally cross-linked PolyB and DNA, unlike previous research that mimicked the process. Prior to this study, researchers had identified the enzymes involved in BER but didn't fully understand how they worked together.

"When we have nicks in DNA, bad things can happen, like the double strand breaking in DNA," said Thomas Spratt, a professor of biochemistry and molecular biology at Penn State University College of Medicine who was not a part of the research team. "What Zucai found provides us with something we didn't understand before, and he used many different methods to reach his findings."

"In addition to revealing PolyB's functional dynamics, the team proposed a modified BER pathway and is testing the pathway in human cells.

"'We have been able to dig deeper into a fundamental pathway for which the pioneer Tomas Lindahl shared the Nobel Prize in Chemistry in 2015," Suo said."

Comment: the logical assumption I make is this is a designed damaged control system which appeared the same time DNA appeared as a living code. Since we know damage happens the appearance had to be simultaneous with the start of the use of DNA

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A new study in bacteria and yeast:

https://phys.org/news/2022-03-ribosomes-collide-bacteria-molecular.html

"Molecular machines known as ribosomes quite literally follow instructions encoded in a linear strand of genetic material. As they travel along the strand, they build a protein. Sometimes, though, this machinery malfunctions.

"Earlier research in yeast, whose cells resemble those of animals, had shown that ribosomes stall when they get into trouble. Like a car that stops too suddenly, a stalled ribosome can be rear-ended by the one behind it. Green's lab had previously identified a yeast molecule that responds to these collisions. Like a tiny Jaws of Life, the molecule cuts the stalled ribosome free. It's the first step in a rescue effort that ultimately lets the cell salvage and reuse these valuable, protein-making machines.

"Bacterial cells' ribosomes can get jammed up too, but scientists doubted that bacteria respond to collisions the same way yeast do. That's because researchers already knew that bacteria have their own distinct method for rescuing wrecked ribosomes, says Jamie Cate, a biochemist and structural biologist at the University of California, Berkeley, who was not involved in the project.

"No one knew exactly what kicked off the bacterial rescue effort, but they expected that it would be something entirely different from yeast, Cate says. Instead, the new research suggests that both bacteria and yeast initiate this process the same way—by summoning blade-like first responders.

***

"In Green's lab in Baltimore, Buskirk and first author Kazuki Saito identified the first responder in bacteria as a molecule called SmrB and explored how it carried out its job. Beckmann's structure "was the final piece of the puzzle," Buskirk says.

***

"Biochemical experiments revealed that SmrB, like its yeast counterpart, cuts the wrecked ribosomes apart. And not only do the two molecules share a job description, bacterial SmrB and its yeast counterpart are also close relatives, the team found. Researchers haven't yet been able to visualize how the yeast version interacts with ribosomes during a collision. So, the similar but simpler SmrB may give scientists a foothold for understanding how the process works in other organisms.

"'Everything else about these rescue pathways is very different," Green says. "We didn't anticipate we would find an aspect that appears to be universal.'"

Comment: this system must be universal or life would end. This is like all the other editing systems discovered. They had to be present at the initiation of DNA coding and decoding. For me it clearly shows God, the designer, recognized in his design where trouble could happen from molecular mistakes

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Found in mice, a newly found coding base thought to be epigenetically originated:-http://www.washingtonpost.com/entertainment/tv/unreal-and-another-period-from-female-creators-sharp-jabs-at-reality/2015/06/22/c7944832-16cc-11e5-9ddc-e3353542100c_story.html?wpisrc=nl_headlines&wpmm=1-If true this opens up a much more Lamarckian view of innovation.-
"An epigenetic mark known as 5-formylcytosine (5fC) may be more than a transitory state that helps regulate gene expression. According to a study published yesterday (June 22) in Nature Chemical Biology, 5fC is stable in the mouse genome and may represent a fifth nucleotide in the DNA alphabet.-'It had been thought this modification was solely a short-lived intermediate, but the fact that we've demonstrated it can be stable in living tissue shows that it could regulate gene expression and potentially signal other events in cells, coauthor Shankar Balasubramanian of the Cancer Research UK Cambridge Institute said in a press release.-"While the function of the modified baseessentially a methylated cytosine with added oxygenremains unclear, its position within the genome points to a role in gene expression. This modification to DNA is found in very specific positions in the genomethe places which regulate genes, lead author Martin Bachman, who conducted the research while at the University of Cambridge, said in the release. In addition, it's been found in every tissue in the bodyalbeit in very low levels. High-resolution mass spectrometry revealed 5fC to be most common in the mouse brain, but even there it was present at only 10 parts per million or less.-"But when the researchers enriched cultures of mouse cells or mice's diets with stable isotopes of carbon and hydrogen, they found no uptake into 5fC bases, suggesting the modification is stable.-'If 5fC is present in the DNA of all tissues, it is probably there for a reason, added Balasubramanian. This will alter the thinking of people in the study of development and the role that these modifications may play in the development of certain diseases.'

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He is being resurrected:-http://darwins-god.blogspot.com/2015/07/its-official-lamarckism-has-now-joined.html-:We suggest that the original Chicken or Egg dilemma (how did chicken come to be?) is not a paradox, it is explained by evolution, and that each evolutionary change could map to either a pure Darwinian world (or Weissmanian really), in which the metaphorical Egg must have preceded the Chicken, or to a Lamarckian world in which the metaphorical chicken comes first.-"Soon Lamarckian mechanisms will be self-evident. Evolutionists have already begun to prepare the way for this tectonic shift in their thinking. First, their venerable prophet must be rescued and protected from the fallout."

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In C elegans, the tiny round worm, starvation can have lasting effects over two generations:-http://phys.org/news/2015-07-starvation-effects.html-"Baugh and his Duke team starved thousands of C. elegans worms for one or eight days at the first stage of larval development after hatching. When feeding was resumed, the worms that had starved longer grew more slowly, and ended up smaller and less fertile. They also proved more susceptible to a second bout of starvation.-"The starved worms also had offspring that were smaller, fewer and less fertile. However, these children and grandchildren of famine turned out to be more resistant to starvation and a heat-tolerance test. More of them were also male instead of the usual hermaphroditic, self-fertilizing form.-"In their natural conditions, it appears the worms are able to increase their growth rate and fertility in times of plenty and then to turn these traits back down in hard times. "They have a memory of famine," Baugh said. The net result is "a combination of fitness costs and benefits that unfolds over generations," the authors wrote in a study that appears early online in the journal Genetics."

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Work in rats shows epigenetic changes in first generation offspring with more changes in third generation:-http://www.sciencedaily.com/releases/2015/08/150803083351.htm-"Earlier work by Skinner has found epigenetic effects from a host of environmental toxicants, connecting plastics, pesticides, fungicide, dioxin and hydrocarbons to diseases and abnormalities as many as three generations later.-"His recent study exposed gestating female rats to the fungicide vinclozolin. Sperm in the first generation of male offspring showed epimutations, or alterations in the methyl groups that stick to DNA and affect its activation.-"Third generation, or great-grand offspring, had increased genetic mutations, which the researchers saw in increased DNA structure changes known as copy-number variations. Multiple generations of control animals had no such variations.-"This, said Skinner, suggests that environment has a more important role in mutations, disease and evolution than previously appreciated, and appears to be one of the main drivers of intergenerational changes, not simply a passive component. In short, Skinner and his colleagues say, the environment and epigenetics can drive genetics.-"'There's not a type of genetic mutation known that's not potentially influenced by environmental epigenetic effects," Skinner said."

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I would like to see the results of this at say 5, 10, and 20 generations. Are the effects permanent? If the environment is changed, the the changes revert?

--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.

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Histones are spools around which DNA winds to fit into the nucleus. Modifying histones can change inheritance for two generations out:-http://www.sciencedaily.com/releases/2015/10/151008142622.htm-"The researchers were curious about whether histones might play a role in transmitting heritable information from fathers to their offspring because they are part of the content of sperm transmitted at fertilization. Histones are distinct from our DNA, although they combine with it during cell formation, acting a bit like a spool around which the DNA winds.-"So, to test their theory about the possible role of histones in guiding embryo development the researchers created mice in which they slightly altered the biochemical information on the histones during sperm cell formation and then measured the results. (It's a bit like putting a nick in a spool of thread and seeing how it affects the way the thread then loops around the spool.) They then studied the effects on the offspring.-"What they discovered was that there were dire consequences for the offspring both in terms of their development e.g. where offspring were prone to birth defects and had abnormal skeletal formation, and in terms of their surviving at all. Moreover, what was most surprising, was that these effects could still be seen two generations later.-"'When we saw the decreased survivability across generations and the developmental abnormalities we were really blown away as it was never thought that altering something outside the DNA, i.e. a protein, could be involved in inheritance," said Sarah Kimmins, from McGill's Dept. of Animal Science, and one of the lead authors on the paper.-"Kimmins added, "These findings are remarkable because they indicate that information other than DNA is involved in heritability. The study highlights the critical role that fathers play in the health of their children and even grand-children. Since chemical modifications on histones are susceptible to environmental exposures, the work opens new avenues of investigation for the possible prevention and treatment of diseases of various kinds, affecting health across generations.'"-Comment: the demonstrated complexity of the genome continues to increase beyond an possibility it occurred naturally.

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Male sperm using microRNAs can do this for one generation, more not known"-http://www.the-scientist.com//?articles.view/articleNo/44273/title/Sperm-RNAs-Transmit-Stress/-"In the past several years, it has become clear that parents' life experiences can alter germ cells epigenetically, and that events in parents' lives can influence the health and behavior of their children and even grandchildren. But it can be difficult to establish a causal connection between epigenetic changes and changes in behavior and health. Researchers at the University of Pennsylvania led by Tracy Bale have now demonstrated that an increase in a group of microRNAs (miRNAs) in sperm from stressed mice can lead to altered stress response in adult offspring. The work, published today (October 19) in PNAS, shows that simultaneously injecting nine miRNAs into mouse zygotes recapitulates the changes found in the offspring of stressed mice.-'I think it's a fine paper [and a] well-designed study, said Michael Skinner, who studies epigenetic inheritance at Washington State University and was not involved in the study. It shows a very nice role for noncoding RNA at the early embryonic stage for transmission of the transgenerational phenotype.'-Comment: Still the same species

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The Nobel prize in chemistry goes to three scientists who worked out a major part of an incomplete story of excision of DNA when a mismatch occurs in cell division and DNA copying:- http://www.nobelprize.org/nobel_prizes/chemistry/laureates/2015/popular-chemistryprize2... is an excellent article in lay terms with great diagrams. Just remember that the enzymes used are giant molecules, which raises the obvious question: if chance evolution is true, how did evolution find each very specialized molecule made up of thousands of amino acids and trace metals?- "Our DNA remains astonishingly intact, year after year, due to a host of molecular repair mechanisms:a swarm of proteins that monitor the genes. They continually proof-read the genome and repair any damage that has occurred. The Nobel Prize in Chemistry 2015 is awarded to Tomas Lindahl, Paul Modrich and Aziz Sancar for having mapped these fundamental processes at the molecular level. Their systematic work has made a decisive contribution to the understanding of how the living cell functions, as well as providing knowledge about the molecular causes of several hereditary diseases and about mechanisms behind both cancer development and aging."

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DAVID: The Nobel prize in chemistry goes to three scientists who worked out a major part of an incomplete story of excision of DNA when a mismatch occurs in cell division and DNA copying:-http://www.nobelprize.org/nobel_prizes/chemistry/laureates/2015/popular-chemistryprize2...-DAVID: This is an excellent article in lay terms with great diagrams. Just remember that the enzymes used are giant molecules, which raises the obvious question: if chance evolution is true, how did evolution find each very specialized molecule made up of thousands of amino acids and trace metals?-Thank you for a great article describing an amazing process. It brings home to us the vast scale of the micro-world that lives inside us. There are billions of little workers cooperating night and day to keep our bodies functioning, and they constantly adjust to every move we make. How did they get together in the first place? As always, I agree with you that chance stretches credulity beyond its limits. Perhaps they did it by using their (God-given?) intelligence? If we rid ourselves of our large organisms chauvinism (Shapiro) and acknowledge the possibility that just as we are intelligent specks in a vast universe, the specks in our bodies are also beings with their own form of intelligence, the whole process makes sense.
 
DAVID (under ant colony complexity): Still 50/50. Just as likely I am right and lots of folk agree with me. I know how automatic my cells are in my human body. -You know? It's worth recalling Stephen Talbott's observation: We discover that our highest capacities - our thinking, our formulation of goals and plans, our strivings and passions, our sense of well-being and illness - are objectively imaged in our own biological organism right down to the molecular activity of our cells, as also in the cells of every other living creature. (My bold). But you know?

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> dhw: Thank you for a great article describing an amazing process. It brings home to us the vast scale of the micro-world that lives inside us. ... If we rid ourselves of our large organisms chauvinism (Shapiro) and acknowledge the possibility that just as we are intelligent specks in a vast universe, the specks in our bodies are also beings with their own form of intelligence, the whole process makes sense.-It makes just as much sense to recognize intelligent information running the processes.
> 
> DAVID (under ant colony complexity): Still 50/50. Just as likely I am right and lots of folk agree with me. I know how automatic my cells are in my human body. 
> 
> dhw: You know? It's worth recalling Stephen Talbott's observation: We discover that our highest capacities - our thinking, our formulation of goals and plans, our strivings and passions, our sense of well-being and illness - are objectively imaged in our own biological organism right down to the molecular activity of our cells, as also in the cells of every other living creature. (My bold). But you know?-Still 50/50

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DNA is six feet/ 2 meters long and has to be packed into the nucleus, just so. No knots, and genes need to be placed near modifiers and controllers, even if quite a distance away when stretched out:-http://www.theatlantic.com/science/archive/2015/10/theres-a-mystery-machine-that-sculpts-the-human-genome/411199/-"In the 1970s, biochemists showed that this feat of extreme origami begins when DNA is wrapped around proteins called histones, creating what looks like a string of beads. This reduces the packing problem, but doesn't come close to solving it. The wrapped DNA must be folded and twisted in ever more complicated (and as yet unknown) ways. Eventually, it forms large loops.-***-"They also bring genes into close contact with distant sequences that turn them on or off. So, the 3-D form of the genome also dictates its function. -***-"They also showed that the loops obey certain rules. Most tend to be short. They occur in the same places whether you're looking at a neuron or a skin cell, or a human cell or mouse cell. And they almost always associate with a protein called CTCF, which acts as a fastener. In theory, two CTCF proteins will bind to separate stretches of DNA and then lock together, creating a loop and holding it in place.-"But when Aiden's team looked at CTCF more closely, they found a huge surprise. The protein recognizes and sticks to specific DNA sequences, which act as its landing pads. These sequences point in a particular direction, which means that a pair of them can line up in four possible ways. They don't. In reality, they almost always line up in just one of the four orientations, pointing towards each other in what study co-leader Eric Lander described as a genomic yin and yang.-'That was a total bombshell, says student Suhas Rao who worked on the project. He, like many others, had assumed that loops form when two stretches of free-floating DNA randomly find each other and are fastened by a pair of CTCF proteins. But that can't be right. If it was, the CTCF landing sequences would align in all four possible orientations, rather than the very specific one that Rao saw in his data. The loops must be forming in a completely different way, one that's deliberate and controlled.-"Rao and fellow student Adrian Sanborn think that the key to this process is a cluster of proteins called an extrusion complex, which looks like a couple of Polo mints stuck together. The complex assembles on a stretch of DNA so that the long molecule threads through one hole, forms a very short loop, and then passes through the other one. Then, true to its name, the complex extrudes the DNA, pushing both strands outwards so that the loop gets longer and longer. And when the complex hits one of the CTCF landing sites, it stops, but only if the sites are pointing in the right direction.-This explanation is almost perfect. It accounts for everything that the team have seen in their work: why the loops don't get tangled, and why the CTCF landing sites align the way they do. This is an important milestone in understanding the three dimensional structure of chromosomes, but like most great papers, it raises more questions than it provides answers, says Kim Nasmyth, a biochemist at the University of Oxford who first proposed the concept of an extrusion complex in 2001.-"And then there's the really big problem: No one knows if the extrusion complex exists.-"Since Nasmyth conceived of it, no one has yet proved that it's real, let alone worked out which proteins it contains. CTCF is probably part of it, as is a related protein called cohesin. Beyond that, it's a mystery. It's like a ghostly lawnmower, whose presence is inferred by looking at a field of freshly shorn grass, or the knife that we only know about by studying the stab wounds. It might not actually be a thing.-"Except: The genome totally behaves as if the extrusion complex was a thing. Rao and Sanborn created a simulation that predicts the structure of the genome on the basis that the complex is real and works they way they think it does.-"These predictions were so accurate that the team could even re-sculpt the genome at will."-Comment: I've indicated the 3-D importance when studying the functionality of DNA. And then there is a chicken and egg problem: How did this essential CTCF protein develop to loop DNA when the DNA is essential for its production? Again, design is a good answer.

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DAVID (under ant colony complexity): Still 50/50. Just as likely I am right and lots of folk agree with me. I know how automatic my cells are in my human body. -dhw: You know? It's worth recalling Stephen Talbott's observation: We discover that our highest capacities - our thinking, our formulation of goals and plans, our strivings and passions, our sense of well-being and illness - are objectively imaged in our own biological organism right down to the molecular activity of our cells, as also in the cells of every other living creature. (My bold). But you know?
-DAVID: Still 50/50.-When the odds are 50/50,
According to us clear thinkers
The cowboy who knows
Which way it all goes
Is wearing his horse's blinkers.

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> DAVID: Still 50/50.
> 
> dhw: When the odds are 50/50,
> According to us clear thinkers
> The cowboy who knows
> Which way it all goes
> Is wearing his horse's blinkers.-My meaning of 50/50? 1) Only one side is correct- 2) Both sides are correct- 3) No one is correct-I favor #1. I admit that #2 is a possibility. #3 is not logical. Theists will join me, and I remain with the claim that all the ID scientists are on my side. My horse is comfortable, but a picket fence is painful to the rump. Quote shopping a few hyperbolic statements contorts the brain.

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DAVID: Still 50/50.-dhw: When the odds are 50/50,
According to us clear thinkers
The cowboy who knows
Which way it all goes
Is wearing his horse's blinkers.-DAVID: My meaning of 50/50? 1) Only one side is correct
2) Both sides are correct
3) No one is correct
I favor #1. I admit that #2 is a possibility. #3 is not logical. Theists will join me, and I remain with the claim that all the ID scientists are on my side.-We are talking about cells/cell communities being intelligent, as opposed to being automatons. I agree that only one side is correct. I have no idea at all why you should relate this to theism, since I have pointed out over and over again that this intelligence may have been God-given. We have, however, discussed the relevance of cellular intelligence to evolution (which you believe in, as opposed to separate creation of species), and so I'd be interested to know which ID evolutionists explicitly support your theory that God personally intervened to design every innovation, lifestyle and natural wonder from bacteria to humans, or 3.8 billion years ago supplied the first living cells with a programme for all of them. And I thought you once said that Shapiro was a practising Jew - but maybe my memory is at fault.

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Histone 1 now added to the repair mechanism. Histones 2-5 were previously known to signal for repair:-http://www.nature.com/nature/journal/vaop/ncurrent/full/nature15401.html-"DNA double-strand breaks (DSBs) are highly cytotoxic DNA lesions that trigger non-proteolytic ubiquitylation of adjacent chromatin areas to generate binding sites for DNA repair factors. This depends on the sequential actions of the E3 ubiquitin ligases RNF8 and RNF168 (refs 1, 2, 3, 4, 5, 6), and UBC13 (also known as UBE2N), an E2 ubiquitin-conjugating enzyme that specifically generates K63-linked ubiquitin chains7. Whereas RNF168 is known to catalyse ubiquitylation of H2A-type histones, leading to the recruitment of repair factors such as 53BP1 (refs 8, 9, 10), the critical substrates of RNF8 and K63-linked ubiquitylation remain elusive. Here we elucidate how RNF8 and UBC13 promote recruitment of RNF168 and downstream factors to DSB sites in human cells. We establish that UBC13-dependent K63-linked ubiquitylation at DSB sites is predominantly mediated by RNF8 but not RNF168, and that H1-type linker histones, but not core histones, represent major chromatin-associated targets of this modification. The RNF168 module (UDM1) recognizing RNF8-generated ubiquitylations11 is a high-affinity reader of K63-ubiquitylated H1, mechanistically explaining the essential roles of RNF8 and UBC13 in recruiting RNF168 to DSBs. Consistently, reduced expression or chromatin association of linker histones impair accumulation of K63-linked ubiquitin conjugates and repair factors at DSB-flanking chromatin. These results identify histone H1 as a key target of RNF8-UBC13 in DSB signalling and expand the concept of the histone code12, 13 by showing that posttranslational modifications of linker histones can serve as important marks for recognition by factors involved in genome stability maintenance, and possibly beyond."-***-http://www.sciencedaily.com/releases/2015/10/151023145114.htm-"Histones enable the tight packaging of DNA strands within cells. The strands are two metres in length and the cells usually approx. 100,000 times smaller. Generally speaking, there are five types of histones. Four of them are so-called core histones, and they are placed like beads on the DNA strands, which are curled up like a ball of wool within the cells. The role of the histones is already well described in research, and in addition to enabling the packaging of the DNA strands they also play a central part in practically every process related to the DNA-code, including repairing possibly damaged DNA.-"The four core histones have so-called tails, and among other things they signal damage to the DNA and thus attract the proteins that help repair the damage. Between the histone "yarn balls" we find the fifth histone, Histone H1, but up until now its function has not been thoroughly examined.-"Using a so-called mass spectrometer, a technique developed in collaboration with fellow researchers at the Novo Nordisk Foundation Centre for Protein Research, Niels Mailand and his team have discovered that, surprisingly, the H1 histone also helps summon repair proteins.-"'In international research, the primary focus has been on the core histones and their functionality, whereas little attention has been paid to the H1 histone, simply because we weren't aware that it too influenced the repair process. Having discovered this function in the H1 constitutes an important piece of the puzzle of how cells protect their DNA, and it opens a door onto hitherto unknown and highly interesting territory," Niels Mailand elaborates."-Comment: Ever more complex and with the appearance of 'cleverly planned'. How much evidence is needed before 'design' is accepted?

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> dhw: I'd be interested to know which ID evolutionists explicitly support your theory that God personally intervened to design every innovation, lifestyle and natural wonder from bacteria to humans, or 3.8 billion years ago supplied the first living cells with a programme for all of them. And I thought you once said that Shapiro was a practising Jew - but maybe my memory is at fault.-Shapiro was president of his Temple. When Id'ers look at evolution they dismiss Darwin completely, most don't buy my approach of theistic evolution, and they don't answer your persistent worry about how God did it. No one knows!

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DAVID (referring to his theory that cells have no intelligence of their own but are automatons): Theists will join me, and I remain with the claim that all the ID scientists are on my side.-dhw: I'd be interested to know which ID evolutionists explicitly support your theory that God personally intervened to design every innovation, lifestyle and natural wonder from bacteria to humans, or 3.8 billion years ago supplied the first living cells with a programme for all of them. And I thought you once said that Shapiro was a practising Jew - but maybe my memory is at fault.-DAVID: Shapiro was president of his Temple. -Thank you. So there is one theist who is not joining you.-DAVID: When Id'ers look at evolution they dismiss Darwin completely, most don't buy my approach of theistic evolution, and they don't answer your persistent worry about how God did it. No one knows!-I asked about ID evolutionists, and if they accept common descent, they cannot possibly dismiss Darwin completely. I'm not surprised that they have no answer to the question of how their God did it, and that they don't buy your theories, but I would be surprised if they didn't look for an alternative. They are also quick to reject Darwin's theory (random mutations and natural selection). In any case, why do you call it MY persistent worry? It's all part of the great mystery of life, and you must have been worried enough to investigate the problem, reject Darwin's solution, and come up with your own hypothesis of preprogramming/dabbling.

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> DAVID: Shapiro was president of his Temple. 
> 
> dhw: Thank you. So there is one theist who is not joining you.-What Shapiro thinks privately and what he produces scientifically may not be what you think. In his career he deals with atheistic superiors. His read/write approach to how cells work may be attributed to God in his personal thoughts. That is how I interpret his work.
> 
> dhw: I asked about ID evolutionists, and if they accept common descent, they cannot possibly dismiss Darwin completely. -I sense that many of them do not accept common descent. Many don't like theistic evolution, and Tony's view may be prevalent.

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DAVID: Shapiro was president of his Temple. -dhw: Thank you. So there is one theist who is not joining you.-DAVID: What Shapiro thinks privately and what he produces scientifically may not be what you think. In his career he deals with atheistic superiors. His read/write approach to how cells work may be attributed to God in his personal thoughts. That is how I interpret his work.-Shapiro's belief that cells are sentient conscious beings (as opposed to automatons) is neither theistic nor atheistic. He can attribute their intelligence to God, and his atheistic superiors can attribute it to chance. My point is that he is a theist who does not share your belief that cells are automatons. (See also post on Spetner.)
 
dhw: I asked about ID evolutionists, and if they accept common descent, they cannot possibly dismiss Darwin completely. -DAVID: I sense that many of them do not accept common descent. Many don't like theistic evolution, and Tony's view may be prevalent.-I'm not sure how much I can rely on your sense, but you do believe in common descent, and so even if you are right about the many, my question would relate to how many of the remaining few share your belief in a 3.8-billion-year programme/divine dabbling for all the innovations, lifestyles etc. But you have already answered that in such a way as to make it clear that even among the evolutionary ID-ers you consider to be your supporters, you are actually pretty isolated.

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dhw: I'm not sure how much I can rely on your sense, but you do believe in common descent, and so even if you are right about the many, my question would relate to how many of the remaining few share your belief in a 3.8-billion-year programme/divine dabbling for all the innovations, lifestyles etc. But you have already answered that in such a way as to make it clear that even among the evolutionary ID-ers you consider to be your supporters, you are actually pretty isolated.-They generally don't like the idea of theistic evolution, which places them closer to Tony. But I use their concept of information driving life, and they call for a designer, just as I do.

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dhw: I'm not sure how much I can rely on your sense, but you do believe in common descent, and so even if you are right about the many, my question would relate to how many of the remaining few share your belief in a 3.8-billion-year programme/divine dabbling for all the innovations, lifestyles etc. But you have already answered that in such a way as to make it clear that even among the evolutionary ID-ers you consider to be your supporters, you are actually pretty isolated.-DAVID: They generally don't like the idea of theistic evolution, which places them closer to Tony. But I use their concept of information driving life, and they call for a designer, just as I do.-Just to remind you of our starting point: I have suggested that cellular intelligence is the driving force behind evolution, as opposed to your divine 3.8-billion-year computer programme and/or divine dabbling. You have granted odds of 50/50, but are adamant that you are right, and Theists will join me, and I remain with the claim that all the ID scientists are on my side. Now it appears that most ID scientists don't even share your belief in evolution, let alone in the 3.8-billion-year computer programme, so you are left with dabbling, which without common descent (which you believe in) becomes separate creation. I have to agree with you, however, that all ID scientists share your belief in ID.

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> dhw; Just to remind you of our starting point: I have suggested that cellular intelligence is the driving force behind evolution,-To remind you, It is cellular information provided by intelligence

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> > dhw; Just to remind you of our starting point: I have suggested that cellular intelligence is the driving force behind evolution,
> 
> To remind you, It is cellular information provided by intelligence-David, for me, the above sentence is the whole crux of the matter in this discussion. Why so adamant to say "provided by"? Is it not more probable intelligence and information are two sides of the same coin always existing together being what IS? "Provided by" makes it sound as if at some point in time information didn't exist. That makes no sense. What is intelligence without information? In my view - nothing.

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> > > dhw; Just to remind you of our starting point: I have suggested that cellular intelligence is the driving force behind evolution,
> > 
> > David: To remind you, It is cellular information provided by intelligence
> 
> dhw: David, for me, the above sentence is the whole crux of the matter in this discussion. Why so adamant to say "provided by"? Is it not more probable intelligence and information are two sides of the same coin always existing together being what IS? "Provided by" makes it sound as if at some point in time information didn't exist. That makes no sense. What is intelligence without information? In my view - nothing.-I agree intelligence and information are intertwined. To create anything that survives the requirements of nature requires planning, which requires intelligence. Therefore intelligence creates the planning information for the new development.

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The membrane of the nucleus helps in DNA repair:-http://phys.org/news/2015-10-nuclear-membrane-dark-dna.html-"Previously, the nuclear membrane was thought to be mostly just a protective bubble around the nuclear material, with pores acting as channels to transport molecules in and out. But in a study published on October 26 in Nature Cell Biology, a research team led by Irene Chiolo documents how broken strands of a portion of DNA known as heterochromatin are dragged to the nuclear membrane for repair.-"DNA exists inside of a cell's nucleus in two forms: euchromatin and heterochromatin. Euchromatin gets all of the attention because it encodes most of the genome, while heterochromatin, which is mostly composed of repeated DNA sequences, has long been ignored as "junk DNA."-"'Scientists are now starting to pay a lot of attention to this mysterious component of the genome," said Chiolo, assistant professor at the USC Dornsife College of Letters, Arts and Sciences. "Heterochromatin is not only essential for chromosome maintenance during cell division; it also poses specific threats to genome stability. Heterochromatin is potentially one of the most powerful driving forces for cancer formation, but it is the 'dark matter' of the genome. We are just beginning to unravel how repair works here."-"The reason why we don't experience thousands of cancers every day in our body is because we have incredibly efficient molecular mechanisms that repair the frequent damages occurring in our DNA. But those that work in heterochromatin are quite extraordinary.-"'Repeated sequences tend to recombine with each other during DNA repair," said Taehyun Ryu, USC graduate student and first author on this study. "This would lead to chromosome aberrations as frequently observed in cancer cells. What prevents these outcomes in normal cells was unclear.'"-"'We knew that nuclear membrane dysfunctions are common in cancer cells," Chiolo said. "Our studies now suggest how these dysfunctions can affect heterochromatin repair and have a causative role in cancer progression.'"-"Working with the fruit fly Drosophila melanogaster, the team observed that breaks in heterochromatin are repaired after damaged sequences move away from the rest of the chromosome to the inner wall of the nuclear membrane. There, a trio of proteins mends the break in a safe environment, where it cannot accidentally get tangled up with incorrect chromosomes."-
Comment: Unless DNA is perfectly copied in cell division life will stop for that organism. Now there are many known parallel backups for repair. Good planning?

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Stem cells are the source of all cells. They can differentiate into any type of cell or simply reproduce themselves. They are the cells that make the embryo, but also are crucial for repair and maintenance during life. Gene control is shown here:- http://phys.org/news/2015-10-prkci-gene-stem-cells.html-"In a paper published in Stem Cell Reports, USC researcher In Kyoung Mah from the lab of Francesca Mariani and colleagues at the University of California, San Diego, (UCSD) describe a key gene in maintaining this critical balance between producing too many and too few stem cells. Called Prkci, the gene influences whether stem cells self-renew to produce more stem cells, or differentiate into more specialized cell types, such as blood or nerves.-"In their experiments, the team grew mouse embryonic stem cells, which lacked Prkci, into embryo-like structures in the laboratory. Without Prkci, the stem cells favored self-renewal, generating large numbers of stem cells and, subsequently, an abundance of secondary structures.-"Upon closer inspection, the stem cells lacking Prkci had many activated genes typical of stem cells, and some activated genes typical of neural, cardiac and blood-forming cells. Therefore, the loss of Prkci can also encourage stem cells to differentiate into the progenitor cells that form neurons, heart muscle and blood.-"Prkci achieves these effects by activating or deactivating a well-known group of interacting genes that are part of the "Notch signaling pathway." In the absence of Prkci, the Notch pathway produces a protein that signals to stem cells to make more stem cells. In the presence of Prkci, the Notch pathway remains silent, and stem cells differentiate into specific cell types."-Comment: Another example of the layers of control that must be present to manage the mechanisms of life. How can this be developed in new species, such as those in the Cambrian, without planning? The key to analysis is the fact that prior animals were very simplistic and lacked the organs of the Cambrian denizens. How do you get from stem cells in the pre-Cambrian producing two-three cell types to stem cells that produce 200 cell types? Oh, I forgot, committees of intelligent cells in the pre-Cambrian.

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DAVID: Stem cells are the source of all cells. They can differentiate into any type of cell or simply reproduce themselves. They are the cells that make the embryo, but also are crucial for repair and maintenance during life. Gene control is shown here:
http://phys.org/news/2015-10-prkci-gene-stem-cells.html-David's comment: Another example of the layers of control that must be present to manage the mechanisms of life. How can this be developed in new species, such as those in the Cambrian, without planning? The key to analysis is the fact that prior animals were very simplistic and lacked the organs of the Cambrian denizens. How do you get from stem cells in the pre-Cambrian producing two-three cell types to stem cells that produce 200 cell types? Oh, I forgot, committees of intelligent cells in the pre-Cambrian.-Perhaps by a change in environmental conditions which suddenly allowed for a far greater variety - the same change that would presumably have triggered your God's 3.8-billion-year old computer programme suddenly to switch on 200 cell types instead of 2-3, or that inspired your God to personally dabble and do the same thing.
 
Here, though, is a possible clue to how it was all done :-D AVID: Close study shows some of the termites have differing personalities and the colonies have some sort of group think:
http://www.livescience.com/52644-the-collective-mind-of-the-termite.html?cmpid=NL_LS_we... 
David's comment: dhw will like this. Not convinced he is not anthropomorphizing them.-Yes, I love it. Thank you for the article and for your fair-mindedness in presenting it. Some scientists believe this is precisely how cell communities behave. One tiny quote will sum it up: "The collective intelligence of the colony is quite real, as real as our own intelligence, and we are far from comprehending either. 
Substitute cellular community for colony, and we are back to your 50/50 acceptance that cells are sentient, cognitive beings, which means they are intelligent and potentially just as capable of complex design as termites are. -Sneer if you like at committees of intelligent cells (see under More about how evolution works for more about how sneering works), but your comment might be seen as a vivid illustration of what Shapiro calls large organisms chauvinism. I must confess to a feeling of puzzlement whenever people talk of anthropomorphism in relation to the humanlike behaviour of other organisms. Individuality, sentience, cognition, decision-making, survival strategies, communication and in this particular context cooperation (as we find in committees) did not originate with humans, so if you believe in common descent reaching back to bacteria, why is it so difficult to accept that these characteristics and procedures may have been inherited from them?

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> dhw: Perhaps by a change in environmental conditions which suddenly allowed for a far greater variety - the same change that would presumably have triggered your God's 3.8-billion-year old computer programme suddenly to switch on 200 cell types instead of 2-3, or that inspired your God to personally dabble and do the same thing.
> 
> Here, though, is a possible clue to how it was all done:
> 
> DAVID: Close study shows some of the termites have differing personalities and the colonies have some sort of group think:
> http://www.livescience.com/52644-the-collective-mind-of-the-termite.html?cmpid=NL_LS_we... 
> David's comment: dhw will like this. Not convinced he is not anthropomorphizing them.
> 
> dhw: Yes, I love it. Thank you for the article and for your fair-mindedness in presenting it. Some scientists believe this is precisely how cell communities behave. One tiny quote will sum it up: "The collective intelligence of the colony is quite real, as real as our own intelligence, and we are far from comprehending either. -I believe in species consciousness just like Sheldrake, which explains this, but doesn't explain evolution.-> dhw: Substitute cellular community for colony, and we are back to your 50/50 acceptance that cells are sentient, cognitive beings, which means they are intelligent and potentially just as capable of complex design as termites are. -My 50/50 is that cells are not sentient, but surprise, you have faith in that concept!
> 
> dhw:Individuality, sentience, cognition, decision-making, survival strategies, communication and in this particular context cooperation (as we find in committees) did not originate with humans, so if you believe in common descent reaching back to bacteria, why is it so difficult to accept that these characteristics and procedures may have been inherited from them?-We think through the agency of neurons, and when were they invented? In the pre-Cambrian period about 600 mya, not 3.8 bya. Cells do not think, but react by using well-planned information.

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I have suggested that termites may provide an analogy to answer David's question of how we get from stem cells in the pre-Cambrian producing two-three cell types to stem cells that produce 200 cell types?
 
DAVID: Close study shows some of the termites have differing personalities and the colonies have some sort of group think:
http://www.livescience.com/52644-the-collective-mind-of-the-termite.html?cmpid=NL_LS_we... -dhw: Some scientists believe this is precisely how cell communities behave. One tiny quote will sum it up: "The collective intelligence of the colony is quite real, as real as our own intelligence, and we are far from comprehending either. 
DAVID: I believe in species consciousness just like Sheldrake, which explains this, but doesn't explain evolution.-No, species consciousness would be the product of evolution, as different cell communities over thousands of millions of years combined to create new cellular combinations (i.e. evolutionary innovations leading to new species).
 
dhw: Substitute cellular community for colony, and we are back to your 50/50 acceptance that cells are sentient, cognitive beings, which means they are intelligent and potentially just as capable of complex design as termites are. -DAVID: My 50/50 is that cells are not sentient, but surprise, you have faith in that concept!-No, I offer it as a hypothesis. It is you who have faith in your half of the 50/50. I am hamstrung by my uncertainty (a)over the source of life and intelligence, and (b) over the existence of a God. However, given the choice between your 3.8-billion-year computer programme for all innovations and the concept of the intelligent cell, and bearing in mind the higgledy-piggledy history of evolution, I certainly prefer my hypothesis to yours, on the understanding that it allows for the possibility of your God inventing the intelligent cell.
 
dhw: Individuality, sentience, cognition, decision-making, survival strategies, communication and in this particular context cooperation (as we find in committees) did not originate with humans, so if you believe in common descent reaching back to bacteria, why is it so difficult to accept that these characteristics and procedures may have been inherited from them?
DAVID: We think through the agency of neurons, and when were they invented? In the pre-Cambrian period about 600 mya, not 3.8 bya. Cells do not think, but react by using well-planned information.-You have agreed that there is a 50/50 chance of bacteria being individual, sentient, intelligent beings, so you should allow a 50/50 chance that we have inherited the same characteristics and are not anthropomorphizing them. Neurons and a brain may not be the only tools for thought.
 
What is well-planned information? We're off again! Your hypothesis: cells contain an incredibly well-planned 3.8-billion-year-old computer programme which automatically processes information. My hypothesis: cells contain an autonomous intelligence which processes information.

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> dhw: No, species consciousness would be the product of evolution, as different cell communities over thousands of millions of years combined to create new cellular combinations (i.e. evolutionary innovations leading to new species).-With no explanation as to how those cellular communities can plan for the future giant gaps in complexity.-> DAVID: My 50/50 is that cells are not sentient, but surprise, you have faith in that concept!
> 
> dhw: No, I offer it as a hypothesis. It is you who have faith in your half of the 50/50. I am hamstrung by my uncertainty (a)over the source of life and intelligence, and (b) over the existence of a God. However, given the choice between your 3.8-billion-year computer programme for all innovations and the concept of the intelligent cell, and bearing in mind the higgledy-piggledy history of evolution, I certainly prefer my hypothesis to yours, on the understanding that it allows for the possibility of your God inventing the intelligent cell.-The picket fence allows you to propose everything in every direction and feel comfortable. I also feel comfortable, but I have answers to the nagging questions that feel comfortable.]
> 
> dhw: You have agreed that there is a 50/50 chance of bacteria being individual, sentient, intelligent beings, so you should allow a 50/50 chance that we have inherited the same characteristics and are not anthropomorphizing them. Neurons and a brain may not be the only tools for thought.-So what else can 'think' and plan for complexity?
> 
> dhw: What is well-planned information? We're off again! Your hypothesis: cells contain an incredibly well-planned 3.8-billion-year-old computer programme which automatically processes information. My hypothesis: cells contain an autonomous intelligence which processes information.-Right. You are recognizing that cells have a mechanism to interpret the information which is onboard and uses that information appropriately to run the processes of life. For me reading a code should be automatic if a code reader is present, as you say it is.

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dhw: No, species consciousness would be the product of evolution, as different cell communities over thousands of millions of years combined to create new cellular combinations (i.e. evolutionary innovations leading to new species).
DAVID: With no explanation as to how those cellular communities can plan for the future giant gaps in complexity.-The explanation would be intelligent thought - the same as your own, except that yours was incorporated into a 3.8-billion-year old computer programme for every single innovation by a supernatural intelligence with no explanation as to how it came into being or acquired its knowledge.
 
DAVID: The picket fence allows you to propose everything in every direction and feel comfortable. I also feel comfortable, but I have answers to the nagging questions that feel comfortable.]-Everything in every direction? I have proposed that evolution takes place through the autonomous intelligence of organisms - an intelligence possibly invented by your God. You propose that your God preprogrammed it all or intervened personally. But yes, we are both comfortable.-dhw: You have agreed that there is a 50/50 chance of bacteria being individual, sentient, intelligent beings, so you should allow a 50/50 chance that we have inherited the same characteristics and are not anthropomorphizing them. Neurons and a brain may not be the only tools for thought.
DAVID: So what else can 'think' and plan for complexity?-Well, according to you, there's a God and he ain't got neurons or a brain. And according to you, NDEs show that humans can think' even when the brain is dead. According to many eminent scientists, single cells are intelligent, and the 50/50 chance that they are right would mean that intelligence (which would include the ability to think and plan) does not depend on neurons and a brain.
 
dhw: What is well-planned information? We're off again! Your hypothesis: cells contain an incredibly well-planned 3.8-billion-year-old computer programme which automatically processes information. My hypothesis: cells contain an autonomous intelligence which processes information.
DAVID: Right. You are recognizing that cells have a mechanism to interpret the information which is onboard and uses that information appropriately to run the processes of life. -Right. You are recognizing that the cellular mechanism to interpret information is not to be conflated with the information. But I would add that it also interprets information from outside.-DAVID: For me reading a code should be automatic if a code reader is present, as you say it is.-If the cell is intelligent, I would envisage the processing mechanism in the same terms as the human brain: some actions are automatic, and some are not. In your hypothesis, of course, all its actions are automatic.

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DAVID: With no explanation as to how those cellular communities can plan for the future giant gaps in complexity.
> 
> dhw: The explanation would be intelligent thought -And what does the intelligent thinking in a community of cells? 
> 
> DAVID: So what else can 'think' and plan for complexity?
> 
> dhw: Well, according to you, there's a God and he ain't got neurons or a brain. And according to you, NDEs show that humans can think' even when the brain is dead. According to many eminent scientists, single cells are intelligent, and the 50/50 chance that they are right would mean that intelligence (which would include the ability to think and plan) does not depend on neurons and a brain.-Not' many' scientists. You just name a very few. And the 50/50 is because there are only two possibilities. In my biologist eyes it is 90/10 in my favor.
> 
> 
> dhw: Right. You are recognizing that the cellular mechanism to interpret information is not to be conflated with the information. But I would add that it also interprets information from outside.-The outside info is static, but inside it is process info, a vast difference.
> 
> DAVID: For me reading a code should be automatic if a code reader is present, as you say it is.
> 
> dhw: If the cell is intelligent, I would envisage the processing mechanism in the same terms as the human brain: some actions are automatic, and some are not. In your hypothesis, of course, all its actions are automatic.-Of course.

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DAVID: With no explanation as to how those cellular communities can plan for the future giant gaps in complexity.
dhw: The explanation would be intelligent thought 
DAVID: And what does the intelligent thinking in a community of cells?-What does the intelligent thinking in your brain, which is a community of cells? We don't know how thought emerges from cells. What does the intelligent thinking in a colony of termites? What we do know is that cells and termites communicate, and that somehow they come up with intelligent and complex solutions to all kinds of problems. In any case, as I pointed out in my previous post, since your God presumably has no brain or neurons, and your NDE patients can think intelligently without a brain, and since you favour dualism, you can hardly insist that thinking is confined to brains and neurons.
 
dhw: According to many eminent scientists, single cells are intelligent, and the 50/50 chance that they are right would mean that intelligence (which would include the ability to think and plan) does not depend on neurons and a brain.
DAVID: Not' many' scientists. You just name a very few. And the 50/50 is because there are only two possibilities. In my biologist eyes it is 90/10 in my favor.-I am in no position to conduct a roll call, but a quick google offers the following as evidence that this is not such a way-out concept as you would like to believe:
1.	Microbial intelligence - Wikipedia, the free encyclopedia
en.wikipedia.org/wiki/Microbial_intelligence-"Microbial intelligence (popularly known as bacterial intelligence) is the intelligence shown by microorganisms. The concept encompasses complex adaptive behaviour shown by single cells, and altruistic and/or cooperative behavior in populations of like or unlike cells mediated by chemical signalling that induces physiological or behavioral changes in cells and influences colony structures.
Complex cells, like protozoa or algae, show remarkable abilities to organise themselves in changing circumstances.[1] Shell-building by amoebae reveals complex discrimination and manipulative skills that are ordinarily thought to occur only in multicellular organisms.
Even bacteria, which show primitive behavior as isolated cells, can display more sophisticated behavior as a population. These behaviors occur in single species populations, or mixed species populations. Examples are colonies of Myxobacteria, quorum sensing, and biofilms.
It has been suggested that a bacterial colony loosely mimics a biological neural network. The bacteria can take inputs in form of chemical signals, process them and then produce output chemicals to signal other bacteria in the colony.
The mechanisms that enable single celled organisms to coordinate in populations presumably carried over in those lines that evolved multicellularity, and were co-opted as mechanisms to coordinate multicellular organisms.
Bacteria communication and self-organization in the context of Network theory has been investigated by Eshel Ben-Jacob research group at Tel Aviv University which developed a fractal model of bacterial colony and identified linguistic and social patterns in colony lifecycle [1] (also see Ben-Jacob's bacteria)."

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DAVID: Not' many' scientists. You just name a very few. And the 50/50 is because there are only two possibilities. In my biologist eyes it is 90/10 in my favor.
> 
> dhw: I am in no position to conduct a roll call, but a quick google offers the following as evidence that this is not such a way-out concept as you would like to believe:
> 1.	Microbial intelligence - Wikipedia, the free encyclopedia
> en.wikipedia.org/wiki/Microbial_intelligence
> 
> "Microbial intelligence (popularly known as bacterial intelligence) is the intelligence shown by microorganisms. The concept encompasses complex adaptive behaviour shown by single cells, and altruistic and/or cooperative behavior in populations of like or unlike cells mediated by chemical signalling that induces physiological or behavioral changes in cells and influences colony structures.
> Complex cells, like protozoa or algae, show remarkable abilities to organise themselves in changing circumstances.[1] Shell-building by amoebae reveals complex discrimination and manipulative skills that are ordinarily thought to occur only in multicellular organisms.
> Even bacteria, which show primitive behavior as isolated cells, can display more sophisticated behavior as a population. These behaviors occur in single species populations, or mixed species populations. Examples are colonies of Myxobacteria, quorum sensing, and biofilms.
> It has been suggested that a bacterial colony loosely mimics a biological neural network. The bacteria can take inputs in form of chemical signals, process them and then produce output chemicals to signal other bacteria in the colony.
> The mechanisms that enable single celled organisms to coordinate in populations presumably carried over in those lines that evolved multicellularity, and were co-opted as mechanisms to coordinate multicellular organisms.
> Bacteria communication and self-organization in the context of Network theory has been investigated by Eshel Ben-Jacob research group at Tel Aviv University which developed a fractal model of bacterial colony and identified linguistic and social patterns in colony lifecycle [1] (also see Ben-Jacob's bacteria)."-Wikipedia is produced by individuals with an interest in a subject. Their credentials are not presented, and expertise level not available. That said I agree that each example is well-known and all can be automatic in my opinion. Their DNAs only need contain the proper instructions.

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13513 views


> > > > dhw; Just to remind you of our starting point: I have suggested that cellular intelligence is the driving force behind evolution,
> > > 
> > > David: To remind you, It is cellular information provided by intelligence
> > 
> > dhw: [bbella] David, for me, the above sentence is the whole crux of the matter in this discussion. Why so adamant to say "provided by"? Is it not more probable intelligence and information are two sides of the same coin always existing together being what IS? "Provided by" makes it sound as if at some point in time information didn't exist. That makes no sense. What is intelligence without information? In my view - nothing.
> 
> I agree intelligence and information are intertwined. To create anything that survives the requirements of nature requires planning, which requires intelligence. Therefore intelligence creates the planning information for the new development.-I would put it: Therefore intelligence uses information for new developments. Do you think that would be saying the same thing?

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> > > > > dhw; Just to remind you of our starting point: I have suggested that cellular intelligence is the driving force behind evolution,
> > > > 
> > > > David: To remind you, It is cellular information provided by intelligence
> > > 
> > > dhw: [bbella] David, for me, the above sentence is the whole crux of the matter in this discussion. Why so adamant to say "provided by"? Is it not more probable intelligence and information are two sides of the same coin always existing together being what IS? "Provided by" makes it sound as if at some point in time information didn't exist. That makes no sense. What is intelligence without information? In my view - nothing.
> > 
> > I agree intelligence and information are intertwined. To create anything that survives the requirements of nature requires planning, which requires intelligence. Therefore intelligence creates the planning information for the new development.
> 
> Bbella: I would put it: Therefore intelligence uses information for new developments. Do you think that would be saying the same thing?-Which is cart and which is horse? Only intelligence can make useful information for the function of processes such as life. I think the function then is automatic by following the information plans.

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13573 views


> > > > > > dhw; Just to remind you of our starting point: I have suggested that cellular intelligence is the driving force behind evolution,
> > > > > 
> > > > > David: To remind you, It is cellular information provided by intelligence
> > > > 
> > > > dhw: [bbella] David, for me, the above sentence is the whole crux of the matter in this discussion. Why so adamant to say "provided by"? Is it not more probable intelligence and information are two sides of the same coin always existing together being what IS? "Provided by" makes it sound as if at some point in time information didn't exist. That makes no sense. What is intelligence without information? In my view - nothing.
> > > 
> > > I agree intelligence and information are intertwined. To create anything that survives the requirements of nature requires planning, which requires intelligence. Therefore intelligence creates the planning information for the new development.
> > 
> > Bbella: I would put it: Therefore intelligence uses information for new developments. Do you think that would be saying the same thing?
> 
> Which is cart and which is horse? Only intelligence can make useful information for the function of processes such as life. I think the function then is automatic by following the information plans.-The way I see it, intelligence doesn't "make" or create information it uses information to make/create life and whatever IS. Information - or all that IS, is eternal "material" in a sense, that intelligence uses to create What IS.

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13582 views


> > > > > > > dhw; Just to remind you of our starting point: I have suggested that cellular intelligence is the driving force behind evolution,
> > > > > > 
> > > > > > David: To remind you, It is cellular information provided by intelligence
> > > > > 
> > > > > dhw: [bbella] David, for me, the above sentence is the whole crux of the matter in this discussion. Why so adamant to say "provided by"? Is it not more probable intelligence and information are two sides of the same coin always existing together being what IS? "Provided by" makes it sound as if at some point in time information didn't exist. That makes no sense. What is intelligence without information? In my view - nothing.
> > > > 
> > > > I agree intelligence and information are intertwined. To create anything that survives the requirements of nature requires planning, which requires intelligence. Therefore intelligence creates the planning information for the new development.
> > > 
> > > Bbella: I would put it: Therefore intelligence uses information for new developments. Do you think that would be saying the same thing?
> > 
> > Which is cart and which is horse? Only intelligence can make useful information for the function of processes such as life. I think the function then is automatic by following the information plans.
> 
> The way I see it, intelligence doesn't "make" or create information it uses information to make/create life and whatever IS. Information - or all that IS, is eternal "material" in a sense, that intelligence uses to create What IS.-To be more (or less) clear: Information is the patterns created by intelligence that arises from the Quantum level to become what IS.

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13580 views


> > Bbella: The way I see it, intelligence doesn't "make" or create information it uses information to make/create life and whatever IS. Information - or all that IS, is eternal "material" in a sense, that intelligence uses to create What IS.
> 
> To be more (or less) clear: Information is the patterns created by intelligence that arises from the Quantum level to become what IS.-This sentence of yours sounds a great deal like how I think: What IS is created by an intelligent mind.

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To facilitate repair DNA wiggles!-http://phys.org/news/2015-11-dna-strands-wiggle-genetic.html-"Sometimes, the molecules that make up life exhibit strange behavior. For instance, in simple organisms such as yeast, when genetic material becomes damaged, the affected DNA strands increase their motion, waving about inside the cell like a sail unfurled. -***-"New research by Rockefeller University scientists shows the swaying of strands is, in fact, a pervasive part of DNA repair in mammalian cells. -***-"'This paper shows that an increase in physical mobility of DNA strands is something that happens inside mammalian cells every time there is a break in the DNA," says de Lange, who is also American Cancer Society Professor, and Director of the Anderson Center for Cancer Research at Rockefeller. "These breaksand the subsequent increase in DNA mobilitycan happen as a result of problems during DNA replication, chemotherapy, and other causes.'"-***-"Since that study, de Lange and postdoctoral fellow Francisca Lottersberger in her lab have identified the cellular structures involved in increasing DNA mobility after damage. One of those structures is embedded in the nuclear envelope, the barrier surrounding the chromosomes. Surprisingly, the second structure that boosts mobility in damaged DNAmicrotubulesresides outside the nucleus, in the cytoplasm. Microtubules are highly dynamic rods that can move things around inside the cell, but can also poke the nucleus. Somehow, the microtubules interact with the nuclear envelope to send a signal to increase mobility of damaged DNA.-***-"The next step, de Lange says, is to try to find out why DNA mobility increases following damage. One possibility, she proposes, is that the process serves as a "fail-safe mechanism" when normal repair processes don't work: The more the broken strands move around, the bigger the chances are of them finding each other again, and repairing the break."-Comment: As with everything I've presented, these molecules seem to know what they are doing. I think they are controlled by onboard instructions. I fully expect more research will show that.

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Here is another repair mechanism using a specific molecule:-http://phys.org/news/2015-11-search-and-rescue-proteins-dna-mutations-linked.html-"MutS is the first protein involved in DNA mismatch repair and is responsible for detecting rare errors that can predispose people to certain types of cancer, a hereditary condition called Lynch syndrome or cancer family syndrome. If a person's mismatch repair system is hindered, the mutation rate increases 100-to-1,000 fold, Simmons said.-***-"To see the protein, the researchers fused MutS to a fluorescent tag and activated fluorescence with a laser. They then could track individual molecules moving through the living cell, similar to a spotlight following a person around a crowded room, Simmons said.-"They found that MutS moved fast to canvas the entire nucleoid, and then slowed significantly when it reached the spot where DNA is replicated. MutS identified and fixed mismatches at this replication site.-"Our work indicates that the population that is moving rapidly isn't searching for mismatches but rather searching for the site of replication," Simmons said. "Once there, it slows down and searches for errors as the DNA is being synthesized."-"There are four DNA bases that are arranged in pairs, and each has only one specific pairing partner. The base pairs hold together the two helix strands of DNA, and a mismatch occurs when the wrong partner is paired with the original DNA base. Hereditary information is passed on when these strands of DNA replicate, and mistakes in replication can lead to cancers.-"The mismatched pair kinks the DNA at the replication fork where DNA is made, Biteen said. MutS positions itself at that fork so it's ready to catch any mistakes. As an added bonus, this positioning likely tells MutS which side is correct and which side is the new, altered DNA."-Comment: Since this protein is so specific, how was it found after DNA developed and suffered copy errors. Could it be that DNA and its repair mechanism were designed together?

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A new one is fund and described in its function:

https://phys.org/news/2019-07-molecular-sensor-scouts-dna.html

"In the time it takes you to read this sentence, every cell in your body suffers some form of DNA damage. Without vigilant repair, cancer would run rampant, and now scientists at the University of Pittsburgh have gotten a glimpse of how one protein in particular keeps DNA damage in check.

"According to a study published today in Nature Structural and Molecular Biology, a protein called UV-DDB—which stands for ultraviolet-damaged DNA-binding—is useful beyond safeguarding against the sun. This new evidence points to UV-DDB being a scout for general DNA damage and an overseer of the molecular repair crew that fixes it.

"'If you're going to fix a pothole, you have to find it first. That's what UV-DDB does. It identifies DNA damage so that another crew can come in and patch and seal it," said study senior author Bennett Van Houten, Ph.D., professor of pharmacology and chemical biology at the Pitt School of Medicine and UPMC Hillman Cancer Center.

***

"'UV-DDB is like a helicopter that can land and then roll for a couple blocks," Van Houten said. "It also has the ability to find damage buried in chromosomes and help DNA repair molecules go places they otherwise couldn't, the way a helicopter can navigate really hilly areas."

"When UV-DDB finds damage, it acts like a foreman to help the DNA repair crew get in, fix the faulty bases and detach quickly.

"For the first time, Van Houten's team witnessed this molecular tango along a "tightrope" of DNA slung between two silica beads, using real-time, single-molecule imaging.

"To show that UV-DDB performs the same functions in living cells, Van Houten recruited the help of Marcel Bruchez, Ph.D., of Carnegie Mellon University, and Patricia Opresko, Ph.D., of Pitt. Together they inflicted oxidative damage to the chromosomes' protective endcaps—called telomeres. As in the DNA tightrope experiment, UV-DDB rushed to the scene, and when it wasn't available, cells were more sensitive to oxidative stress.

***

"'It's clear this protein is involved in a very fundamental problem," Van Houten said. "We could not have evolved out of the slime if we didn't have good DNA repair.'" (my bold)

Comment: Note the final bolded statement, which points out the obvious reason why this is a designed system. It had to be present with the first living cells.

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> > David: Which is cart and which is horse? Only intelligence can make useful information for the function of processes such as life. I think the function then is automatic by following the information plans.
> 
> Bbella: The way I see it, intelligence doesn't "make" or create information it uses information to make/create life and whatever IS. Information - or all that IS, is eternal "material" in a sense, that intelligence uses to create What IS.-Do you think the process of creating the universe and life within it began with pre-existing information?

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To save space DNA is wrapped around molecular spools called histones. These are constantly being replaced. This study unravels some of the mechanism involved in storage of DNA in the nucleus, all very dynamic:-http://www.sciencedaily.com/releases/2015/11/151106062841.htm-"DNA represents a dynamic form of information, balancing efficient storage and access requirements. Packaging approximately 1.8m of DNA into something as small as a cell nucleus is no mean feat, but unpacking it again to access the required sections and genes? That requires organization. -"To understand more about the importance of histone replacement, researchers at the Babraham Institute and MRC Clinical Sciences Centre used developing mouse egg cells, oocytes. Developing oocytes provide a system where the mechanics of how DNA is packaged into cells can be explored in the absence of DNA replication, as egg cells do not divide. However, their genomes are highly active as the development of the egg involves widespread turning on and off of genes and DNA modification before the mature egg cell is ready for fertilisation. The work, published in the latest issue of Molecular Cell, relied on the Institute's expertise in single cell analysis, allowing accurate mapping of the epigenetic landscape in precious cells.-"The researchers deleted a histone chaperone protein -- one of a group of proteins that are responsible for replacing histones in the chromatin structure -- and analysed the effects on egg cell development, DNA integrity and accumulation of DNA methylation.-"'Oocytes lacking the Hira histone chaperone showed severe developmental defects which often led to cell death." said Dr Gavin Kelsey, research group leader in the Institute's Epigenetics programme and author on the paper. "The whole system is disrupted, eggs accumulate DNA damage and the altered chromatin means that genes cannot be efficiently silenced or activated. But we also uncovered an intricate relationship between the different epigenetic systems operating in the oocyte, where failure to ensure normal histone levels severely compromised deposition of methylation on the underlying DNA."-"The research addresses the importance of histone turnover in maintaining genomic fidelity and adds to our understanding about the mechanisms in place to protect the integrity of the genome as it is remodeled and reshaped."-Comment: Extreme complexity to protect the information in DNA.

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Looking at DNA as a written code/language, its grammar is highly complex, more so than spoken language:-http://www.sciencedaily.com/releases/2015/11/151109140252.htm-A new study from Sweden's Karolinska Institutet shows that the 'grammar' of the human genetic code is more complex than that of even the most intricately constructed spoken languages in the world. The findings, published in the journal Nature, explain why the human genome is so difficult to decipher.-***-" The sequencing of the human genome in the year 2000 revealed how the 3 billion letters of A, C, G and T, that the human genome consists of, are ordered. However, knowing just the order of the letters is not sufficient for translating the genomic discoveries into medical benefits; one also needs to understand what the sequences of letters mean. In other words, it is necessary to identify the 'words' and the 'grammar' of the language of the genome.-"The cells in our body have almost identical genomes, but differ from each other because different genes are active (expressed) in different types of cells. Each gene has a regulatory region that contains the instructions controlling when and where the gene is expressed. This gene regulatory code is read by proteins called transcription factors that bind to specific 'DNA words' and either increase or decrease the expression of the associated gene.-***-"[R]esearchers at Karolinska Institutet have previously identified most of the DNA words recognised by individual transcription factors. However, much like in a natural human language, the DNA words can be joined to form compound words that are read by multiple transcription factors. However, the mechanism by which such compound words are read has not previously been examined. Therefore, in their recent study in Nature, the Taipale team examines the binding preferences of pairs of transcription factors, and systematically maps the compound DNA words they bind to.-"Their analysis reveals that the grammar of the genetic code is much more complex than that of even the most complex human languages. Instead of simply joining two words together by deleting a space, the individual words that are joined together in compound DNA words are altered, leading to a large number of completely new words.-"'Our study identified many such words, increasing the understanding of how genes are regulated both in normal development and cancer," says Arttu Jolma. "The results pave the way for cracking the genetic code that controls the expression of genes.' "-Comment: The layer of controls for expression of genes is still being unscrambled. How deep do the complex layers upon layers go? The more complexity, the more likely design.

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Studies in acorn worms finds that 70% of human genes are found in them. We are much more complex which means that multiple layers of controls of gene translation and expression have been added to us:-http://www.sciencedaily.com/releases/2015/11/151118155119.htm-"A team from the Okinawa Institute of Science and Technology Graduate University (OIST) and its collaborators has sequenced the genomes of two species of small water creatures called acorn worms and showed that we share more genes with them than we do with many other animals, establishing them as our distant cousins.-"The study found that 8,600 families of genes are shared across deuterostomes, a large animal grouping that includes a variety of organisms, ranging from acorn worms to star fishes, from frogs to dogs, to humans. This means that approximately 70% of our genes trace their ancestry back to the original deuterostome. By comparing the genomes of acorn worms to other animals, OIST scientists inferred the presence of these genes in the common ancestor of all deuterostomes, an extinct animal that lived half a billion years ago.-***-" Around 550 million years ago, a great variety of animals burst onto the world in an event known as the Cambrian explosion. This evolutionary radiation revealed several new animal body plans, and changed life on Earth forever, as complex animals with specialized guts and behavioural features emerged. Thanks to the genome sequencing of multiple contemporary animals of the deuterostome group, we can go back in time to unveil aspects of the long-lost ancestor of this diverse group of animals.-***-"The team compared the genomes of the two acorn worms with the genomes of 32 diverse animals and found that about 8,600 families of genes are homologous, that is, evolutionarily-related, across all deuterostomes and so are confidently inferred to have been present also in the genome of their deuterostome ancestor. Human arms, birds' wings, cats' paws and the whales' flippers are classical examples of homology, because they all derive from the limbs of a common ancestor. As with anatomical structures, genes homology is defined in terms of shared ancestry. Because of later gene duplications and other processes, these 8,600 homologous genes correspond to at least 14,000 genes, or approximately 70%, of the current human genome.-"'Our analysis of the acorn worm genomes provides a glimpse into our Cambrian ancestors' complexity and supplies support for the ancient link between the pharyngeal development and the filter feeding life style that ultimately contributed to our evolution," explains Dr Simakov."-Comment: From studies like this it is hard to deny an evolutionary process. But we do not know how evolution works.

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Studying the ribosome shows tremendous increasing complexity:-http://www.sciencedaily.com/releases/2015/11/151130152206.htm-"Some of the keys to unlocking the origin of life lie encrypted in the ribosome, life's oldest and most universal assembly of molecules. Today's ribosome converts genetic information (RNA) into proteins that carry out various functions in an organism. But the ribosome itself has changed over time. Its history shows how simple molecules joined forces to invent biology, and its current structure records ancient biological processes that occurred at the root of the Tree of Life, some 3.8 billion years ago.-***-"Like rings in the trunk of a tree, the ribosome contains components that functioned early on in its history. The center of the trunk records the tree's youth, and successive rings represent each year of the tree's life, with the outermost layer recording the present. Just as the core of a tree's trunk remains unchanged over time, all modern ribosomes contain a common core dating back 3.8 billion years. This common core is the same in all living organisms, including humans.-***-"'By taking ribosomes from a number of species -- humans, yeast, various bacteria and archaea -- and looking at the outer portions that are variable, we saw that there were very specific rules governing how they change," said Williams. "We took those rules and applied them to the common core, which allowed us to see all the way back to the first pieces of RNA." (my bold)-"Some clues along the way helped. For instance, though RNA is now responsible for creating proteins, the very earliest life had no proteins. By looking for regions of the ribosome that contain no proteins, the researchers could determine that those elements existed before the advent of proteins. -***-"While the ribosomal core is the same across species, what's added on top differs. Humans have the largest ribosome, encompassing some 7,000 nucleotides representing dramatic growth from the hundred or so base pairs at the beginning.-"What we're talking about is going from short oligomers, short pieces of RNA, to the biology we see today," said Williams. "The increase in size and complexity is mind-boggling." (my bold)-Comment: The rules in bold above are pattern planning. And the complexity (in bold) demands an acceptance of design.

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DNA is grouped around genes to facilitate expression:-http://www.sciencedaily.com/releases/2015/12/151210130724.htm-"[W]e need to think about the structure of the genome in 3D space because that is how we now understand that genes are regulated," says Xiong Ji, a postdoctoral researcher in the Young lab and a co-author of the Cell Stem Cell paper.-"One of Ji's co-authors, graduate student Daniel Dadon, agrees. "This three-dimensional information helps us to interpret regulatory and mutational data with unprecedented accuracy. It's not just a bag of genes and regulatory elements in the nucleus -- this is a highly organized structure that confers function."-"Previous research in mouse ES cells by Young's lab and others determined that a chromosome's DNA is formed into loops that are anchored at their bases by proteins called CTCFs. The benefits of the loops are two-fold. First, the loops help organize and package two meters of DNA to fit into a nucleus that is approximately 5 micrometers in diameter. Second, each loop creates an insulated neighborhood that restricts the action of a regulatory element to genes that resides in the same loop. As graduate student and co-author Diego Borges-Rivera states, "The genome's 3D shape is a key mechanism underlying gene regulation."-"By studying human ES cells, scientists in the Young lab and the lab of Whitehead Founding Member Rudolf Jaenisch created an initial genome map consisting of 13,000 loops established by CTCF anchors and determined that the average insulated neighborhood is 200 kb in length and contains a single gene. The team found that most of the the mapped CTCF anchor sites in the human ES cells genome are maintained in other human cell types and furthermore, that these loop anchor sequences are highly conserved in primate genomes. Such a surprising degree of conservation indicates that these neighborhoods create a foundational framework for gene regulation that is maintained throughout development and across species."-Comment: Mentioned many times before, the 3-D relationships are carefully laid out, as if designed, and put to shame the argument from 'junk DNA'.

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The structure of this massive enzyme made up of thousands of amino acids is now pictured:-http://phys.org/news/2015-12-dna-enzyme-atomic.html-"An enzyme crucial to the process of DNA repair in our cells has been mapped in atomic detail by researchers at the University of Dundee, the UK's top-rated University for Biological Sciences.-"DNA repair plays a key role in human diseases such as cancer. Researchers say that revealing the 3D molecular structure of a key enzyme involved in this process could be an important step towards developing future drugs.-"DNA is the genetic `library' of the cell and is so important that it must be repaired when damaged. It is the only kind of molecule in the cell that is subject to such repair. In one such process, DNA temporarily forms interconnections, called junctions, that much be processed by special enzymes, including one called GEN1, which has now been mapped by the Dundee team.-"'GEN1 was the first of these proteins to be identified, and only relatively recently," said Professor David Lilley, from the School of Life Sciences at the University of Dundee, who has led this new work.-"'We have now determined the molecular structure of GEN1 in fine detail. This is an important step towards understanding DNA repair and how we may be able to develop drugs in future."-Comment: Usual point. How did this complex molecule develop through chance evolution. It is absolutely required to protect DNA from mistakes in cell division, and it had to appear when DNA appeared. Only design fits.

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It is important to control groups of genes at once, since more than one gene may be involves in certain processes:-http://phys.org/news/2015-12-genetic-theorists-reveal-mechanism-gene.html-"The regulatory switch the lab studied has three components: an NFkB protein transcription factor, IkB inhibitor proteins and the DNA that houses the genes.-"NFkB proteins are a family of dimeric (two-part) proteins that bridge extracellular signals and gene expression, alighting on DNA to activate the manufacture of specific proteins in response to outside stimuli. They organize many cellular functions, including the inflammatory response, immune response to infection and the programmed cell death that inhibits cancer.-***-"Because NFkB proteins can activate so many processes at once, timing is important, he said. "NFkB isn't just sending out one signal, turning on the manufacture of one new protein. It's running a broadcast network, turning on many genes, including IkB," Wolynes said. "The stripping mechanism means that instead of leaving all the genes turned on and letting each one figure out when to turn off, IkB strips the NFkB and makes sure they all get turned off. Transcription ends at that point."-"He said this shutdown appears to happen all at once. "If you have a process that turns on 100 different genes, you probably want them all also to turn off at the same time. You don't necessarily want five random genes taking their time, because that would lead to disorganized cell behavior."-"'In the classical picture of gene switches, we don't talk about time," Potoyan said. "We just understand that a gene turns on and off. But here, timing is critical because there are hundreds of genes being regulated. In molecular stripping, all the transcription sites become visible to IkB, which broadcasts the signal for every NFkB to unbind at once.-***-"'We believe this stripping process may be very general for master regulator genes," he said. "It's a system that violates that 40- to 50-year-old paradigm of how a gene switch works. That's one of the reasons we think this study is important.'" -Comment: Genome complexity increases. My standard observation: How did evolution found this complex enzyme with such exact function? Design?

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13445 views

New research shows DNA making coils to allow itself to open up and create different functions:- http://www.scientificamerican.com/article/how-strange-twists-in-dna-orchestrate-life/?W... newest findings, published in Nature Communications in October, capture the dynamic nature of supercoiled DNA and point to what could be a new solution to one of DNA's longstanding puzzles. The letters of the genetic code, known as bases, lie hidden within the helixso how does the molecular machinery that reads that code and replicates DNA get access? Specialized proteins can unzip small segments of the molecule when it's replicated and when it's converted into RNA, a process known as transcription. But Zechiedrich's work illustrates how DNA opens on its own. Simply twisting DNA can expose internal bases to the outside, without the aid of any proteins. Additional work by David Levens, a biologist at the National Cancer Institute, has shown that transcription itself contorts DNA in living human cells, tightening some parts of the coil and loosening it in others. That stress triggers changes in shape, most notably opening up the helix to be read.-"The research hints at an unstudied language of DNA topology that could direct a host of cellular processes. It's intriguing that DNA behaves this way, that topology matters in living organisms, said Craig Benham, a mathematical biologist at the University of California, Davis. I think that was a surprise to many biologists.-***-"Zechiedrich and her collaborators have spent the last two decades making small pieces of supercoiled DNA, whose behavior better mimics DNA in the living cell. Essentially, they take a short strand of DNA and twist itonce, twice, three times or moreeither with or against the coil. Then they glue the ends together. The end result is a tiny circle of DNA coiled in one direction or another. Zechiedrich, her collaborator and Baylor colleague Jonathan Fogg and others have shown that these twisted coils dance, shimmying through a microscopic ballet. Each molecule can assume a variety of shapes, from simple circles to figure eights, racquets, handcuffs, needles and rods. Linear DNA is stiff and inflexible, said De Witt Sumners, a mathematician at Florida State University in Tallahassee. But when you get it bent into a small circle, the duplex opens up and adopts a large number of interesting shapesthis is completely unexpected.-***-"The findings align with Harris's models, which show that supercoiling can split the two strands of the helix, rotating the DNA bases that normally lie inside the helix to the outside, a phenomenon known as base flipping. Other simulations show that twisting a bit more flips out additional bases, creating a bubble of inside-out DNA. Zechiedrich theorizes these bubbles might provide trigger points for replication or gene expression. This challenges the standard view, in which proteins latch onto DNA and launch these events. Who's driving the bus in cellular metabolism? said Sumners. It's a very dynamic processDNA and proteins each influences how the other acts and reacts.'-Comment: 3-D DNA coiling and uncoiling and forming knots show how fluid and dynamic the living cells are. It helps explain how 23,000+ genes make a human

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The study shows how 3-D proximity can active genes related to disease prevention:-http://medicalxpress.com/news/2016-09-scientists-distant-dna-affect-disease.html-"A person's DNA sequence can provide a lot of information about how genes are turned on and off, but new research out of Case Western Reserve University School of Medicine suggests the 3-D structure DNA forms as it crams into cells may provide an additional layer of gene control. As long strands of DNA twist and fold, regions far away from each other suddenly find themselves in close proximity. The revolutionary study suggests interactions between distant regions may affect how genes are expressed in certain diseases.-"Peter Scacheri, PhD, Associate Professor of Genetics and Genome Sciences at Case Western Reserve University School of Medicine has been studying how specific regions of DNA physically interact with disease genes. His most recent study, published in Nature Genetics, discovered regions of DNA he termed "outside variants" that physically interact with high-risk mutations in a person's DNA sequence called single nucleotide polymorphisms, or SNPs. The outside variants suggest a new level of gene regulation and may help explain how identical SNPs can lead to different clinical outcomes.
"Our previous work showed that there was more to the expression of a disease gene than just the nearby regulatory elements on the DNA strand, and it seemed logical to look at variants that are brought in close physical proximity to the gene when DNA is packaged in the cell," said Scacheri. "By looking at these 'outside variants,' we can determine the risk associated with disease with better precision than by just looking at the known variants."-***-"Once the researchers discovered outside variants, they studied DNA samples to determine the impact of the regions on disease gene levels. The team used computer models to compare gene levels associated with their newly identified outside variants to those associated with previously identified SNPs. The team discovered outside variants physically interacted with known SNPs within the DNA samples and both genetic elements joined forces to mediate disease risk. Through the models, Scacheri's team was able to use outside variants to better predict disease risk.-"According to Scacheri, "The big surprise was when we crunched the numbers and compared the risk associated with the amount of heritability that could be explained by the outside variants. By our calculations, outside variants accounted for a whopping 2-3 times more of the heritability than explained by the current models. That was far more than we had expected."
Further characterization of outside variants revealed they have much in common with enhancer clusters. Proteins that help activate disease genes commonly attach to both regions. In fact, 77% of outside variants identified by the researchers were located near protein attachment sites similar to those found in enhancer clusters. The similarities between outside variants and enhancer clusters support the team's conclusion that multiple elements work together to control disease genes.-***-"The study provides a better understanding of how folded DNA employs distant genetic regions to control how genes are turned on or off. Three dimensional models of DNA may therefore reveal other genetic elements that can help explain the complex processes of gene control, and ultimately disease heritability. The outside variants identified in the study may also provide additional biomarkers to assess a person's risk of disease."-Comment: As noted previously the 3-D relationships in DNA affect gene expression and control. Where a gene is located is part of its function. How did Darwin style chance evolution arrange for that? The complexities in the genome function I have presented are beyond the capacity of a Darwin style evolutionary process.

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Another take on the recent article showing the 3-D relationships of coiled and packed
DNA strongly effect gene expression:-https://www.sciencedaily.com/releases/2016/09/160920151438.htm-"A person's DNA sequence can provide a lot of information about how genes are turned on and off, but new research out of Case Western Reserve University School of Medicine suggests the 3-D structure DNA forms as it crams into cells may provide an additional layer of gene control. As long strands of DNA twist and fold, regions far away from each other suddenly find themselves in close proximity. The revolutionary study suggests interactions between distant regions may affect how genes are expressed in certain diseases.-***-" His most recent study, published in Nature Genetics, discovered regions of DNA he termed "outside variants" that physically interact with high-risk mutations in a person's DNA sequence called single nucleotide polymorphisms, or SNPs. The outside variants suggest a new level of gene regulation and may help explain how identical SNPs can lead to different clinical outcomes.-***-"The study investigated SNPs associated with six autoimmune diseases, rheumatoid arthritis, systemic lupus, Crohn's disease, multiple sclerosis, ulcerative colitis, and celiac disease. The SNPs were previously identified through genome-wide association studies, increasingly popular research tools that search DNA sequence data for regions associated with disease. The large-scale studies tend to zero in on SNPs in "enhancer clusters" of DNA, regions known to contort and interact with disease genes. The researchers identified outside variant DNA regions that seemed to be dependent on known disease SNPs, but were found far beyond enhancer clusters normally associated with the diseases.-***-"The study provides a better understanding of how folded DNA employs distant genetic regions to control how genes are turned on or off. Three dimensional models of DNA may therefore reveal other genetic elements that can help explain the complex processes of gene control, and ultimately disease heritability. The outside variants identified in the study may also provide additional biomarkers to assess a person's risk of disease.-"'We found outside variants associated with several autoimmune-related disorders, including multiple sclerosis, Crohn's disease, and arthritis. The next step is to see if this extends to other common diseases, like heart disease and diabetes," said Scacheri, indicating his research team plans to "determine whether we can use outside variants in a diagnostic or preventive medicine setting to better identify individuals who are most at risk for developing these diseases.'"-Comment: 3-D studies of DNA are extremely important. Again raises the issue of how did DNA initially develop in early life, as a code better and more complex than any humans have invented?

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Another article on the importance of the 3-D relationships of DNA and gene expression:

https://www.quantamagazine.org/20160105-supercoiled-dna/?utm_source=Quanta+Magazine&...

"double-helix DNA is further wrapped into complex shapes that can play a profound role in how it interacts with other molecules. “DNA is way more active in its own regulation than we thought,” said Lynn Zechiedrich, a biophysicist at Baylor College of Medicine and one of the researchers leading the study of so-called supercoiled DNA. “It’s not a passive [molecule] waiting to be latched on to by proteins.”

***

"Simply twisting DNA can expose internal bases to the outside, without the aid of any proteins. Additional work by David Levens, a biologist at the National Cancer Institute, has shown that transcription itself contorts DNA in living human cells, tightening some parts of the coil and loosening it in others. That stress triggers changes in shape, most notably opening up the helix to be read.

***

"DNA rarely gets to relax. It’s subject to a continual onslaught of molecules that bind it — the enzymes that untangle, unwind and then replicate DNA; the molecules that mark which genes are active and which are silent; and the proteins that pack the lengthy molecule into a manageable size. All of these molecules contort DNA into new shapes, blocking it from the repose of the simple double helix.

***

"How the cell decides to activate a certain gene, for example, involves a complex assembly of molecules in the right place at the right time.

***

"Levens and collaborators found that transcription twists DNA, leaving a trail of undercoiled (or negatively supercoiled) DNA in its wake. Moreover, they discovered that the DNA sequence itself effects how the molecule responds to supercoiling. For example, the researchers identified a specific sequence of DNA that’s prone to opening when stressed, like a weak spot in an old inner tube. The segment acts as a sort of chemical cruise control; as the amount of supercoil rises and falls, it slows or speeds the pace at which molecular machinery reads DNA.

***

"supercoiling can split the two strands of the helix, rotating the DNA bases that normally lie inside the helix to the outside, a phenomenon known as base flipping. Other simulations show that twisting a bit more flips out additional bases, creating a bubble of inside-out DNA. Zechiedrich theorizes these bubbles might provide trigger points for replication or gene expression. This challenges the standard view, in which proteins latch onto DNA and launch these events. “Who’s driving the bus in cellular metabolism?” said Sumners. “It’s a very dynamic process — DNA and proteins each influences how the other acts and reacts.'” (my bold)

Comment: Yes, who is driving the bus? All of these molecules, DNA and others in the cell, act as if they were thinking workers in a human factory turning out a product. They must work on information that coordinates their movements. Every cell in the human body or other organisms is doing this at every moment of their lives. Too complex for chance. It requires mental planning.

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QUOTE: “Who’s driving the bus in cellular metabolism?” said Sumners. “It’s a very dynamic process — DNA and proteins each influences how the other acts and reacts.'” (David’s bold)

DAVID’s comment: Yes, who is driving the bus? All of these molecules, DNA and others in the cell, act as if they were thinking workers in a human factory turning out a product. They must work on information that coordinates their movements. Every cell in the human body or other organisms is doing this at every moment of their lives. Too complex for chance. It requires mental planning.

It is all truly amazing, and what a revealing image you have used. Maybe they ARE thinking workers. And maybe your God made them that way.

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QUOTE: “Who’s driving the bus in cellular metabolism?” said Sumners. “It’s a very dynamic process — DNA and proteins each influences how the other acts and reacts.'” (David’s bold)

DAVID’s comment: Yes, who is driving the bus? All of these molecules, DNA and others in the cell, act as if they were thinking workers in a human factory turning out a product. They must work on information that coordinates their movements. Every cell in the human body or other organisms is doing this at every moment of their lives. Too complex for chance. It requires mental planning.

dhw: It is all truly amazing, and what a revealing image you have used. Maybe they ARE thinking workers. And maybe your God made them that way.

It is all very revealing. But not amazing enough to have you recognize God had to plan life. Perhaps the individual molecules are operating through a form of quantum consciousness. All of their activity has purpose, and demonstrates planning.

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dhw: It is all truly amazing, and what a revealing image you have used. Maybe they ARE thinking workers. And maybe your God made them that way.

DAVID: It is all very revealing. But not amazing enough to have you recognize God had to plan life. Perhaps the individual molecules are operating through a form of quantum consciousness. All of their activity has purpose, and demonstrates planning.

The question here is whether the purposeful activity of all of these molecules, DNA and others in the cell, denotes that they ARE thinking workers or are mere automatons. That has been the debate between us. I say they may be thinking workers. You say they are automatons. Whichever they are, when I say “maybe your God made them that way”, I mean maybe your God made them (or if you prefer it, planned them) that way.

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DAVID’s comment: Yes, who is driving the bus? All of these molecules, DNA and others in the cell, act as if they were thinking workers in a human factory turning out a product. They must work on information that coordinates their movements. Every cell in the human body or other organisms is doing this at every moment of their lives. Too complex for chance. It requires mental planning.

dhw: It is all truly amazing, and what a revealing image you have used. Maybe they ARE thinking workers. And maybe your God made them that way.

DAVID: It is all very revealing. But not amazing enough to have you recognize God had to plan life. Perhaps the individual molecules are operating through a form of quantum consciousness. All of their activity has purpose, and demonstrates planning.

dhw: The question here is whether the purposeful activity of all of these molecules, DNA and others in the cell, denotes that they ARE thinking workers or are mere automatons. That has been the debate between us. I say they may be thinking workers. You say they are automatons. Whichever they are, when I say “maybe your God made them that way”, I mean maybe your God made them (or if you prefer it, planned them) that way.

IF we could show molecules think, that would support your vision of the reality of life. Separated out from a living environment, the individual molecules just sit there. Their function only appears in the full milieu of life

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dhw: The question here is whether the purposeful activity of all of these molecules, DNA and others in the cell, denotes that they ARE thinking workers or are mere automatons. That has been the debate between us. I say they may be thinking workers. You say they are automatons. Whichever they are, when I say “maybe your God made them that way”, I mean maybe your God made them (or if you prefer it, planned them) that way.

What do you expect them to do - grow legs and start looking for their buddies? Of course their function only appears in the full milieu of life! If someone put your brain in a glass jar, do you think it would do anything other than sit in the glass jar? All living communities depend on their individual members cooperating, and all living bodies are living communities of living communities. That doesn't mean the individual members don't think, even if their thinking powers are limited to the fulfilment of particular functions. But you are right, IF we could show that the hypothesis is right, it would mean the hypothesis is right! The same applies to your hypothesis of a 3.8-billion-year-old computer programme, divine dabbling, and indeed the very existence of your God.

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David IF we could show molecules think, that would support your vision of the reality of life. Separated out from a living environment, the individual molecules just sit there. Their function only appears in the full milieu of life

dhw: What do you expect them to do - grow legs and start looking for their buddies? Of course their function only appears in the full milieu of life! If someone put your brain in a glass jar, do you think it would do anything other than sit in the glass jar?

Exactly my point. That is why life is a miracle, all those dead molecules coming to life in the right arrangement. You don't want to see the miracle, because it implies you have to accept God!

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DAVID: IF we could show molecules think, that would support your vision of the reality of life. Separated out from a living environment, the individual molecules just sit there. Their function only appears in the full milieu of life

dhw: What do you expect them to do - grow legs and start looking for their buddies? Of course their function only appears in the full milieu of life! If someone put your brain in a glass jar, do you think it would do anything other than sit in the glass jar? You omitted the continuation: All living communities depend on their individual members cooperating, and all living bodies are living communities of living communities. That doesn’t mean the individual members don’t think, even if their thinking powers are limited to the fulfilment of particular functions.

DAVID: Exactly my point. That is why life is a miracle, all those dead molecules coming to life in the right arrangement. You don't want to see the miracle, because it implies you have to accept God!

I thought your point was that cells can’t think. How on earth you can believe, after all these years of discussion, that I don’t see the miracle of life just because I offer the hypothesis that cells may have a (possibly God-given) intelligence, is quite beyond me.

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DAVID: Exactly my point. That is why life is a miracle, all those dead molecules coming to life in the right arrangement. You don't want to see the miracle, because it implies you have to accept God!

dhw: I thought your point was that cells can’t think. How on earth you can believe, after all these years of discussion, that I don’t see the miracle of life just because I offer the hypothesis that cells may have a (possibly God-given) intelligence, is quite beyond me.

I'm delighted you see the miracle. What causes miracles? That brings us to the supernatural, doesn't it? Of course cells can't think. Your theories are all an avoidance of considering God as the source, even your 'possibly God-given' allowances which never say God gave the cells intelligently planned instructions, which to me is the logical conclusion.

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dhw: I thought your point was that cells can’t think. How on earth you can believe, after all these years of discussion, that I don’t see the miracle of life just because I offer the hypothesis that cells may have a (possibly God-given) intelligence, is quite beyond me.

DAVID: I'm delighted you see the miracle. What causes miracles? That brings us to the supernatural, doesn't it?

No, it doesn’t. Tony tried to play the same silly verbal game. The word miracle can ALSO mean “something very lucky or very good which you did not expect to happen or did not think was possible. It’s a miracle you weren’t killed!” (Longman Dictionary of Contemporary English).

DAVID: Of course cells can't think.

Of course those experts who tell us cells can think are wrong. David knows best.

I am an agnostic. If I could accept any theory that excludes God, I would be an atheist. The fact that I offer a theory which includes the possibility of God but runs contrary to your personal interpretation of your God’s thinking – an interpretation which is simply riddled with contradictions and anomalies – does not mean I am avoiding considering God as the source. It means I am offering an alternative hypothesis which even you agree fits in with the history of life as we know it. But I can understand why you are so keen to divert attention away from your own illogical dogma by manufacturing a false motive for my hypothetical but logical alternative! ;-)

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DAVID: I'm delighted you see the miracle. What causes miracles? That brings us to the supernatural, doesn't it?

dhw: No, it doesn’t. Tony tried to play the same silly verbal game. The word miracle can ALSO mean “something very lucky or very good which you did not expect to happen or did not think was possible. It’s a miracle you weren’t killed!” (Longman Dictionary of Contemporary English).

Correct. The use of the word miracle has several levels, but your referred to level is a play on the underlying meaning of supernatural. Your word game avoids the underlying import.

DAVID: Of course cells can't think.

dhw: Of course those experts who tell us cells can think are wrong. David knows best.

Those experts cannot tell us the difference: cells are simply following intelligent instructions.

DAVID: Your theories are all an avoidance of considering God as the source, even your 'possibly God-given' allowances which never say God gave the cells intelligently planned instructions, which to me is the logical conclusion.

dhw: I am an agnostic. If I could accept any theory that excludes God, I would be an atheist. The fact that I offer a theory which includes the possibility of God but runs contrary to your personal interpretation of your God’s thinking – an interpretation which is simply riddled with contradictions and anomalies – does not mean I am avoiding considering God as the source. It means I am offering an alternative hypothesis which even you agree fits in with the history of life as we know it. But I can understand why you are so keen to divert attention away from your own illogical dogma by manufacturing a false motive for my hypothetical but logical alternative!

;-) I'm doing everything I can with the facts I present to knock you off your favorite fence. I'm not illogical. Add God and it all works.

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DAVID: I'm delighted you see the miracle. What causes miracles? That brings us to the supernatural, doesn't it?
dhw: No, it doesn’t. Tony tried to play the same silly verbal game. The word miracle can ALSO mean “something very lucky or very good which you did not expect to happen or did not think was possible. It’s a miracle you weren’t killed!” (Longman Dictionary of Contemporary English).
DAVID: Correct. The use of the word miracle has several levels, but your referred to level is a play on the underlying meaning of supernatural. Your word game avoids the underlying import.

There is no “play”, no “word game” on my part. You accuse me of not seeing the miraculousness of life, and when I assure you that I do, you pretend that the word can only relate to an act of God. You know as well as I do that the word has another meaning, as confirmed by your knowledgeable “correct”. Game over.

DAVID: Of course cells can't think.
dhw: Of course those experts who tell us cells can think are wrong. David knows best.
DAVID: Those experts cannot tell us the difference: cells are simply following intelligent instructions.

Those experts who say that cells are simply following instructions cannot tell the difference. Stalemate.

DAVID: Your theories are all an avoidance of considering God as the source, even your 'possibly God-given' allowances which never say God gave the cells intelligently planned instructions, which to me is the logical conclusion.
dhw: I can understand why you are so keen to divert attention away from your own illogical dogma by manufacturing a false motive for my hypothetical but logical alternative! ;-)
DAVID: ;-) I'm doing everything I can with the facts I present to knock you off your favorite fence. I'm not illogical. Add God and it all works.

I am aware of what you are trying to do, and I appreciate our discussions more than I can ever say. However, you won’t knock me off my fence by kidding yourself that a hypothesis which allows for God is designed to avoid God. And to achieve your admirable purpose, you will need to present a more reasonable alternative to the theistic form of my hypothesis (God set it all in motion, then sat back to watch, though perhaps with an occasional dabble) than God only wanted humans and we don’t know why he specially designed the whale, the weaverbird’s nest and the monarch butterfly’s lifestyle in order to achieve his one and only purpose. (But – non sequitur – all organisms need and provide energy and belong to an eco-niche.)

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DAVID: I'm doing everything I can with the facts I present to knock you off your favorite fence. I'm not illogical. Add God and it all works.

dhw: I am aware of what you are trying to do, and I appreciate our discussions more than I can ever say. However, you won’t knock me off my fence by kidding yourself that a hypothesis which allows for God is designed to avoid God. And to achieve your admirable purpose, you will need to present a more reasonable alternative to the theistic form of my hypothesis (God set it all in motion, then sat back to watch, though perhaps with an occasional dabble) than God only wanted humans and we don’t know why he specially designed the whale, the weaverbird’s nest and the monarch butterfly’s lifestyle in order to achieve his one and only purpose.

My reasonable hypothesis is that God exists and is purposeful. He might be a deistic God as you describe, but I prefer to think of Him as a theistic God, fully engaged with purpose and using evolution by actively speciating forms until He got to humans. There will be no more appearances of very unique species, just adaptation and minor modifications like the human brain being slightly smaller.

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DAVID: ;-) I'm doing everything I can with the facts I present to knock you off your favorite fence. I'm not illogical. Add God and it all works.
dhw: I am aware of what you are trying to do, and I appreciate our discussions more than I can ever say. However, you won’t knock me off my fence by kidding yourself that a hypothesis which allows for God is designed to avoid God. And to achieve your admirable purpose, you will need to present a more reasonable alternative to the theistic form of my hypothesis (God set it all in motion, then sat back to watch, though perhaps with an occasional dabble) than God only wanted humans and we don’t know why he specially designed the whale, the weaverbird’s nest and the monarch butterfly’s lifestyle in order to achieve his one and only purpose.
DAVID: My reasonable hypothesis is that God exists and is purposeful.

As an agnostic, I can understand very well why you think this is a reasonable hypothesis. Our debate here concerns the nature of his purpose.

DAVID: He might be a deistic God as you describe, but I prefer to think of Him as a theistic God, fully engaged with purpose and using evolution by actively speciating forms until He got to humans. There will be no more appearances of very unique species, just adaptation and minor modifications like the human brain being slightly smaller.

I know you prefer to stick to your dogma, and I accept that human consciousness makes us a very special species, but the idea that the WHOLE of evolution – every innovation, lifestyle and natural wonder extant and extinct – was preprogrammed 3.8 billion years ago, apart from the odd dabble, and this was done for the sole purpose of producing humans, is what I find unreasonable.

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dhw: I know you prefer to stick to your dogma, and I accept that human consciousness makes us a very special species, but the idea that the WHOLE of evolution – every innovation, lifestyle and natural wonder extant and extinct – was preprogrammed 3.8 billion years ago, apart from the odd dabble, and this was done for the sole purpose of producing humans, is what I find unreasonable.

You find God unreasonable. The supreme achievement of life's evolution is humans. Why not the main purpose?

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dhw: …the idea that the WHOLE of evolution – every innovation, lifestyle and natural wonder extant and extinct – was preprogrammed 3.8 billion years ago, apart from the odd dabble, and this was done for the sole purpose of producing humans, is what I find unreasonable.

DAVID: You find God unreasonable. The supreme achievement of life's evolution is humans. Why not the main purpose?

Of course I don’t find God unreasonable. It is your interpretation of your God’s motives that I find unreasonable. But once again there is a subtle change in your position. “The main purpose” leaves lots of room for manoeuvre, as opposed to your insistence that it was his only purpose and everything else was related to it. You have slipped this in before when cornered, and I have commented on it. So please tell us more. What other purposes do you think your God may have had in starting life?

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dhw: …the idea that the WHOLE of evolution – every innovation, lifestyle and natural wonder extant and extinct – was preprogrammed 3.8 billion years ago, apart from the odd dabble, and this was done for the sole purpose of producing humans, is what I find unreasonable.

DAVID: You find God unreasonable. The supreme achievement of life's evolution is humans. Why not the main purpose?

dhw: Of course I don’t find God unreasonable. It is your interpretation of your God’s motives that I find unreasonable. But once again there is a subtle change in your position. “The main purpose” leaves lots of room for manoeuvre, as opposed to your insistence that it was his only purpose and everything else was related to it. You have slipped this in before when cornered, and I have commented on it. So please tell us more. What other purposes do you think your God may have had in starting life?

Main purpose is still main purpose. The phrase is to allow for other possible minor purposes, but each time I think about it, I don't find any.

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Biochemical control to isolate and separate areas of DNA found adding to evidence of very complex gene expression controls:

https://phys.org/news/2017-05-great-mystery-dna.html

"After decades of research aiming to understand how DNA is organized in human cells, scientists at the Gladstone Institutes have shed new light on this mysterious field by discovering how a key protein helps control gene organization.

***

"The extreme compacting of DNA into chromosomes is like taking a telephone cord that stretches from San Francisco to New York, and stuffing it into a backpack," described Benoit Bruneau, PhD, a senior investigator at Gladstone and lead author of a new study. "The organization of chromosomes is not random, but rather very complex, and it is critical for normal development. When this process goes wrong, it can contribute to various diseases."

"Chromosomes are coiled into loops and then organized into many large domains called topologically associating domains, or TADs. Within each TAD, several genes and the elements that regulate them are packaged together, and they are insulated from those in neighboring TADs.

"'Imagine TADs are like adjoining rooms: like the genes in each TAD, people in each room can talk to one another, but not to people in the next room," explained Elphège Nora, PhD, postdoctoral scholar in Bruneau's laboratory and first author of the study. "In previous work, we showed that TADs package genes together and insulate them from neighboring genes. The burning question then became: what controls this TAD organization?"

"In the new study, published in the renowned scientific journal Cell, the scientists discovered that the key to organizing these TADs is a protein called CTCF.

"CTCF is a fascinating protein," said Bruneau, who is also a professor at the University of California, San Francisco. "It can be found at the boundaries of TAD domains, and was previously thought to be involved in many aspects of chromosome organization. We wanted to see what would happen to the structure of chromosomes if we removed all the CTCF from cells."

***

"'We noticed that, in the absence of the CTCF protein, the insulating boundaries of TAD domains had almost fully disappeared, so that genes and regulatory elements could now interact with those in adjacent TADs," added Nora. "This would be like removing the wall between adjoining rooms, so that people could now freely interact with others in the neighboring room."

"However, the absence of CTCF had little effect on how genes connect within a single TAD. This indicates that CTCF is required for insulating TADs from one another, but not for packaging genes within these domains. This represents the first conclusive study to show that the two mechanisms are separate and controlled by different proteins.

***

"We looked at a level of organization called compartmentalization, which separates active and inactive genes within a cell nucleus," said Nora. "This helps the cell identify which genes to use. For example, skins cells don't need eye-related genes, so these genes would be tightly packaged in a compartment and put away, because the cell will never use them. We used to think that boundaries of TAD domains were a prerequisite for the organization of these compartments."

"'To our surprise, we found that is not the case," said Bruneau. "When we deleted the CTCF protein, which caused TAD boundaries to disappear, we saw no effect on the organization of the larger compartments. This interesting finding revealed that CTCF and TAD structure are not required for compartmentalization but, rather, that an independent mechanism is responsible for this chromosome organization."

"'Our findings redefine the role of CTCF in gene regulation and provide new insights about the fundamental processes that govern genome organization" added Bruneau. "With this knowledge, we can now start reevaluating the cause of several diseases, as chromosome organization-including TADs-is often disrupted in many cancers and involved in significant developmental defects, such as congenital heart disease.'"

Comment: More and more 3-D DNA controls are found and new layers are sure to be found. These 3-D studies show the level of complexity in that DNA is more than just a linear code but has domains that must be separate and insolated and ones that must be in proximity. Not just a TAD of new complexity. Not by chance. Only a planning mind can create this. Logical.

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It is found very important in embryology as the 3-D DNA controls myocardial development:

https://www.sciencedaily.com/releases/2017/11/171121121438.htm

"The genome stores information about an organisms development. Each cell carries this information tightly packed on a two-meter long DNA strand in the cell nucleus and specific epigenetic mechanisms control access to the 'blueprint of life'. Because every cell type in a mammalian organism requires access to genomic areas in a tempo-spatial specific manner, the epigenome is crucial for determining cellular identity. It is already known that various epigenetic mechanisms are associated with cell differentiation. Particularly indispensable is the methylation of DNA, in which methyl groups are attached to specific nucleotides of double-stranded DNA. Recent studies also show that differentiation processes are accompanied by a reorganization of the three-dimensional folding of the DNA. Up until now, however, it has been unclear what comes first during cardiomyocyte differentiation: the reorganization of the DNA's folding in the cellular nucleus or the DNA's methylation -- and whether these mechanisms are dependent on one another.

"In order to address this question, the team lead by the Freiburg pharmacologists used modern sequencing methods. These made it possible to map the three-dimensional genome organization as well as epigenetic mechanisms during the differentiation of cardiomyocytes across the entire genome. For this purpose, the researchers established methods for isolating cardiomyocytes in various developmental stages from healthy mouse hearts. This cell-type-specific analysis was essential to demonstrate that there is a close interplay between epigenetic mechanisms and the spatial folding of the DNA in the cardiomyocytes' nucleus. The comparison of different stages of development showed that the type of spatial folding of DNA defines which methylation patterns are formed and which genes are activated. The researchers proved that the spatial arrangement of the DNA is not dependent on the DNA methylation with cells, among other things, that have no DNA methylation at all. The three-dimensional genome organization is thus a central switchboard for determining cellular identity. In the future, the researchers want to use this switch to control cellular functions."

Comment: A four-chambered mammalian heart has different cardiomycytes for each chamber since each operates for different purposes and different pressures. For example the right ventricle must have much lower pressure than the left ventricle to protect the lung arteries which cannot tolerate high pressure. Embryology is a proof that Darwin had no idea how organisms developed in proposing his tiny-step approach to evolution. Advanced design requires feedback that the new design is successful. Therefore advanced planning to make the right designs for reproduced complex multicellular organisms, which first appeared in the Cambrian Explosion is required. Embryology reeks of design as the only possible source. A designer is required.

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Special mechanism using two proteins prevents knotting of DNA:

https://www.sciencedaily.com/releases/2019/04/190422100945.htm

"The findings help explain how about 2 metres of DNA can be neatly packaged in each of our cells, in a space that is about the width of a hair.

"Scientists have identified two sets of proteins in cells that work together to keep the strands unknotted, avoiding tangles that would hamper vital biological processes.

"These proteins are found in many organisms, and scientists believe that their role in managing DNA may be common throughout nature.

"One family of proteins -- known as SMC -- acts like a belay device used by rock climbers, which passes ropes through a series of loops.

'These proteins have been found to work alongside another set, known as TopoII, which was previously thought to help solve tangles, but in a way that was not well understood.

***

"They found that SMC acts like a belay, sliding back and forth to enlarge or reduce loops in linked segments of DNA. Knots are first squeezed and compressed by SMC, and subsequently they are easily detected and resolved by TopoII.

"Their study is the first to explain how the two families of proteins keep DNA tangle-free under the confined, crowded conditions of the cell. The research, published in Proceedings of the National Academy of Science, was supported by the European Research Council.

"Dr Davide Michieletto, of the University of Edinburgh's School of Physics and Astronomy, who led the study, said: "DNA's long strands might be expected to become horribly tangled -- a bit like pulling knotted headphones out of your pocket. But instead, nature has created these amazing machines to address this problem in a remarkable way, seemingly across many species.'"

Comment: The DNA double helix looks like a coiled spring, but it is not simply compressed like a spring to fit into a nucleus. It is compressed, twisted and carefully packed. This creates 3-D relationships that are vital to DNA controls through genes influencing each other. Living organisms cannot survive if DNA becomes irreparably knotted up. This means that when DNA was developed, this rescue mechanism had to be present at the same time. Chance Darwinism cannot have created this. Clear evidence of design.

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A study in pigeons shows immunity transferred through two generations:-http://phys.org/news/2015-11-immunity-pigeons.html-Suspecting that older generations were passing along immunity capabilities to more than just their own chicks, the researchers conducted a several year study of urban pigeons. They started by injecting 60 females with a protein called haemocyaninit helps to transport oxygen in some invertebrates but does not do anything beneficial to pigeons. They also injected 60 additional female pigeons with a saline solution to serve as a control group. The team then injected the same protein into all of the offspring of the test pigeons, and then two years later, into all of the third generation of offspring as well. The purpose of the injections was to cause the birds to produce antibodies as a part of an immune responseafter the birds were injected, blood tests were taken to see how strong of a response was triggered. They discovered that the immune response of the third generation was stronger for those chicks whose grandmothers had received haemocyanin than for those whose grandmothers had received the saline. This of course suggested that in reacting to the protein initially, the grandmother pigeons had developed an immune response that they had somehow passed down through their offspring, to their grand-chicks.-Comment: Lamarck lives!

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This is a long article covering much of current research:-http://www.the-scientist.com/?articles.view/articleNo/44628/title/Ghosts-in-the-Genome/-"These and other model systems provide evidence that inheritable epigenetic information exists alongside the inheritable DNA sequence. In addition to RNAs and prion proteins, epigenetic information carriers include covalent modifications to nucleotides and histones, providing a wide variety of mechanisms that enable organisms to transmit information extragenomically. (See illustration above.) And the increasing acceptance of transgenerational epigenetics has, in turn, spurred renewed interest in the possibility that ancestral environmental conditions might influence the phenotypes of future generations.-"This idea, often referred to as the inheritance of acquired characters, was one aspect of Jean-Baptiste Lamarck's early evolutionary theories. But the current use of Lamarckian inheritance to refer to transgenerational epigenetic inheritance is something of a misnomer. In fact, the inheritance of acquired characters was hardly the defining feature of Lamarck's beliefs. His evolutionary theory did not include the basic concept of natural selection, and did not have a place for phenotypic variation existing prior to environmental challenges. Moreover, both Darwin and Lamarck believed that traits acquired in one's lifetime could be passed on. Famously, Darwin even developed a model of inheritance that invoked gemmules, which carried information from all parts of the body to alter the characteristics of the next generation.-"Today, a number of studies document a link between ancestral environmental conditions and changes in offspring behavior or metabolism, potentially validating some of the thinking of both seminal evolutionary theorists on this topic. It is now becoming clear that the environments of both the mother and the father can influence offspring phenotype.-***-"One way to experimentally probe the question of how a father transmits information to his offspring is to breed rodents using assisted reproductive technologies, such as artificial insemination or in vitro fertilization (IVF), that use purified sperm to fertilize ova. In the case of Nestler's social-defeat paradigm, IVF experiments using sperm from control or defeated male mice did not reproduce the effect in offspring, indicating either that the relevant paternal information is located outside of sperm (perhaps in the seminal fluid), or that the disruptive process of IVF and embryo culture might somehow prevent accurate transmission of sperm information to progeny. In contrast, in Diaz and Ressler's study pairing odorants with foot shocks, odor sensitivity was also affected in offspring generated via IVF using sperm from exposed versus unexposed male mice."-Comment: Many parts of the genome and the reproductive process can carry epigenetic information, including perhaps such items as seminal fluid!

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Short tandem repeats, presumed to be junk are not. They modify gene expression:-http://medicalxpress.com/news/2015-12-repetitive-dna-hidden-layer-functional.html-"In the first study to run a genome-wide analysis of Short Tandem Repeats (STRs) in gene expression, a large team of computational geneticists led by investigators from Columbia Engineering and the New York Genome Center have shown that STRs, thought to be just neutral, or "junk," actually play an important role in regulating gene expression. The work, which uncovers a new class of genetic variants that modulate gene expression, is published on Nature Genetics's Advance Online Publication website on December 7. -***-"Genomic variants are what makes our DNA different from each other, and come, Erlich explains, "like spelling errors in different flavors." The most common variants are SNPs (single nucleotide polymorphisms). Computational geneticists have been focused mostly on SNPs that look like a single letter typomother vs. mutherand their effect on complex human traits.-"Erlich's study looked at Short Tandem Repeats (STRs), variants that create what look like typos: stutter vs. stututututututter. Most researchers, assuming that STRs were neutral, dismissed them as not important. In addition, these variants are extremely hard to study. "They look so different to analysis algorithms," Erlich notes, "that they just usually classify them as noise and skip these positions."-"Erlich used a multitude of statistical genetic and integrative genomics analyses to reveal that STRs have a function: they act like springs or knobs that can expand and contract, and fine-tune the nearby gene expression. Different lengths correspond to different tensions of the spring and can control gene expression and disease traits. He is calling these variants eSTRs, or expression STRs, to note that they regulate gene expression."-Comment: With 0nly 22,000+ genes these extra layers of controls explain how humans got so complex.

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Environmental challenges have caused the stickleback fish to change and adapt. Same species but obvious changes in 50 years:-http://www.sciencedaily.com/releases/2015/12/151214165724.htm-"Evolution is usually thought of as occurring over long time periods, but it also can happen quickly. Consider a tiny fish whose transformation after the 1964 Alaskan earthquake was uncovered by University of Oregon scientists and their University of Alaska collaborators.-"The fish, seawater-native threespine stickleback, in just decades experienced changes in both their genes and visible external traits such as eyes, shape, color, bone size and body armor when they adapted to survive in fresh water. The earthquake -- 9.2 on the Richter scale and second highest ever recorded -- caused geological uplift that captured marine fish in newly formed freshwater ponds on islands in Prince William Sound and the Gulf of Alaska south of Anchorage.-***-"'And this is not just a plastic change, like becoming tan in the sun; the genome itself is being rapidly reshaped," she said. "Stickleback fish can adapt on this time scale because the species as a whole has evolved, over millions of years, a genetic bag of tricks for invading and surviving in new freshwater habitats. This hidden genetic diversity is always waiting for its chance, in the sea.'"-Comment: As with guppies, alterations can be quite rapid.

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Technically only species can mate. However many so-called species do mate. However when the individuals are truly far apart as species there is a gene that stops hybridization:-http://phys.org/news/2015-12-gene-species.html-"A University of Utah-led study identified a long-sought "hybrid inviability gene" responsible for dead or infertile offspring when two species of fruit flies mate with each other.-***-"A big surprise is that the gene that makes fruit fly hybrids inviable - named gfzf - is a "cell cycle-regulation gene" or "cell cycle-checkpoint gene" normally involved in stopping cell division and replication if defects are detected. But when mutated and disabled in the new study, the gene allowed the survival of male hybrids of the two fruit fly species.-"The gfzf gene evolves quickly, which is what biologists expect from hybrid inviability genes. But is also was a surprise because cell cycle-checkpoint genes usually evolve slowly because they are "conserved" genes essential in most organisms."-Comment: This is a key finding in explaining how 'true' species stay separate. Organisms that are considered entirely separate, but can cross-breed (horses and donkeys) really aren't. This is the fallacy of identifying only by phenotype. Dogs and wolves easily mate. They are really the same species.

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Most methylation occurs on cytosine , but some is now found an adenine:-http://www.sciencedaily.com/releases/2015/12/151221133734.htm-"Epigenetics has so far focused mainly on studying proteins called histones that bind to DNA. Such histones can be modified, which can result in genes being switched on or of. In addition to histone modifications, genes are also known to be regulated by a form of epigenetic modification that directly affects one base of the DNA, namely the base C. More than 60 years ago, scientists discovered that C can be modified directly through a process known as methylation, whereby small molecules of carbon and hydrogen attach to this base and act like switches to turn genes on and off, or to 'dim' their activity. Around 75 million (one in ten) of the Cs in the human genome are methylated.-"Now, researchers at the Wellcome Trust-Cancer Research UK Gurdon Institute and the Medical Research Council Cancer Unit at the University of Cambridge have identified and characterised a new form of direct modification -- methylation of the base A -- in several species, including frogs, mouse and humans.-"Methylation of A appears to be far less common that C methylation, occurring on around 1,700 As in the genome, but is spread across the entire genome. However, it does not appear to occur on sections of our genes known as exons, which provide the code for proteins.-"'These newly-discovered modifiers only seem to appear in low abundance across the genome, but that does not necessarily mean they are unimportant," says Dr Magdalena Koziol from the Gurdon Institute. "At the moment, we don't know exactly what they actually do, but it could be that even in small numbers they have a big impact on our DNA, gene regulation and ultimately human health.'"-Comment: It means, s ENCODE research showed, less and less junk.

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RNA's are the molecules that carry out gene activity and instructions. This long article describes many activities with methylation:-http://www.the-scientist.com/?articles.view/articleNo/44873/title/RNA-Epigenetics/-"Analyzing the human transcriptome in this way, we identified more than 12,000 methylated sites in mRNA molecules derived from approximately 7,000 protein-coding genes. The transcripts of most expressed genes, in a variety of cell types, were shown to be methylated, indicating that m6A modifications are widespread. In addition, about 250 noncoding RNA sequencesincluding well-characterized long noncoding RNAs (lncRNAs), such as the XIST transcripts that have a key role in X-chromosome inactivationare decorated by m6A. In almost all cases, the epigenetic mark was found on adenosines embedded in the predicted A/Gmethylated AC sequence. We found that this pattern was consistently preceded by an additional purine (A or G) and followed by a uracil (U), extending the known consensus sequence to A/GA/Gmethylated ACU.2-***
"These findings clearly indicate the importance of m6A decoration in regulating the expression of diverse transcripts. Moreover, our parallel study of the human and mouse methylome by m6A-seq has uncovered a remarkable degree of conservation in both consensus sequence and areas of enrichment, further supporting the importance of m6A function.2 But research into understanding how m6A marks themselves are regulated, and how this affects various cellular processes, is only just beginning.-***-"Recently, C.H. and colleagues identified another m6A reader protein, YTHDF1, with a very different functionstimulating protein synthesis by ramping up the efficiency of translation machinery.8 The dueling functions of YTHDF2 and YTHDF1 provide a mechanism by which cells can adjust gene expression promptly and precisely to environmental stimuli. Finally, G.R. and his group have identified an additional reader protein, the RNA-binding protein heterogeneous nuclear ribonucleoprotein A2B1 (HNRNPA2B1),2 which directly binds a set of m6A decorated transcripts and mediates alternative splicing.9-"Clearly, m6A plays diverse roles in regulating cellular function, starting with basic processes such as gene expression, translation, and alternative splicing. As work on this epigenetic mark continues, we will undoubtedly link m6A to numerous phenotypes, and its dysregulation may undergird various diseases and syndromes.-***
"It's quickly becoming clear that m6A decoration has diverse cellular and physiological functions. But perhaps the best illustration of its critical ability to precisely control processes at the cellular level is its involvement in early embryogenesis. Cell-fate decisions are coordinated by alterations in global gene expression, which are orchestrated by epigenetic regulation. Well-established epigenetic marks, such as DNA methylation and histone modifications, are known to mediate embryonic stem cell (ESC) cell-fate decisions, and it turns out that m6A modification is no different.-***-"Dynamic m6A RNA markings, the new kid on the epigenetic block, herald the era of tripartite epigenetics where modifications of DNA, RNA, and proteins join hands to fine-tune gene expression and to execute prompt and precise responses to environmental stimuli and stresses. Indeed, m6A is just one of 140 modified RNA nucleotides that likely affect the function of the nucleic acid messenger and key cellular actor in diverse ways. Molecular approaches are paving the way for the study of additional RNA modifications."-Comment: These brief quotes show how rich this article is in describing how complex the transcription process is directing gene functions.

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Adapting to heat is handled by epigenetic methylation:-https://www.newscientist.com/article/dn28733-guinea-pigs-beat-climate-change-by-tweaking-their-own-dna/-"Hot stuff. For the first time, wild mammals have been seen responding to higher temperatures by altering chemical structures on their DNA. These epigenetic changes may adjust the activity of specific genes, and some are passed on to offspring.-***-"Evolution by genetic mutation and natural selection can be slow. But epigenetic changes that affect how genes are expressed, such as attaching methyl molecules onto DNA, are much faster and more flexible. Experiments in a type of brine shrimp and the plant Arabidopsis thaliana have shown that such heat-induced epigenetic responses can even be inherited by the next generation.-***-"So far, experiments like these have largely focused on organisms that have been bred in artificial lab conditions to become very genetically similar. To see if this can happen in more genetically diverse animals, Weyrich's team studied guinea pigs sourced from South America. They allowed five males to mate with females in an enclosure at a normal ambient temperature of below 5 °C, and then again with other females after spending two months at 30 °C.-"This is a higher temperature difference than they might experience with more gradual climate change, but after two months at this higher temperature, Weyrich's team found signs of significantly altered methylation in at least 10 genes that seem to be linked to regulating body temperature. That these genes were differentially methylated before and after heat is stunning, says Weyrich.-***-"These epigenetic responses may help organisms cope, but they won't make them adapt more quickly, says team member Jörns Fickel, because they don't affect the DNA sequence. Instead, they might buy a species time to evolve permanent adaptations to a warmer climate.-"However, it is not known if every animal can respond in this way. Some organisms may not have an epigenetic heat response to fall back on when temperatures rise.-"The team also identified differences in the methylation patterns of the offspring conceived before and after heat treatment, suggesting that temperature can affect the next generation.-"But intriguingly, the changes found in the later batch of pups were not very similar to the changes seen in their fathers. Weyrich's team believe this may be because the fathers underwent their own set of immediate epigenetic responses to temperature, and then passed on a different set of preparedness changes to their offspring via the sperm they developed during the hot two months."-Comment: Minor modification of same species. Nothing like a proposed inventive mechanism

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Alterations carried in sperm:-http://www.sciencemag.org/news/2015/12/are-you-inheriting-more-genes-your-father-"Male mice bequeath an unexpected legacy to their progeny. Two studies published online this week in Science reveal that sperm from the rodents carry pieces of RNAs that alter the metabolism of their offspring. The RNAs spotlighted by the studies normally help synthesize proteins, so the findings point to an unconventional form of inheritance.-***-"The new work highlights a different class of RNAs, transfer RNAs (tRNAs). In one study, genomicist Oliver Rando of the University of Massachusetts Medical School in Worcester and colleagues delved into a case of epigenetic inheritance in which the progeny of mice fed a low-protein diet show elevated activity of genes involved in cholesterol and lipid metabolism. When Rando's group analyzed sperm from the protein-deprived males, they uncovered an increased abundance of fragments from several kinds of tRNAs. The researchers concluded the sperm acquired most of these fragments while passing through the epididymis, a duct from the testicle where the cells mature. -"In the second study, a team from the Chinese Academy of Sciences in Beijing and other institutions also homed in on tRNA fragments. After feeding male mice either a high-fat or low-fat diet, the scientists injected the animals' sperm into unfertilized eggs. They then tracked the metabolic performance of the offspring, which ate a normal diet. Although progeny of the fat-eating fathers remained lean, they showed two abnormalities often found in their dads and in people who are obese or diabetic: abnormal absorption of glucose and insensitivity to insulin. To determine whether tRNA fragments were responsible for the traits, the researchers inserted the fragments into eggs fertilized with other sperm. Fragments that came from fathers that ate the high-fat diet resulted in offspring that also showed impaired glucose absorption.-***-"Although tRNAs are best known for roles in protein synthesis, their fragments are turning up in other cellular situations. Pieces of functional units that are pretty well understood can have interesting moonlighting functions, Rando says. Both studies suggest that the RNA bits alter gene activity. Rando and colleagues blocked one of the tRNA fragments inside embryonic stem cells and increased the activity of about 70 genes. -"Bale says both papers are really impressive for digging deep into epigenetic mechanisms. And Nadeau says they should help overcome the challenge of identifying the molecules that are responsible for inheritance outside of DNA sequences.'-Comment: In view of the discussion about an inventive mechanism, all this shows is minor adaptations, nothing that suggests a road to speciation. But to a degree Lamarck lives!

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Scientists, by knocking out genes, have cultured a living bacterium with a probably the smallest number of genes and live:-http://phys.org/news/2016-03-microbe-stripped-down-dna-hint-secrets.html-"Scientists have deleted nearly half the genes of a microbe, creating a stripped-down version that still functions, an achievement that might reveal secrets of how life works.-***-"The newly created bacterium has a smaller genetic code than does any natural free-living counterpart, with 531,000 DNA building blocks containing 473 genes.-***-"But even this stripped-down organism is full of mystery. Scientists say they have little to no idea what a third of its genes actually do.-"We're showing how complex life is, even in the simplest of organisms," researcher J. Craig Venter told reporters. "These findings are very humbling."-***-"The genome is not some one-and-only minimal set of genes needed for life itself. For one thing, if the researchers had pared DNA from a different bacterium they would probably have ended up with a different set of genes. For another, the minimum genome an organism needs depends on the environment in which it lives.-"And the new genome includes genes that are not absolutely essential to life, because they help the bacterial populations grow fast enough to be practical for lab work.-"The genome is "as small as we can get it and still have an organism that is ... useful," Hutchison said.-***-"The work began with a manmade version of a microbe that normally lives in sheep, called M. mycoides (my-KOY'-deez). It has about 900 genes. The scientists identified 428 nonessential genes, built their new genome without them, and showed that it was complete enough to let a bacterium survive.-Experts not involved with the work were impressed.-"'I find this paper really groundbreaking," said Jorg Stulke of the University of Goettingen in Germany, who is working on a similar project with a different bacterium. In an email, he said the researchers seem to have gotten at least very close to a minimum genome for M. mycoides."-Comment: Venter's point is very important. It emphasizes how difficult it is to originate life.

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More comments are turning up about this study. Mycoplasma are the smallest-sized genome bacteria known to science:-http://www.the-scientist.com/?articles.view/articleNo/45658/title/Minimal-Genome-Created/&utm_campaign=NEWSLETTER_TS_The-Scientist-Daily_2016&utm_source=hs_email&utm_medium=email&utm_content=27687509&_hsenc=p2ANqtz--4n26M6bsQU03tj-zax8knAqXfUryF8naWRUKE94_KOTB9LPtXzXPGNvZzGpiH4nU-mc-XxccQt2Uy0slX8PHp_Ve4WQ&_hsmi=27687509/-"The team's starting point was the bacterium Mycoplasma genitalium, which has the smallest known genome of any living cell with just 525 genes. However, it also has a very slow growth rate, making it difficult to work with. To practice synthesizing genomes and building new organisms, the team therefore turned to M. genitalium's cousins, M. mycoides and M. capricolum, which have bigger genomes and faster growth rates. In 2010, Venter's team successfully synthesized a version of the M. mycoides genome (JCVI-syn1.0) and placed it into the cell of a M. capricolum that had had its own genome removed. This was the first cell to contain a fully synthetic genome capable of supporting replicative life.-***-"Ultimately the team removed 428 genes from the JCVI-syn1.0 genome to create JCVI-syn3.0 with 473 genes (438 protein-coding genes and 35 RNA genes)considerably fewer than the 525 genes of M. genitalium. Interestingly, the functions of around one-third of the genes (149) remain unknown. I was surprised it was that high, said Hood, but I also think we kid ourselves about how much we know about the genomes of organisms. There's still an enormous amount of dark matter.'-Comment: There are two approaches to studying origin of life, bottom up or top down. Bottom up, starting with inorganic Earth has been a total failure so far. Top down is this attempt to see what a minimum set of genes might be. Very large:-" Let's see now. 473 genes having 531kb. In other words this minimal organism has over 500,000 base pairs. This means that the search space for this relatively simple lifeform is 2^500,000!"-From this ID website:-http://darwins-god.blogspot.com/2016/03/mycoplasma-mycoides-just-destroyed.html-Comment: The above quote assumes looking from bottom up and searching for just the right combination of genome bases to make the organism when starting from scratch. What top down does is point out how difficult it is to find any way to imagine a bottom up natural beginning to life, yet we live. A good reason to look at a supernatural source.

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DAVID: From this ID website: - http://darwins-god.blogspot.com/2016/03/mycoplasma-mycoides-just-destroyed.html - David's comment: The above quote assumes looking from bottom up and searching for just the right combination of genome bases to make the organism when starting from scratch. What top down does is point out how difficult it is to find any way to imagine a bottom up natural beginning to life, yet we live. A good reason to look at a supernatural source. - You will not, I hope, be surprised to hear that I agree. The complexity of the cell is such that belief in chance requires just as massive a leap of faith as belief in an unknown, single, eternally conscious, sourceless mind that can create both a universe and a cell.
However, I really have no sympathy with the following argument put forward by the ID website: - QUOTE: Now, this latest research has upped the ante. It is just getting worse. A minimal organism consisting of 473 genes is many orders of magnitude beyond evolution's capabilities. Simply put, the science contradicts the theory. What the science is telling us is that evolution is impossible, by any reasonable definition of that term. - Evolution is not a theory of the origin of life, but of how different species developed out of the original forms. There is absolutely no reason why theists should not believe that their God created those original cells - and indeed millions of theists do believe just that. The complexity of the cell is an argument against abiogenesis but not against evolution and not for creationism. This sort of distortion is what gets ID a bad name.

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> dhw: You will not, I hope, be surprised to hear that I agree. The complexity of the cell is such that belief in chance requires just as massive a leap of faith as belief in an unknown, single, eternally conscious, sourceless mind that can create both a universe and a cell. - You do not surprise me at all.
> 
> dhw: Evolution is not a theory of the origin of life, but of how different species developed out of the original forms. There is absolutely no reason why theists should not believe that their God created those original cells - and indeed millions of theists do believe just that. The complexity of the cell is an argument against abiogenesis but not against evolution and not for creationism. This sort of distortion is what gets ID a bad name. - Agreed. Do not conflate. Origin of life and the process of evolution are two intertwined but separate points to be considered.

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Virus-fighting genes in primates appear to possibly speed their evolution:-http://phys.org/news/2016-04-primate-evolution-fast-lane.html-"The pace of evolution is typically measured in millions of years, as random, individual mutations accumulate over generations, but researchers at Cornell and Bar-Ilan Universities have uncovered a new mechanism for mutation in primates that is rapid, coordinated, and aggressive. The discovery raises questions about the accuracy of using the more typical mutation process as an estimate to date when two species diverged, as well as the extent to which this and related enzymes played a role in primate evolution. -***-"As primates evolvedincluding chimpanzees, Neanderthals, and modern humansthe number of types of viruses tailored for targeting primates multiplied. APOBECs in our cells mount a vigorous defense, bombarding the viral genome with clusters of mutations to render them unable to continue an infection. However, having such a mutation-based defense is risky for cells, since "friendly fire" could wreak havoc on our genome as well. Indeed, the enzymes have been shown to cause mutations in the tumor cells of breast and other cancers.-***-"The discovery is particularly significant because the enzyme has a tendency to alter regions of the genome that code for proteins as well as the areas responsible for their regulation. It's a vestige of their primary function in viral defense: Many viruses are composed of single stranded DNA or RNA, and DNA being actively used as a template for proteins is temporarily single stranded and unwound from the double helix. To the enzyme, they look the same.-"The researchers looked for the signature of past mutations in humans and our closest hominid relatives, focusing on one of the enzymes in the APOBEC family, APOBEC3, since it has expanded into several subtypes during primate evolution, each with unique mutational signatures.-"They knew that the enzyme recognizes a specific motif in the DNA and it targets only one of the DNA bases for mutation. Another telltale sign: multiple mutations occurring close together. Using conservative criteria, they identified thousands of such instances unique to primate genomes and, as negative control, did not identify any in other vertebrates such as mice that lack many of the APOBEC3 genes.-***-"'What is appealing is that it's an accelerated evolutionary mechanism that could generate a large change in a gene in a single generation," said Levanon. "It's like playing the lotteryit could not have an impact, or it could have a major one."-"'These events potentially mutate dozens of DNA bases in a small region less than the size of a gene. It is reasonable to think that most of these mega-mutations will be deleterious and will disappear in evolutionary time, but we do see a large number that survived," added Keinan. "Importantly, those that survived are overrepresented in functionally important parts of the genome, which suggests that some of these mutations have been maintained by natural selection because they conferred an advantage'." -Comment: Human evolution with its large brain seems fast. These enzymes could be the cause or a cause. The other issue is enzymes are very large with specific functions. How did the evolutionary process find the right giant molecule quickly to fight the infection by viruses, and immediately protect the animal? If that did not happen we could not see the evidence of the advance now. Saltation vs. landscape problem.

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DAVID: Virus-fighting genes in primates appear to possibly speed their evolution:
http://phys.org/news/2016-04-primate-evolution-fast-lane.html-QUOTE: "'What is appealing is that it's an accelerated evolutionary mechanism that could generate a large change in a gene in a single generation," said Levanon. "It's like playing the lotteryit could not have an impact, or it could have a major one."-There seem to be new discoveries all the time in this field, and I can't help wondering whether eventually they will come together to confirm the existence and nature of an autonomous inventive mechanism (let's call it the intelligent cell) that has produced saltations throughout evolution.-David's comment: [] How did the evolutionary process find the right giant molecule quickly to fight the infection by viruses, and immediately protect the animal? If that did not happen we could not see the evidence of the advance now. Saltation vs. landscape problem.-So now we have God supervising every new viral infection (which presumably he devised in the first place) and personally providing the right giant molecule to fight it? Or preprogramming the first cells so that their descendants would come up with the right new molecules at all the right times? Or could there be another explanation, such as God providing organisms (not the evolutionary process) with a mechanism enabling them to find or perhaps design the giant molecule?

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> dhw: So now we have God supervising every new viral infection (which presumably he devised in the first place) and personally providing the right giant molecule to fight it? Or preprogramming the first cells so that their descendants would come up with the right new molecules at all the right times? Or could there be another explanation, such as God providing organisms (not the evolutionary process) with a mechanism enabling them to find or perhaps design the giant molecule?-I've always agreed it is a possibility.

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dhw: So now we have God supervising every new viral infection (which presumably he devised in the first place) and personally providing the right giant molecule to fight it? Or preprogramming the first cells so that their descendants would come up with the right new molecules at all the right times? Or could there be another explanation, such as God providing organisms (not the evolutionary process) with a mechanism enabling them to find or perhaps design the giant molecule?-DAVID: I've always agreed it is a possibility.-You have always insisted that the inventive mechanism has to be guided by God, which is the exact opposite of what I propose.

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Venter's team dos not now what one-third of the genes do but they cannot be removed for life to continue:-"Scientists say they've pared down a microbe's genome to the minimum necessary for life - a mere 473 genes - but they still don't know what a third of those genes do.-'These findings are very humbling in that regard, said genomics pioneer Craig Venter, one of the authors of the study published today by the journal Science.-"Syn 3.0 builds on two decades of work to figure out the genetic mechanisms of life - including the creation of Syn 1.0, the first organism to make use of a synthesized genome.-***-"The other challenge had to do with those 149 mystery genes. Because the functions of the genes are unknown, the researchers didn't know they were needed until they were gone. That shows how far geneticists still have to go in understanding how life works.-'We know about two-thirds of essential biology. We're missing a third, Venter said.-Project leader Clyde Hutchison, a researcher at the J. Craig Venter Institute, said some of the genes appear to play a role in transporting small molecules around the cell. But the details still have to be worked out, and that's a priority for future research, he said.-***-"Syn 3.0 isn't likely to stand as the ultimate minimal genome for life. For one thing, the code was optimized so that it reproduced readily in a lab medium rather than in the natural environment. For another, different species may well have different sets of essential genes. There will be lots of minimal genomes as these same approaches get applied to other types of biological cells, Venter said.-"The fact that researchers are still in the dark about a third of even the smallest viable genome is likely to serve as a cautionary tale as researchers take greater advantage of gene-editing tools. It's vastly premature to talk about editing the human genome until we know a whole lot more, Venter said.-"Venter said the project also suggests that it's too limiting to think about life's machinery in purely gene-centric terms. I think we've shown that we need a genome-centric view of life, looking at functions across the genome, he said. Life is much more like a symphony orchestra than a piccolo player.'-Comment: Layer upon layer of complexity. Obviously more than just coding for proteins.

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We can identify how genes relate to different functioning parts of an animal or plant, but we have no idea how that control is expressed:-http://www.wsj.com/articles/the-effect-of-environment-on-genes-1470938931-"Suppose scientists want to know what a genelet's call it Gene Zhas to do with behavior. Using genetic-engineering wizardry, they generate a line of mice lacking Gene Z (knockout mice), plus another line with an extra copy of Gene Z (transgenic overexpression mice). Then they see if there's something different about the behavior of either group when compared with unmanipulated control mice.-***-"Genes like our fictional Gene Z, with neurogenetic effects on behavior, are often sensitive to small differences in the environment. Gene Z's effects on anxiety might differ between two labs because the mice in the two are fed different kinds of food; nutrition influences brain chemistry and thus potentially Gene Z's effects on the brain.-***-"People are often impressed with the deterministic power of genes, believing they explain everything about our biology and behavior. Many genes do indeed have consistent, powerful effects, but far more of them show a marked environmental dependency than most scientists had previously anticipated. Thus, what Dr. Crabbe and others show is that in many cases, you can't really say what a gene generically doesso perhaps be a bit skeptical about such pronouncements. Instead, you can only safely say what a gene does in the environment(s) in which it has been studied. -"This is pertinent to mice living in different laboratories. But just imagine how much that would apply to a species that can live in dramatically different environmentsin deserts, tundra and rain forests, in hunter-gatherer bands and in dense cities, in close-knit communities or as hermits. There is no species that matches humans in the range of ecosystems, habitats and social system in which it lives. And that suggests there is no species freer from the power of genes than humans."-Comment: This article looks at the possible epigenetic environmental changes in genetic studies. It clearly shows we do not know how genes exert their controls. All we can see is what gene is related to what function and the environment may well alter that function. What this all means is that we recognize the genome does more than just code for proteins, but we are still just at the beginning of how to understand the multitude of layers of functional controls that must be present, especially the HAR's, the human accelerated regions that produce evolutionary jumps just presented yesterday. I continue to believe it is not be chance.

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1st article: 
DAVID: Surprise! Epigenetic mechanisms are different in prokaryotes and eukaryotes according to this review article:
http://www.la-press.com/the-evolution-of-epigenetics-from-prokaryotes-to-humans-and-its...
David's comment: the main point of this very technical article is that the difference in handling DNA in the two types of organisms results in very different ways of applying epigenetic changes. The main point for me is going from unicellular organisms to multicellular is a giant step for evolution to have accomplished, and that step is no more explained than the origin of life itself. The origin of life, multicellularity, and the Cambrian explosion have no explanation in the Darwin theory. -I don't think even Darwin would dispute your comments, so I don't know why you have mentioned him. His theory of evolution was not meant to explain the origin of life or of multicellularity, and he himself acknowledged the problem of the Cambrian explosion (his dilemma), which he hoped (in vain) might be solved by new fossil discoveries.-I shan't pretend to have understood the technicalities of this article, but I am struck by one particular sentence: It was as if nature was experimenting to optimally utilize the gene pool without changing individual gene sequences. As far as we know, Nature is not a consciously experimenting scientist. A theist will perhaps argue that every experiment is carried out by a god. The alternative has to be that every experiment is carried out by the organisms themselves. The effects of such experiments would be accumulative, as every experiment would create new information to be incorporated into new structures. Two possibilities, then: a) a god does it directly; b) the organisms do it themselves. The second of these still leaves open the question of how life and the ability to self-organize originated, but it offers an explanation for the Cambrian, as does the first alternative, which raises the question of how a god originated (usually glossed over by the non-explanation of first cause).
 
xxxx-2nd article:
David's comment: This article looks at the possible epigenetic environmental changes in genetic studies. It clearly shows we do not know how genes exert their controls. All we can see is what gene is related to what function and the environment may well alter that function. What this all means is that we recognize the genome does more than just code for proteins, but we are still just at the beginning of how to understand the multitude of layers of functional controls that must be present, especially the HAR's, the human accelerated regions that produce evolutionary jumps just presented yesterday. I continue to believe it is not be chance. -I agree, and yet again I wish you would consider the possibility that it is not the environment that alters gene function but the cells that alter themselves as an intelligent reaction to the environment. With this simple adjustment of perspective, you not only get rid of chance, but you also allow your God the luxury of not having to preprogramme or dabble every single adjustment that every single cell /cell community makes to every single change in the environment! (NB, in case you have forgotten, this explanation does not exclude God as the originator of cellular intelligence.)

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dhw: Nature is not a consciously experimenting scientist. A theist will perhaps argue that every experiment is carried out by a god. The alternative has to be that every experiment is carried out by the organisms themselves. The effects of such experiments would be accumulative, as every experiment would create new information to be incorporated into new structures. Two possibilities, then: a) a god does it directly; b) the organisms do it themselves. The second of these still leaves open the question of how life and the ability to self-organize originated, but it offers an explanation for the Cambrian, as does the first alternative, which raises the question of how a god originated (usually glossed over by the non-explanation of first cause).-Your second alternative is not supported by the fossils, as Darwin hoped. The current findings in the shale layers in China show the abrupt dramatic appearance of whole multicellular sea animals with the equivalent of arms, legs, organ systems, eyes, etc. with no reasonable antecedent experimental forms. In the preceding pre-Cambrian layer there are simple sheets of cells (Ediacarans) and bilatarian bags of simple cells. Tell me how the complex forms appear with no layer of trial and error forms you propose? Your proposal does not fit the findings. 
> 
> xxxx
> 
> 2nd article:
> David's comment: What this all means is that we recognize the genome does more than just code for proteins, but we are still just at the beginning of how to understand the multitude of layers of functional controls that must be present, especially the HAR's, the human accelerated regions that produce evolutionary jumps just presented yesterday. I continue to believe it is not by chance. [/i]
> 
> dhw: I agree, and yet again I wish you would consider the possibility that it is not the environment that alters gene function but the cells that alter themselves as an intelligent reaction to the environment. ..... (NB, in case you have forgotten, this explanation does not exclude God as the originator of cellular intelligence.)-As you infer, we know that epigenetic effects exist, but so far they are not proven to cause speciation. On the other hand the discovery of HAR's offers a new road to study. I suggest they are God's tool.

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dhw: Two possibilities, then: a) God does it directly; b) the organisms do it themselves. The second of these still leaves open the question of how life and the ability to self-organize originated, but it offers an explanation for the Cambrian, as does the first alternative, which raises the question of how a god originated (usually glossed over by the non-explanation of first cause).
DAVID: Your second alternative is not supported by the fossils, as Darwin hoped. The current findings in the shale layers in China show the abrupt dramatic appearance of whole multicellular sea animals with the equivalent of arms, legs, organ systems, eyes, etc. with no reasonable antecedent experimental forms-I wrote that Darwin acknowledged the problem of the Cambrian explosion (his dilemma), which he hoped (in vain) might be solved by new fossil discoveries. I don't know why you have repeated what I said, when the whole point of my own hypothesis is that if cell communities have the ability to do their own inventing, innovations will take place as saltations, not as gradual transitions. What would be the use of half an arm/leg/liver/kidney?- DAVID:  Tell me how the complex forms appear with no layer of trial and error forms you propose? Your proposal does not fit the findings.-I am not proposing trial and error forms. (See above, and see comment on 2nd article.)-DAVID: (under HARS) I still believe the preponderance of evidence points to a mind behind all of reality
dhw: But believing in a mind behind reality is not the same as believing that such a mind directly designed every innovation and natural wonder, and in the context of evolution, that is what BBella and I are disputing.
DAVID: But I don't separate those parts. That is why I have the dilemma of pre-planning or dabbling. The HAR's look like a dabble. Perhaps something equivalent happened in the Cambrian. Unfortunately we cannot check the DNA.-You don't separate what parts? The theistic version of my hypothesis is that God gave organisms the intelligence to design their own innovations and natural wonders. Where is the separation?-David's comment: (under Early mammal primate) What I find fascinating is how alike those bones are to current anatomy. Looks like pre-planning. -Looks like common descent to me. Organisms providing new structures within the framework of old structures. But for you every difference and every similarity looks like pre-planning!-xxxx-2nd article:
dhw: yet again I wish you would consider the possibility that it is not the environment that alters gene function but the cells that alter themselves as an intelligent reaction to the environment. ..... 
DAVID: As you infer, we know that epigenetic effects exist, but so far they are not proven to cause speciation. On the other hand the discovery of HAR's offers a new road to study. I suggest they are God's tool.-Even if they are God's tool, they can still be part of an autonomous mechanism which is capable of innovation as well as adaptation. But of course nothing has been proven yet. That is why we can only hypothesize.

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> dhw: I wrote that Darwin acknowledged the problem of the Cambrian explosion (his dilemma), which he hoped (in vain) might be solved by new fossil discoveries. I don't know why you have repeated what I said, when the whole point of my own hypothesis is that if cell communities have the ability to do their own inventing, innovations will take place as saltations, not as gradual transitions. What would be the use of half an arm/leg/liver/kidney?
> 
> DAVID:  Tell me how the complex forms appear with no layer of trial and error forms you propose? Your proposal does not fit the findings.
> 
> dhw: I am not proposing trial and error forms. (See above, and see comment on 2nd article.)-Whole Cambrian organisms are very complex with several organ systems that have to invented and coordinated in function. You want existing simple organisms in the pre-Cambrian to invent these giant steps without trial and error. That requires a planning mind. Your proposal is impossible unless God has implanted a perfect inventive mechanism, a possibility I accept. But that makes God primary to the control of evolution.->dhw: The theistic version of my hypothesis is that God gave organisms the intelligence to design their own innovations and natural wonders.-As described above, I accept this.-> 
> David's comment: (under Early mammal primate) What I find fascinating is how alike those bones are to current anatomy. Looks like pre-planning. 
> 
>dhw:Looks like common descent to me. Organisms providing new structures within the framework of old structures. But for you every difference and every similarity looks like pre-planning!-Of course common descent. Dinosaurs had similar femurs, but I was looking just at the tiny mammals that succeeded them. One can look at femurs back before the dinosaurs. Pattern pre-planning.
> 
> xxxx
> 
> David: the discovery of HAR's offers a new road to study. I suggest they are God's tool.[/i]
> 
> dhw: Even if they are God's tool, they can still be part of an autonomous mechanism which is capable of innovation as well as adaptation. But of course nothing has been proven yet. That is why we can only hypothesize.-I've been theorizing there is a drive to complexity. HAR's may be a sign of it.

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Cells open up genes to begin the anti-inflammation function:-https://www.sciencedaily.com/releases/2016/08/160816152919.htm-"...scientists show that when immune cells encounter a bacteria, a number of genes become active. During this process, nucleosomes, which coat DNA and essentially block genes, are gone, leaving the genes open and ready to enlist in the fight against bacteria.-"These particular genes are related to inflammation.-***-"'What causes some cells to express these genes while other cells do not?" she asked. "Does the packaging of DNA play a role in deciding which genes are expressed? We believe that it's more about the regulation and the mechanics of how the transcriptional machinery is recruited than the genes themselves."-"Floer likens the process to Michigan winters. In the Midwest, it's always snowing. Finding an open parking space that's not covered with snow becomes a statewide pastime. Complicating matters, imagine that you have an electric car, and you need a special spot. There are only a few of them, and they have to be cleared of snow.
Specifically, the team extracted stem cells involved in inflammation and fighting infections from the bone marrow of mice. They grew them in petri dishes to become mature macrophages, white blood cells that devour any diseased protein in their path. In their experiments, they showed that cell-type specific transcription factors bind to macrophage-specific genes and recruit the nucleosome remodeler -- the cellular snowplows. Once bonded, nucleosome remodelers keep the gene regulatory sites open by clearing away the blizzard of nucleosomes.-"In addition, Floer's team discovered that the remodelers function at these sites long before the genes are expressed and doing their jobs. This means that they are recruited at some point during differentiation of stem cells into their specific, adult cells.-"'We find that as a cell differentiates into a specific cell type, it acquires all of the necessary information early on that dictates its behavior as an adult cell," Floer said.-"The next phase of this research will be expanded genome wide. Floer's team focused only on a handful of genes. Along with tackling an entire genome, the team will experiment with environmental changes during differentiation to see what factors enhance the prevalence of cellular snowplows..."-Comment: Since infections kill, I wonder how these cells develop their capacity to fight infection with potential fatal infections all around. It doesn't seem to be possible step by step.

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DAVID: Whole Cambrian organisms are very complex with several organ systems that have to invented and coordinated in function. You want existing simple organisms in the pre-Cambrian to invent these giant steps without trial and error. That requires a planning mind. Your proposal is impossible unless God has implanted a perfect inventive mechanism, a possibility I accept. But that makes God primary to the control of evolution.-Primary in the sense that he started it all, but absolutely not in the sense of control. My hypothesis (theistic version) specifically entails his handing control to the organisms themselves, except when he dabbles. Perfect is also misleading. We must always remember that if common descent is true (and I think it is), then every change has to take place in existing individual organisms. When the environment changes, many organisms go extinct. That means failure on a massive scale. But what I am proposing is that some individual organisms - probably very few initially - have the intelligence to work out new designs, and of course this means that all the cell communities within those organisms must cooperate (or "coordinate their function"). With today's postings alone, you have given us one example after another of how this process works for adaptation and therefore might work for innovation:
 
DAVID: (Under Fruiting bodies) Some unicellular organisms under stress will form fruiting bodies, an early form of multicellularity, and if the stress is severe enough some of the cells become spores to insure survival
http://www.the-scientist.com/?articles.view/articleNo/46673/title/First-Micrographs-of-...
Your comment: Some amoeba also can do this. It is obvious that stress in the environment causes developments of this kind. That is the 'why' part. It is the 'how' part that puzzles me. If the stress is severe and they don't get to the spore phase quickly they don't survive. This is a protective process that had to be developed over time. Non-survivors don't develop anything. Did it appear magically all at once?-Many of them will not have survived. But some very bright ones did. They worked out a way to do it. No magic is required if you acknowledge that they are sentient, cognitive, decision-making beings.-DAVID: (under How cells fight infection:) Since infections kill, I wonder how these cells develop their capacity to fight infection with potential fatal infections all around. It doesn't seem to be possible step by step.-No, it doesn't. And of course many infections do kill. But some cells are bright enough to work out how to fight infection.
 
DAVID: (under New oxygen research) Note the oxygen cycle system keeps oxygen at the same steady level. Again, the theory is that this level was necessary for evolution to progress, although it didn't have to progress. Bacteria are still here and very successful just as they were.-The intelligence demonstrated in the earlier examples is what leads to the next step: once conditions offer new opportunities, some organisms (probably a small minority) are intelligent enough to find new ways of exploiting them. That is where the mechanism for adaptation (i.e. intelligence plus the ability to alter their own structure) becomes a mechanism for innovation. Once again, if only you would acknowledge that cells/cell communities may be intelligent, sentient cognitive beings in their own right, you would accept this is as a feasible hypothesis. -DAVID: As described above, I accept this.-As described above, you will then have to accept that(theistic version)God created a mechanism that ceded control of evolution to the organisms themselves - except for the occasional dabble. And if your God gave organisms the intelligence to invent new organs, I hope you will also accept that organisms will also have the intelligence to work out all the natural wonders which you have hitherto insisted were also specially and directly designed by your God.-David's comment: (under Early mammal primate) What I find fascinating is how alike those bones are to current anatomy. Looks like pre-planning. 
dhw:Looks like common descent to me. Organisms providing new structures within the framework of old structures. But for you every difference and every similarity looks like pre-planning!
DAVID: Of course common descent. Dinosaurs had similar femurs, but I was looking just at the tiny mammals that succeeded them. One can look at femurs back before the dinosaurs. Pattern pre-planning.-Why do you tack on pre-planning? Common descent simply means that the patterns were inherited. If innovations are successful, they will be passed on, and later organisms will invent their own variations.-DAVID: the discovery of HAR's offers a new road to study. I suggest they are God's tool.
dhw: Even if they are God's tool, they can still be part of an autonomous mechanism which is capable of innovation as well as adaptation. But of course nothing has been proven yet. That is why we can only hypothesize.
DAVID: I've been theorizing there is a drive to complexity. HAR's may be a sign of it.-I've been theorizing that there is a drive to survival and/or improvement. HARS may be a sign of it.

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Transcription factors and DNA have an intimate relationship for modification of gene expression and function:-http://phys.org/news/2016-09-dna-function-transcription-factors.html-"Substances known as transcription factors often determine how a cell develops as well as which proteins it produces and in what quantities. Transcription factors bind to a section of DNA and control how strongly a gene in that section is activated. Scientists had previously assumed that gene activity is controlled by the binding strength and the proximity of the binding site to the gene. Researchers at the Max Planck Institute for Molecular Genetics in Berlin have now discovered that the DNA segment to which a transcription factor binds can assume various spatial arrangements. As a result, it alters the structure of the transcription factor itself and controls its activity. Neighbouring DNA segments have a significant impact on transcription factor shape, thus modulating the activity of the gene. -***-"The researchers discovered that transcription factors can assume various shapes depending on which DNA segment they bind to. "The shape of the bond, in turn, influences whether and how strongly a gene is activated," Meijsing explains.-"Consequently, transcription factors can bind to DNA segments without affecting a nearby gene.-"One example is glucose production in the liver. If the blood contains too little glucose, the adrenal glands release glucocorticoids, which act as chemical messengers. These hormones circulate through the body and bind to glucocorticoid receptors on liver cells. The receptors simultaneously act as transcription factors and regulate gene activity in the cells. In this way, the liver is able to produce more glucose, and the blood sugar level rises again.-"'Sometimes glucocorticoid receptor binding results in strong activation of neighbouring genes, whereas at other times little if anything changes," Meijsing reports. The scientists found that the composition of DNA segments to which the receptors bind help determine how strongly a gene is activated. However, these segments are not in direct contact with the receptors acting as transcription factors; they only flank the binding sites. Yet, that is evidently enough to have a significant influence on the interaction.-"'The structure of the interface between the transcription factor and genome segments must therefore play a key role in determining gene activity. In addition, adjacent DNA segments influence the activity of the bound transcription factors. These mechanisms ultimately ensure that liver cells produce the right substances in the right amounts," Meijsing says."-Comment: the glucocorticoid example is a wonderful description of how the body is coordinated in its feedback controls of various important chemical levels. I again ask, how did evolution develop such a complex stepwise system of intimate controls. Hard to imagine it is trial and error.

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This research pinpoints how damaged areas of DNA are discovered, marked for repair. The agent is an enzyme which are large complex molecules:-http://phys.org/news/2016-09-scientists-super-enzyme-dna.html-"New research funded by the MRC and Cancer Research UK, led by the laboratories of Professor Keith Caldecott and Professor Laurence Pearl at the University of Sussex's Genome Damage and Stability Centre, has identified how the enzyme PARP3, short for poly(ADP-ribose) polymerase 3, recognises and signals the presence of broken DNA strands. -"Research has shown that the PARP3 enzyme is involved in the DNA repair process and helps to maintain the integrity of the genetic code, but until now the precise DNA repair activation mechanism triggered by the enzyme was unclear.-***-"When the PARP3 enzyme locates a specific site of DNA damage, it 'marks' the damaged DNA with a molecular signal.-"This signal is created via a chemical change, involving the addition of a molecule called 'ADP-ribose' to the DNA. The DNA is packaged up in a complex called 'chromatin' which contains proteins; the team found that the PARP3 enzyme adds the 'ADP-ribose' molecule to one of these proteins - 'histone H2B'.-"By marking the precise site of damage the enzyme flags the problem up to specialised DNA repair enzymes that will move in to repair the damage, protecting the cell from potentially dangerous DNA breaks.-***-"PARP3 is one of a superfamily of enzymes that are targeted by PARP inhibitor drugs, a new class drugs used to treat hereditary cancer, including ovarian and breast cancer. Knowledge of how the PARP3 enzyme activates DNA repair will also contribute to improving the understanding, and targeting, of PARP inhibitor drugs."-Comment: Note these are automatic molecular reactions which must occur quickly to protect the integrity of DNA and prevent bad mutations. The key issue is that these enzymes have specific lock and key areas which can lock to the problem areas and initiate the repair. How did evolution find such large specific molecules to do this job early in the history of life, without which life could not have safely continued? See this link in Wikipedia to understand how complex these enzymes are in structure. Follow the links in the structure paragraph to see diagrams of the enormous structure:-https://en.wikipedia.org/wiki/PARP3 -Not by chance.

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Scientists have found out how epigenetic tags on DNA are carried forward into new cells:-https://www.sciencedaily.com/releases/2016/09/160907160525.htm-"Epigenetic tags help tell genes -- stretches of DNA that act as biological instruction manuals -- when to switch "on" and "off," ultimately determining cell type and function. DNA methylation, or the addition of methyl tags to DNA, is one of the most well-studied epigenetic signals; errors in this process are commonly found in cancer.-***- "The findings center on a protein called UHRF1, a guardian of the cell's epigenetic information that can recognize patterns of epigenetic tags and promote the addition of new ones. These "reading" and "writing" activities of UHRF1 are well understood on their own but until now, scientists didn't know exactly how or even if these UHRF1 activities worked together.-***-"Here's what they found -- during cell division, UHRF1 recognizes newly copied DNA at sites that are missing methyl tags. At the same time, it also recognizes a protein associated with DNA called histone H3 and attaches another small protein called ubiquitin on that histone. This ubiquitin protein acts as a molecular flag, signaling to another protein called a DNA methylation enzyme that a methyl tag is needed there. The group discovered that ubiquitin attachment on the histone is promoted by the pre-existing pattern of epigenetic signals recognized by UHRF1. This is the first time an epigenetic signal has been shown to impact ubiquitylation and connects the patterns of epigenetic information in a new way.-"'While the functions of the individual parts of UHRF1 were already known, we didn't appreciate the interdependence of these functions in adding ubiquitin to histones," said Joe Harrison, Ph.D., a postdoctoral fellow in the Kuhlman Laboratory at UNC and the paper's first author. "This exquisite regulation of an ubiquitin ligase has not been previously described and is very exciting for the field of ubiqutin biology.'"-Comment: Once again we see amazing complexity of how a molecule can act to preserve or change DNA by watching DNA methylation flagging. Unless one thinks molecules do this intelligently through their own thought, this is done automatically.

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Another part of the DNA repair process is found using a large enzyme:-http://phys.org/news/2016-09-dna.html-"To find out what activates SIRT6, the researchers alternately applied chemical inhibitors to human skin cells to determine which proteins were essential in getting the gene to repair the broken DNA strands. They discovered that one protein was involved in activating the gene in response to oxidative stressc-Jun N-terminal kinase, which goes by the simpler term JNK. When JNK was inhibited, SIRT6 was not activated and the broken strands of DNA were not repaired efficiently. -"To communicate stress signals within cells, JNKs add phosphate groups to proteins, and the Rochester study found the amino acid residue on SIRT6 that is modified by JNK. Once modified, SIRT6 can attract the enzyme PARP1 (Poly [ADP-ribose] polymerase 1) to the damaged site, where the enzyme undertakes a chemical process to repair the DNA. In effect, the activated gene serves as a first responder, recruiting DNA repair enzymes to the accident site and getting them to work.-"The study is the latest work by Gorbunova and Seluanov to shed light on the molecular mechanisms that drive the aging process. Their previous work involved understanding the prominence of an inferior DNA repair process later in life, as well as how errant DNA fragmentscalled jumping genesare typically kept inactive."-Comment: Note these are automatic molecular reactions. Once again Note the use of giant enzymes which raise the issue of how did evolution find this type of molecule. I'm still suggesting saltation.

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Long thought to be part of 'junk DNA' long non-coding RNAs (lncRNA)are found to have function in developing heart cells:-https://www.sciencedaily.com/releases/2016/09/160908164948.htm-"Several years ago, biologists discovered a new type of genetic material known as long noncoding RNA. This RNA does not code for proteins and is copied from sections of the genome once believed to be "junk DNA." Now, in a related study, biologists have discovered how an enigmatic type of RNA helps to control cell fate. -"Several years ago, biologists discovered a new type of genetic material known as long noncoding RNA. This RNA does not code for proteins and is copied from sections of the genome once believed to be "junk DNA."-"Since then, scientists have found evidence that long noncoding RNA, or lncRNA, plays roles in many cellular processes, including guiding cell fate during embryonic development. However, it has been unknown exactly how lncRNA exerts this influence.-"Inspired by historical work showing that structure plays a role in the function of other classes of RNA such as transfer RNA, MIT biologists have now deciphered the structure of one type of lncRNA and used that information to figure out how it interacts with a cellular protein to control the development of heart muscle cells. This is one of first studies to link the structure of lncRNAs to their function.-
***-"In the new study, the researchers decided to investigate which regions of the 600-nucleotide RNA molecule are crucial to its function. "We knew Braveheart was critical for heart muscle cell development, but we didn't know the detailed molecular mechanism of how this lncRNA functioned, so we hypothesized that determining its structure could reveal new clues," Xue says.-***-"This analysis revealed that Braveheart has several distinct structural regions, or motifs. The researchers then tested which of these motifs were most important to the molecule's function. To their surprise, they found that removing 11 nucleotides, composing a loop that represents just 2 percent of the entire molecule, halted normal heart cell development.-"The researchers then searched for proteins that the Braveheart loop might interact with to control heart cell development. In a screen of about 10,000 proteins, they discovered that a transcription factor protein called cellular nucleic acid binding protein (CNBP) binds strongly to this region. Previous studies have shown that mutations in CNBP can lead to heart defects in mice and humans.-"This analysis revealed that Braveheart has several distinct structural regions, or motifs. The researchers then tested which of these motifs were most important to the molecule's function. To their surprise, they found that removing 11 nucleotides, composing a loop that represents just 2 percent of the entire molecule, halted normal heart cell development.-"The researchers then searched for proteins that the Braveheart loop might interact with to control heart cell development. In a screen of about 10,000 proteins, they discovered that a transcription factor protein called cellular nucleic acid binding protein (CNBP) binds strongly to this region. Previous studies have shown that mutations in CNBP can lead to heart defects in mice and humans."-Comment: This study again shows the enormous complexity in layers of control within DNA in cell development and raises the issue (once again) of how did a chance evolutionary process find the structure of lncRNA to perform this duty in heart cell development. Secondly a key argument used by Darwinists is that 'junk DNA' was 80% of all DNA. Therefore, it was developed by chance evolution, as discarded DNA, resulting from new advances that supplanted older forms. Obviously, junk DNA is a false premise, as 80% of DNA is found to be functional. Living organisms clearly show chance did not create life, God did.

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Genes are modified by methylation, and there are controls of this:-http://medicalxpress.com/news/2016-09-inherited-parental-methylation-shifts-functional.html-"Parental imprintinga form of gene control passed down from parents to offspringis far more dynamic than previously thought and may contribute to changes in the brain and other tissues over time. This finding by Whitehead Institute scientists challenges current understandings of gene regulation via DNA methylation, from development through adulthood. -"'All of this dynamic variation between individuals and within individuals is really very surprising," says Whitehead Founding Member Rudolf Jaenisch, who is also a professor of biology at MIT. "We don't yet understand the significance of this. Is it functionally important and does it reflect, particularly in the brain, the history of neuronsactivity states, for example? These are all interesting possibilities."
Methylationthe attachment of molecules, known as methyl groups, to DNAis an epigenetic phenomenon that affects gene expression. Generally, methylated genes are turned off while unmethylated genes are active and ready for transcription. Although advances in sequencing technology have yielded informative methylation maps in a variety of tissues, such approaches only capture static "snapshots" of methylation and are unable to reveal the dynamics of methylation in real time in tissues and individual cells.-***-"To investigate active methylation in individual cells, Jaenisch lab postdoctoral researcher Yonatan Stelzer developed a reporter system that tracks genomic methylation in real-time. When a target gene is unmethylated, the reporter is also unmethylated, triggering expression of a glowing protein that illuminates the cell. When the target is methylated, so too is the reporter. The glowing protein is then unexpressed, leaving the cell dark. As the target gene's methylation changes, so does the reporter's.-"In the latest research, described online this week in the journal Cell Reports, Stelzer used the reporter system in mice to discover that imprinted methylation in developing and adult tissues is actively regulated rather than merely maintained in stable fashion.-"'What we see with the reporter in adult tissues is very surprising and much more complex than we had thought," says Stelzer, ..."The regulation of imprinted methylation results in these very consistent patterns in different tissues and even in a cell-type dependent manner. In the case of neural cells, it means that imprinted methylation is dynamically shaping the adult brain over time and could play a role in aging. Because this imprinting affects hundreds of genes that are non-coding, including microRNAs and non-coding RNAs, it's a very interesting fine-tuning mechanism for the dosage of gene expression in the brain and elsewhere in the body.'"-Comment: Methylation is an active modification process, but as we always see in genetic controls, a mechanism is present to turn on but also to turn off. In the Darwinian chance form of evolution one would wonder if both parts of the controls develop together. Seem unlikely in a hunt and peck system.

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DNA is under surveillance to check for incorrect copies as cells divide and copy DNA. p53 is a chemical which drives repair genes:-http://medicalxpress.com/news/2016-09-regulatory-rna-essential-dna-response.html-"researchers at the Stanford University School of Medicine have discovered a new player in this high-stakes molecular game in the form of a novel regulatory RNA they've named DINO. This RNA molecule binds to and stabilizes a well-known tumor suppressor protein called p53 that mobilizes a cell's response to DNA damage. When mutated, p53 is one of the most infamous bad guys in the cancer world.-"'It's so important for a cell to keep track of potentially dangerous changes to its genome," said professor of dermatology Howard Chang, MD, PhD. "But if cells reacted to every little ding, they would find themselves responding inappropriatelythey would stop growing and maybe even self-destruct unnecessarily. You don't want to do this unless the DNA damage is severe. We've discovered that DINO is an integral part of this decision-making circuit."-***-"DNA damage is a natural byproduct of cell division because it is impossible to faithfully copy each of the 3 billion nucleotides that make up our genomes without making at least a few errors. Damage can also be caused by exposure to certain chemical agents, ultraviolet light and ionizing radiation.-"Most of the time these problems are recognized and quickly repaired by the cell. That's where p53 comes in. When it is doing its job, p53 recognizes and responds to DNA damage by increasing the expression of genes involved in DNA repair and cell division. In this way it functions as a tumor suppressor. When mutated, however, p53 loses its ability to modulate the cell's response to DNA damage. Mutations in p53 are among the most common causes of many types of cancer.-"Chang and his collaborators found that p53 also increases the expression of DINO. DINO, in turn, binds to and stabilizes p53 in a kind of positive feedback loop, amplifying its signal throughout the nucleus. (my bold)-***-"DINO is a member of a group of RNA molecules known as long noncoding RNAs, or lncRNAs. These molecules have been implicated in a growing number of critical regulatory roles throughout the cell. This is the first time that a lncRNA has been shown to be involved in this critical DNA damage-response pathway in living animals.
Chang and his colleagues found that when DINO expression is artificially increased, cells respond as if their DNA has been damaged even in the absence of any genome changes. In contrast, when DINO expression is inhibited, the cell responds less robustly to signals from p53.-
"'DINO expression allows the cell to fine-tune its response to DNA damage and respond appropriately," said Chang.-
"Because, as an RNA, DINO is made in the cell's nucleus where p53 is active, the researchers believe it may provide a more rapid and precise response to DNA damage than would a regulatory protein, which would be synthesized in the cytoplasm."-Comment: Another example of a feedback loop with automatic molecular actions. This had to be present from the beginning of life using DNA as the genome code, since copying DNA has to be closely monitored or life would not last. Saltation.

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A more flexible DNA interpretation allows for more variability in evolution:

http://www.the-scientist.com/?articles.view/articleNo/47097/title/Protozoans-Found-With...

"The genetic code—the digital set of instructions often laid out in tidy textbook tables that tells the ribosome how to build a peptide—is identical in most eukaryotes. But as with most rules, there are exceptions. During a recent project on genome rearrangement in ciliates, Mariusz Nowacki, a cell biologist at the University of Bern in Switzerland, and his team stumbled across two striking deviants.

"Ciliates, complex protozoans with two nuclei, are known to translate RNA transcripts in unorthodox ways. Nowacki’s team, however, discovered that Condylostoma magnum and an unclassified Parduczia species had gone even further, reassigning all of the traditional “stop” codons (UGA, UAA, and UAG) to amino acids. “It didn’t make sense in the beginning,” says Nowacki. “Nobody would expect that there would be a stopless genetic code.”

"Puzzled, Nowacki’s team wanted to find out what the ciliates’ actual stop codons looked like. The group turned to transcripts of the ciliates’ histone proteins because their sequences are highly conserved across all eukaryotes. Using protein mass spectrometry and ribosome profiling, the researchers determined that the Parduczia species always interpreted UAA and UAG as glutamine codons, but read UGA as a tryptophan codon in some cases and as a stop codon in other cases. Even stranger, in C. magnum all three traditional stop codons functioned as either a stop or an amino acid signal.

“'For the cells to survive, they have to be able to resolve this ambiguity,” says Nowacki. The data showed that the ribosomes somehow knew to interpret the same combination of three nucleotides as either “stop” or “go” in the appropriate context—so Nowacki’s team started looking for contextual clues.

"The researchers discovered that the appearance of the ambiguous codons declined dramatically near the end of transcripts, cutting down on the potential confusion. Additionally, C. magnum and the Parduczia species had a remarkably short length of untranslated mRNA between the translated part of the transcript and the 3’ poly(A) tail, compared with other eukaryotes. The team suggests that proteins coating or interacting with the poly(A) tail may act as roadblocks to translation when the ribosome bumps up against them. In yeast, poly(A)-binding proteins have been shown to play a role in translation termination.

"I think it’s a very good explanation,” says Andre Cavalcanti, a molecular biologist at Pomona College in California, though it raises the question of whether the codon reassignment or the short untranslated region (UTR) evolved first. “Not every ciliate that reassigns the genetic code has UTRs as short as these, which seems to be a requirement of the model,” he added in an email to The Scientist. “Different ciliates might adapt in different ways.”

"To test its hypothesis, Nowacki’s team is planning to tinker with the length of the UTR in C. magnum. If the researchers can push the poly(A) tail farther away from the true stop codon, Nowacki predicts, they may see more readthrough.

“'We were able to identify a novel biology in sea creatures, in creatures that were never looked at before,” says Nowacki. “It shows that [the genetic code] is not necessarily frozen and unambiguous." (my bold)

Comment: This DNA variability allows for more adaptation ability and may help explain how bacteria adapt to extreme environments. These variations could have been given by God at the beginning of life. Less dabbling required.

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12570 views

Bacteria contain enzymes to protect themselves from attack. These enzymes are giant molecules modified and used in research labs to study DNA by breaking it up an reinserting genes:

http://www.wsj.com/articles/a-genetic-chain-saw-to-target-harmful-dna-1477081818

Many people are excited by the potential of the genetic tool Crispr-Cas9 to serve as a kind of molecular scissors to cut and repair malfunctioning DNA.

***

"Crispr, which stands for Clustered Regularly Interspaced Short Palindromic Repeats, is thought to have evolved in bacteria over millions of years. Crispr is the immune system of the bacteria, capturing an invader’s DNA and integrating it into the genome of the bacteria to fend off future attacks.

"Several years ago, scientists demonstrated a way to reprogram an enzyme called Cas9 in the Crispr system to enable the editing of genes—opening up the potential to someday cure genetic diseases.

***

"There are actually six major types of Crispr systems in nature, each of which uses different enzymes to perform tasks. Dr. Barrangou wants to use the Crispr-Cas3 system to take on antibiotic resistance.

"The Cas9 and Cas3 enzymes have some things in common. For one thing, both can be programmed to target DNA. But Cas9 cuts DNA like a surgeon’s scalpel, causing a break that can then be repaired. Cas3, says Dr. Barrangou, operates more like Pac-Man, chewing up DNA and causing extensive damage that can’t be readily fixed. Dr. Barrangou says that the goal is to get harmful bacteria to commit cell suicide.

“'Cas3 is a meaner system and more cumbersome than Cas9,” he says. “But if you want to cut a tree and get rid of it, you bring a chain saw, not a scalpel.”
Dr. Barrangou and his colleagues founded a company called Locus Biosciences in Raleigh, N.C., to use reprogrammed Crispr-Cas3 to develop antimicrobials and tackle infectious diseases that are increasingly resistant to antibiotics, such as C.difficile, E.coli and MRSA. Challenges remain, including testing the delivery of Crispr to the bacteria. “We aren’t trying to edit it,” says Paul Garofolo, Locus’s CEO. “We are trying to kill it.”

"This new focus on the potential of other Crispr systems can be traced at least in part, scientists say, to a 2015 study in the journal Cell identifying a new system called Cpf1 that cuts differently than Cas9. Researchers contend that Cpf1 may ultimately allow for more precise gene editing in humans than Cas9.

Comment: Note these are man-made modifications of bacterial defense enzymes. What is always striking to me is that bacteria in evolving these huge molecules had to invent them. Enzymes are giant in size and have loci which will grab both sides of a reaction, hold the molecules together and force a reaction that would otherwise take years to occur. Chance logically cannot create this. Saltation is logical.

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12533 views

DNA is constantly copied and mistakes occur. Enzymes are found to facilitate quick repair:

http://phys.org/news/2016-10-key-dna-replication-protein.html

"PrimPol is used in cells when normal repair proteins encounter damaged sections of DNA, often caused by anticancer chemotherapy drugs. The protein can skip over the damage to rescue DNA replication, says the study's senior investigator, Aneel K. Aggarwal, PhD, Professor of Pharmacological and Oncological Sciences at ISMMS

***

"DNA damage happens constantly—more than 100,000 events occur in every human cell each day. PrimPol is necessary for the cell to repair DNA damage, but sometimes this may not be to the individual's benefit, as in the case of resistance to chemotherapeutic agents, says the study's co-lead author, Olga Rechkoblit, PhD, Assistant Professor of Pharmacological Sciences at ISMMS.

"The basic steps involved in DNA replication are known. The first step involves unzipping the intertwined double helix DNA structure, creating a "Y" shape known as a replication fork. These two strands act as templates for making the new DNA strands. A short piece of RNA known as a primer (produced by a primase enzyme) acts as the starting point for the synthesis of new DNA.

"'It had been believed that DNA polymerase and primase activities in human cells were the province of separate enzymes. Then PrimPol was discovered, and the understanding of DNA replication changed dramatically. PrimPol was found to be capable of both restarting and performing DNA synthesis after DNA replication stalls," says Dr. Rechkoblit.

***

"While scientists were excited by the discovery of the enzyme, they didn't understand how it worked. Drs. Aggarwal and Rechkoblit organized a team of investigators from Cornell University in New York, Argonne National Laboratory in Illinois, and the University of Texas Medical Branch in Galveston to find out.

"'Because the three-dimensional structure of the enzyme is so different from that of other DNA polymerases, it required a group effort to elucidate its structure," says Dr. Aggarwal.

"The clinical implications are clear, Dr. Rechkoblit says.

"Many chemotherapy agents kill cancer cells by damaging their DNA and preventing the completion of DNA replication. PrimPol, on the other hand, promotes the replication progression and, thus, cell survival," she says. "Knowing the structure of PrimPol described in the current study is invaluable for designing an inhibitor for this enzyme as a future cancer therapy."

The actual structure of the enzyme is shown at this site:

http://advances.sciencemag.org/content/2/10/e1601317.full

Comment; Without copy corrections life could not survive. This huge enzyme is necessary at the beginning of life. God must have given it. considering its size and complexity.

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12605 views

Parts of DNA must be spliced together by the spliceosome to create the instructions for action:

http://phys.org/news/2016-11-gene.html

"Ribonucleic acids - RNAs for short - serve as intermediates in the ordered translation of the hereditary information stored in the DNA into blueprints for the synthesis of specific proteins. In the cell nucleus, defined segments of the DNA are first transcribed into RNA copies called messenger RNA precursors (pre-mRNAs). In many cases, these primary transcripts contain interspersed sequences that interrupt the actual protein-coding sequence. These "introns" must be removed and the coding sequences spliced before the information can be used for protein synthesis. Indeed, a given gene may encode for several different forms of a protein by a process called alternative splicing, which plays an important role in post-transcriptional gene regulation - for differently spliced mRNA strands code for different protein forms that may also differ in their function. All splicing operations are carried out by a complex molecular machine in the cell nucleus, which is referred to as the spliceosome.

***

"The spliceosome found in human cells is made up of many different subunits, which must be assembled onto the mRNA precursor in a series of carefully choreographed steps. The binding specificity of individual subunits is crucial for both spliceosome assembly and function. "The assembly factor we have studied, called the U2 Auxiliary Factor or U2AF for short, is critical for the correct recognition of the splicing sites at one end of the introns," says Lena Voithenberg, first author of the new paper. U2AF itself is made up of two different subunits. In its free form, the larger of the two is a highly dynamic protein, as Voithenberg and her colleagues demonstrated by means of single-molecule fluorescence microscopy.

***

"We found that the large subunit rapidly switches its conformation from an open to a closed structure on timescales of micro- to milliseconds," Voithenberg explains. Only the open form can bind to the RNA. - Moreover, the proportion of molecules in this conformation depends on the relative binding affinity of the RNA sequences available: Sequences that show a high affinity for the binding subunit therefore have a higher probability of being recognized - and cleaved - than those with a lower affinity. According to the Munich researchers, their results suggest that the different structural conformations adopted by the large subunit of U2AF serve to regulate the splicing efficiency at different splicing sites. This in turn has obvious implications for how mRNA precursors are cleaved and spliced, which in turn affects not only the structure of the final protein, but also the rate at which it is synthesized.

Comment: Another example of the complexity of layers of the genome. Note the picture in the article of the molecule itself. Same issue: how does evolution discover these necessary forms? Question is not answered in current evolutionary science studies.

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12685 views

DNA must be copied exactly or life would end. Constant repair of errors is essential:

https://www.sciencedaily.com/releases/2016/11/161101100725.htm

"Scientists at The Australian National University (ANU) and Heidelberg University in Germany have found an essential component in the DNA repair process which could open the door to the development of new cancer drugs.

"Lead researcher Associate Professor Tamás Fischer from ANU said the research found hybrid structures composed of DNA and RNA play an important role in restoring the genetic information after the DNA is damaged. RNAs are short-lived copies of the genetic information stored in DNA.

"The study also discovered that RNase H enzymes that target these hybrid structures are also essential for the efficient and precise repair of damaged DNA.

***

"RNase H enzymes have been studied and used in molecular biology for many years but their biological function was not entirely clear until now.
"Our study reveals that these enzymes are essential for DNA repair and this is probably one of their most important functions and the reason that they are present in every living cell."

"Dr Fischer said one of the most surprising findings was that RNA -- DNA hybrids, which were previously thought to only negatively affect the integrity of the human genome -- are actually also involved in protecting the DNA."

Comment: This presents a chicken and egg problem. First DNA and then copy protection mechanisms, or did both appear together. Logically both appeared at the same time for ear.ly life to survive. Enzymes are giant molecules. How did evolution find them? Only God can do this.

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12558 views

The activity of transposons which can change genetic messages is explored:

http://journals.aps.org/prl/abstract/10.1103/PhysRevLett.117.208101

Abstract: "Transposable elements, or transposons, are DNA sequences that can jump from site to site in the genome during the life cycle of a cell, usually encoding the very enzymes which perform their excision. However, some transposons are parasitic, relying on the enzymes produced by the regular transposons. In this case, we show that a stochastic model, which takes into account the small copy numbers of the active transposons in a cell, predicts noise-induced predator-prey oscillations with a characteristic time scale that is much longer than the cell replication time, indicating that the state of the predator-prey oscillator is stored in the genome and transmitted to successive generations. Our work demonstrates the important role of the number fluctuations in the expression of mobile genetic elements, and shows explicitly how ecological concepts can be applied to the dynamics and fluctuations of living genomes."

Report on the contents of the paper:

http://phys.org/news/2016-11-motion-genes-human-genome.html

"These are genes that are active and are doing genome editing in real time in living cells, and this is a start of trying to really understand them in much more detail than has been done before," said Goldenfeld,

***

"Goldenfeld and Xue embarked on this work because of their interest in transposons, small regions of DNA that can move themselves from one part of the genome to another during the lifetime of a cell—a capability that has earned them the name "jumping genes." Collectively, various types of transposons make up almost half of the human genome. When they move around, they may create mutations in or alter the activity of a functional gene; transposons can therefore create new genetic profiles in a population for natural selection to act on, in either a positive or negative way.

***

"the physical structure of the DNA that makes up the genome acts like an environment, in which two types of transposons, long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), have a competitive relationship with one another. In order to replicate, SINEs steal the molecular machinery that LINEs use to copy themselves, somewhat like a cuckoo bird tricks other birds into raising her chicks for her while abandoning their own.

***

"This method has been successfully applied in ecology to describe predator-prey interactions; Xue and Goldenfeld simulated the movements of transposons within the human genome with the same mathematical method. Their models included a detailed accounting for how Alu elements steal the molecular machinery L1 elements use to copy themselves.

"Xue and Goldenfeld's results predicted that populations of LINE and SINE elements in the genome are expected to oscillate the way those of, for example, wolves and rabbits might.

"'We realized that the transposons' interaction actually was pretty much like the predator-prey interaction in ecology," said Xue. "We came up with the idea, why don't we apply the same idea of predator-prey dynamics . . .we expected to see the oscillations we see in the predator-prey model. So we first did the simulation and we saw the oscillations we expected, and we got really excited."

"In other words, too many SINEs and the LINEs start to suffer, and soon there are not enough for all the SINEs to exploit. SINEs start to suffer, and the LINEs make a come-back. Xue and Goldenfeld's model made the surprising prediction that these oscillations occur over a timescale that is longer than the human lifespan—waves of Alu elements and L1 elements pushing and pulling at each other in slow motion across generations of the human genomes that carry them."

Comment: It is amazing to see different types of transposons struggling with each other, but it certainly adds flexibility to genome changes. This adds to the complexity of the genome. DNA is not a simple code by any measure.

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12459 views

A complex study shows how areas of DNA are protected during cell division, and also how methylation marks can be removed:

http://medicalxpress.com/news/2016-11-enzyme-implications-infertility-cancer.html

"To "turn off" particular regions of genes or protect them from damage, DNA strands can wrap around small proteins, called histones, keeping out all but the most specialized molecular machinery. Now, new research shows how an enzyme called KDM4B "reads" one and "erases" another so-called epigenetic mark on a single histone protein during the generation of sex cells in mice.

***

"At the heart of their new discovery, says Taverna, is the fact that genes housed in a cell's nucleus are not the whole story when it comes to the proteins they ultimately make. If genes are the sentences of a book, the story can be altered dramatically depending on which sentences are read and skipped over, and in what order. Histone proteins, Taverna explains, act like removable tape sealing closed particular pages of the book. When DNA is wrapped around them, genetic regions are "silenced" and go unread by other proteins—a classic epigenetic control mechanism, since it changes how the genome is read without changing its sentences.

***

"That research revealed a new site for methyl groups on one histone. That spot, a lysine known as H3K23, has little to no methyl tags in active Tetrahymena nuclei but is loaded up with three methyl groups (H3K23me3) in "mating nuclei" undergoing early meiosis, the special version of cell division that creates sex cells.

***

"In those experiments on Tetrahymena, the team learned that H3K23me3 appears in regions of the genome that should never be cut by enzymes during meiosis. DNA cuts normally occur during meiosis to allow for the mixing of genetic material and the proper sorting out of chromosomes in dividing cells, so H3K23me3 could protect nearby regions of the genome by "taping them up" so they can't be accessed.

"In a hunt for what controls that part of the process, researchers at the University of Wisconsin-Madison led by John Denu, Ph.D., developed a way to find out which proteins bind to which histone tags. Specifically, they identified a family of three similar enzymes called lysine demethylases, or KDM4s, which have been implicated in the development of some cancers in humans. KDM4A binds H3K23me3 plus two other histone tags and KDM4C binds another histone tag, but KDM4B binds only H3K23me3.

***

"While KDM4B's structure proved elusive, the scientists were able to figure out the structure of KDM4A bound to H3K23me3. By comparing the differences between the KDM4s and by tweaking three of KDM4A's amino acid building blocks to make it act like KDM4B, the scientists report they were able to learn the basis for the binding preferences of all three KDM4s.

"'Now that we know the 'rules' that determine how KDM4s bind, we can imagine ways to intervene to change their interactions with histone tags," says Taverna. "That in turn means we can test what happens when we enhance their activity or turn it down, and better understand their roles in disease."

"To that end, biochemical tests revealed that after KDM4B "reads" H3K23me3, it "erases" the methyl groups from a nearby lysine, H3K36me3. The researchers say that more work is needed to understand the significance of this rare combination of activities, but Taverna speculates that the "demethylation"—that is, removing the epigenetic marks—of H3K36 helps to "tape up," silence and protect nearby DNA.

"'We know from our work in Tetrahymena that H3K23me3 is most often found in regions of the genome that should never suffer DNA damage because that would harm reproduction," he says. "During meiosis, when H3K23me3 is most prevalent, DNA is prone to damage, which explains why Tetrahymena lacking H3K23me3 struggle to reproduce.'"

Comment: "Cut and paste" is an active component of working with DNA to produce protein products. Think of putting together a scrapbook. For us it requires thought and planning. At the genome level these are unthinking molecules literally doing the same thing. These types of complex biochemical editing reactions did not develop by chance.

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12426 views

A whole family of human proteins act to control gene expression:

http://medicalxpress.com/news/2016-11-surprizing-largest-group-human-proteins.html

"Teams led by Professors Timothy Hughes and Jack Greenblatt, of the University of Toronto's Donnelly Centre, have shown that proteins called C2H2-zinc fingers (C2H2-ZF) can control gene activity in new and surprizing ways. Reporting in the December issue of Genome Research, the researchers also reveal DNA binding sites for more than a hundred C2H2-ZFs as part of an ongoing effort to decode genome sequences that do not code for genes.

"Despite being the largest group of human proteins—counting 700 members—the C2H2-ZFs are poorly understood partly because their sheer abundance and diversity make them hard to study. Yet knowing how they work is important because they help orchestrate gene activity. Of 20,000 human genes, only a subset is active in the cell at any given time. This subset determines if the cell will, say, build blood, or the brain or go haywire to become cancer.

***

"The C2H2-ZF proteins work by directly binding the DNA to control the genes nearby. Named after their finger-like structures that, aided by zinc ions, clasp the DNA, C2H2-ZFs have previously been thought to act by stifling a wide range of genes. In a previous study that included about 40 C2H2-ZFs, the team showed that each protein recognized a unique DNA snippet as its landing site in the genome, raising the possibility that the rest of the group could be just as diverse.

***

"In addition to binding the DNA, it turned out that each C2H2-ZF can partner with a motley of other proteins that could potentially tweak its ability to switch genes on and off in a unique way. The finding upended the previous thinking in which C2H2-ZF proteins were seen as limited in their ability to bind other proteins—half of them were thought to interact with a single protein that helps them gag target genes, while the rest lack the usual molecular features that help proteins contact one another.

"Our key finding is that there's almost as much diversity in the protein-protein interactions as there is in the DNA binding sequences. It tells us that the way the C2H2-ZF proteins work is almost certainly more complicated than we would have expected," said Hughes, who is also a professor in U of T's department of molecular genetics.

"The kinds of proteins that C2H2-ZFs interact with suggest that their roles go beyond clamping down on genes and may even act to turn genes on or help package DNA inside the cell.

"The study also shines light on how the C2H2-ZF evolved to become the largest and most diverse group of proteins we have. The DNA sequences that C2H2-ZF proteins recognize look a lot like they had come from viruses, some of which plagued our mammalian ancestors as long as 100 million years ago. This kind of viral DNA has been called "selfish DNA" because it spreads by inserting itself randomly in a host's genome.

"It is thought that the C2H2-ZF proteins evolved to shut down this selfish DNA, their legion expanding to keep up with new intruders. Once the viral DNA was squashed for good, the C2H2-ZF proteins were able to take on new roles in shutting down mammalian genes. And now, this new data suggest that the C2H2-ZF proteins branched out even more than previously thought to acquire wholly unexpected functions by binding to other proteins.

***

""Even today, 15 years after the human genome was sequenced, if you give any piece of DNA to a geneticist and ask them what this does, generally they are unable to tell you that. But the more we learn about how human proteins recognize the DNA and what they do, the better our ability will be to interpret genome sequences and say what the significance of the variants is," said Hughes. " (my bold)

Comment: This last bolded paragraph tells the real story. We still know so very little about how it all works and its lots more complicated than we every thought it would be. Not by chance!

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12418 views

There is a way to correct stalled transcription problems by an existing mechanism. Absolutely correct transcription is vital for life to continue:

http://phys.org/news/2016-12-ribosome-recycling-drug.html

Ludwig Maximilian University of Munich researchers have elucidated a mechanism that recycles bacterial ribosomes stalled on messenger RNAs that lack termination codons.

***

One of these processes is the recycling of stalled ribosomes. Wilson and his research group have just completed a comprehensive structural study of ribosome recycling. The results of the study, which appears in the leading journal Nature, may identify promising points of attack for future antibiotics.

Ribosomes are the organelles that translate the nucleotide sequences encoded in messenger RNA molecules (mRNAs) into the amino-acid sequences of the corresponding proteins. The ribosome "reads" the nucleotide sequence in a fixed direction and is released from the mRNA only when it reaches a defined termination signal. Errors in synthesis or processing may, however, lead to the production of mRNAs that lack termination signals, causing the ribosome to stall while still attached to the mRNA and the growing protein. Cells have evolved several ways of detaching stalled ribosomes from the truncated mRNAs and recycling them for re-use.

Wilson's team has now employed cryo-electron microscopy to determine the structure of the bacterial recycling factor ArfA. Their analysis reveals how ArfA recognizes the stalled ribosome on a defective mRNA and recruits a so-called release factor, which detaches the incomplete protein. This then enables the stalled ribosome to be released from the mRNA in the normal manner by dissociation into its two component subunits. The subunits are then free to interact with another mRNA, thus allowing protein synthesis to proceed.

Comment: This mechanism could not have developed after the transcription mechanism developed by itself. It is obvious they had to be developed together all at once or continued replication of life would not have survived. Only God could do this.

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12447 views

The role of miRNA is vast in modifying gene transcription:

http://phys.org/news/2016-12-atlas-rna-universe.html

In the last few years, small snippets of RNA, which may have played a key role in the planet's earliest flickering of life, have been uncovered and examined in great detail. Their discovery, first in the tiny soil-dwelling nematode worm C. elegans and shortly thereafter, across the web of life, marks a revolution in biology, with broad implications in the fight against nearly every known disease.

These abbreviated RNA fragments, known as microRNA (miRNA) are composed of just 18-22 nucleotides. They are too short to code for proteins, (in the manner of longer messenger RNA or mRNA strands). Instead, they act as a subtle and extremely sophisticated network of gene regulators.

To accomplish this, miRNAs find complementary sections of mRNA targets and bind with a specific location known as the 3'UTR (for UnTranslated Region). After binding to the UTR, the miRNA inactivates mRNA, interfering with its translation to protein.

***

Over the course of evolution, higher species have become heavily invaded by miRNA, which have undergone radical expansion in vertebrates, while the number of genes has remained stable. Astonishingly, worms, flies, and humans all have roughly 20,000 protein coding genes, though humans have far more miRNA than simpler species. Mangone insists this intriguing puzzle begs for a convincing explanation.

"What we found is that these miRNAs started parasitizing cells because they needed to target and regulate more gene expression, modulating entire pathways not just single genes," Mangone says.

***

These tiny strips of RNA, many with very similar nucleotide sequences, form miRNA families, capable of targeting disparate gene pathways. While these miRNA families were originally thought to provide redundancy and robustness in gene regulation, the new study suggests a different explanation for miRNA abundance and proliferation in higher species.

The research findings show that miRNA not only target specific genes but expand their network of action through minor mutations in specific portions of their sequence, which Mangone named "evolutionary hotspots." This allows particular miRNA family members to extend their range of modulating activity while maintaining a common set of core targets.

***

The results of the study are thought-provoking and run counter to previously proposed ideas about the nature and function of miRNAs. The study explores miRNA families, finding that the mutations that give rise to them do not occur randomly, with respect to either sequence location or function. Rather, mutations occur in preferential regions—evolutionary hotspots—indicating the mutations are functional and maintained through evolution. Contrary to the common conception of single miRNAs regulating single genes, the study observed that each miRNA tends to control multiple members in the same regulatory pathways.

Finally, the study explores the specific sequence locations in miRNAs known as the seed regions, often assumed to be essential for binding with the 3'UTRs. "We show in this manuscript that there are a lot of targets that do not have the seed region, yet they are still targeted, suggesting that just the presence of the seed region in the 3' UTR doesn't correlate with the binding on the miRNA. There are other rules, but now we begin to understand the language that these miRNAs speak."

Comment: We don't know how this all works so far, but it is obvious that the layers of the genome are very deep and are the reason that 22,000 gens in humans can create all of our complexities. Not by chance!

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12478 views

Cells are constantly reproducing themselves as daughters. DNA must be constantly monitored against mistakes, and it is:

http://www.businessinsider.com/breakthrough-prize-winner-dna-research-2016-12

"That DNA tells our cells what to do. When they divide, that information is copied from one cell to another.

"But life is hard on our cells. They become damaged every moment of every day, exposed the radiation of the sun, the heat of our laptops, the chemicals we absorb from air pollution, the alcohol we drink, and more. Aging itself damages them.

"This damage can easily become a harmful mutation, causing cells to replicate in an out of control way, leading to disease and cancer. With the constant assault, it's a wonder this doesn't happen all the time.

"It's only thanks to a mechanism in our cells that can recognize when something has gone wrong that we aren't all riddled with cancer.

"That mechanism, known as the DNA damage response, functions like an individual intelligent agent, able to monitor when things are going wrong and then try to come up with a way to deal with them.

***

"Discoveries explaining how that mechanism works are so significant that on December 4, geneticist Stephen Elledge was awarded one of five $3 million Breakthrough Prizes in life sciences.

***

"Elledge's research on the DNA damage response certainly fits the bill. While we've thought that cells had some way to respond to damage ever since the 1940s, Elledge has helped reveal the biological components involved in the process.

"'One of the remarkable properties of nature’s most remarkable molecule, DNA, is self-awareness: it can detect information about its own integrity and transmit that information back to itself," Elledge wrote in JAMA after he was awarded a prestigious Lasker award in 2015 for his work.

"When this response detects damaged DNA, it can respond in several ways. It may try to repair the damage, but it may also activate the immune system, cause the cell to destroy itself, or trigger a process known as senescence — which helps prevent tumors but is also largely responsible for aging."

Comment: There is no way life could have continued with a DNA code controlling it, unless such a defense mechanism against mistakes was present at all times. Only a saltation could have produced this result. Not by chance.

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12418 views

Great care is taken on opening and copying DNA. If it is not accurate life would not continue:

https://www.sciencedaily.com/releases/2016/12/161213093123.htm

"For years, scientists have puzzled over what prompts the intertwined double-helix DNA to open its two strands and then start replication. Knowing this could be the key to understanding how organisms -- from healthy cells to cancerous tumors -- replicate and multiply for their survival.

"A group of USC scientists believe they have solved the mystery. Replication is prompted by a ring of proteins that bond with the DNA at a special location known as "origin DNA." The ring tightens around the strands and melts them to open up the DNA, initiating replication.

***

"When the origin DNA melts, the double helix divides into separate strands, Chen explained. Those DNA strands then become the template for faithful duplication of other strands -- a Xerox copy of their parental DNA. As soon as replication is complete, one double helix DNA now becomes two exact copies of the same double helix.

"'DNA replication is critical for heredity and survival," said Chen, who also is affiliated with the Norris Comprehensive Cancer Center at the Keck School of Medicine at USC. "The origin DNA's opening is an essential step for DNA replication in our cells and for some tumor viral pathogens to replicate and spread."

"Why is origin DNA so special? Regular DNA sequences contain the A, T, G and C nucleotides, more or less in equal ratio. But origin DNA sequences contain more A and T nucleotides than usual.

"To prompt replication, the scientists used a helicase from a "Large Tumor Antigen" or Large T. The antigen comes from a virus, SV40, linked to human cancers such as brain and bone cancers, mesothelioma and lymphoma. The six proteins from Large T comprise a "helicase" that mimics the structure of the healthy cells' helicases.

"The scientists obtained a 3-D view of the atomic structure of the helicase using X-ray crystallography, a technique for examining nano-biomolecules and their structures at the atomic level that has been refined over centuries. Chen said the images revealed that the proteins which surrounded the DNA had attached to it, then tightened like a vice until the bonds between the two strands of the double helix broke -- or melted -- the origin DNA.

"Although the scientists used a cancerous virus to study replication, healthy cells replicate in a similar way, Chen said."

Comment: Note the giant size and complexity of the helicase mechanism. Its function is based on the sequence of amino acids and of the folding patterns. Such a set of six molecules had to be 'found' by evolution as it advanced from the initial cells. But think about it. It really had to present in the initial cells' DNA or copy errors would have ended life before it got very far. Only true solution. It had to be supplied at the beginning! Not by accident.

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12434 views

Recent research shows a complex mechanism of flowering control:

http://www.ibs.re.kr/cop/bbs/BBSMSTR_000000000738/selectBoardArticle.do?nttId=14075

"Epigenetic regulation is one of the major mechanisms to control flowering time. It regulates gene expression through chemical modifications of DNA and its interacting proteins, but without changing the DNA sequence. If you think of the DNA contained in each cell as a big book that contains all the information, these chemical modifications can be thought as bookmarks that tell the cell which pages to read and which to skip over time. A particular type of chemical modification called acetylation, occurring on DNA bounded proteins (histones), can be promoted or removed by specific proteins. Arabidopsis has at least 18 proteins that remove these chemical modifications and are referred to as histone deacetylases (HDACs). Which are the targets of HDACs, how they coordinate with each other and how they interact with other proteins is still unclear. This study discovered the proteins that interact to one of these chemical modifications that controls the time of flowering.

"IBS researchers concentrated on the ninth HDAC, known as HDA9. This protein is known to regulate several biological processes, such as flowering time, seed dormancy and stress responses. The team found that plants lacking this protein bloomed earlier and have enlarged fruits, indicating that the regulation of the stem cells activity was compromised. The same happens when POWERDRESS (PWR) (a protein already studied by the same research team for its regulation of floral stem cells), or both HDA9 and PWR are missing.

"The scientists discovered that PWR and HDA9 form a protein complex that removes the chemical modifications from a protein bound to DNA called histone 3. In the same way as removing a bookmark from the "DNA book" indicates that you do not need to read the pages next to the bookmark, removing this chemical modification reduces the production of AGL19, a protein that causes early flowering. In this way, plants maintain normal flowering time.

"'PWR, HDA9 and AGL19 regulate flowering time. A plant with reduced PWR and HDA9 has increased AGL19 levels and flowers earlier," explains Kim. "The opposite situation, that is the overexpression of PWR and HDA9, has not been tested yet."

"The next challenge for the team is to study other chemical modifications (or "bookmarks") on plants' histones and clarify how these different chemical modifications together regulate flowering."

Comment: The article does not mention the size of the deacetylases, but the name implies they are enzymes, and therefore giant molecules of a particular shape. How did plant evolution develop just the right molecule of this type to control flowering. It certainly suggests design or saltation. Note this is a different epigenetic modification, not methylation but acetylation.

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12359 views

An experiment shows parent plants pass on drought resistance to progeny:

http://www.the-scientist.com/?articles.view/articleNo/47727/title/Transgenerational-Epi...

"The notion that organisms pass down adaptations acquired during their lifetimes to their offspring was overturned long ago by Darwinian evolution. But the concept is getting a second chance, with more nuance. Growing evidence shows that a parent’s environment sometimes does influence offspring, though the underlying process is something of a black box.

"Sonia Sultan and Jacob Herman of Wesleyan University in Middletown, Connecticut, peeked into that box with experiments on a small flowering annual, Polygonum persicaria. They grew some plants in dry soil and other plants in normal soil, then raised offspring from all plants in dry soil. In some members of the progeny, they disrupted 15 percent to 20 percent of DNA methylation—a means of epigenetic regulation—across the genome.

"Plants whose parents endured drought were better prepared to face the same hardship, growing larger as seedlings, setting down deeper roots, and making broader leaves. But in demethylated plants, that effect went away, lending evidence to the idea that epigenetics had a role in this form of adaptation.

"Adjusting offspring traits to better suit the parental environment is itself an evolved trait, notes Julie Etterson, an evolutionary ecologist at the University of Minnesota Duluth who was not involved in the research. The authors used plants from 12 genetically distinct populations and not all of them showed the transgenerational effect, raising questions about when and why this trait is advantageous. Sultan says these environmental hand-me-downs are a phenomenon “not accounted for by standard models of evolution.'”

Comment: We do know the mechanism by which plants add methyl radicals to modify gene expression and change lifestyles, but it certainly works for subsequent adaptations. this is not speciation, just modification and adaptation of an existing species.

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12279 views

New research shows that DNA is organized into neighborhoods with gene modification controls and enhancers close by and limited to effect in aht regikon:

http://www.nytimes.com/2017/01/09/science/dna-tads.html?emc=edit_th_20170110&nl=tod...

"It turns out that the vast informational expanse of the genome is divvied up into a series of manageable, parochial and law-abiding neighborhoods with strict nucleic partitions between them — each one a TAD.

***

"DNA is a super-long molecule packed into a very small space, and it’s clear that it’s not packed randomly,” Dr. Mundlos said. “It follows a very intricate and controlled packing mechanism, and TADs are a major part of the folding protocol.”

***

"researchers soon realized there was much more to the genome than the protein codes it enfolded. “We were caught up in the idea of genetic information being linear and one-dimensional,” said Job Dekker, a biologist at the University of Massachusetts Medical School.

"For one thing, as the sequencing of the complete human genome revealed, the portions devoted to specifying the components of hemoglobin, collagen, pepsin and other proteins account for just a tiny fraction of the whole, maybe 3 percent of human DNA’s three billion chemical bases.

"And there was the restless physicality of the genome, the way it arranged itself during cell division into 23 spindly pairs of chromosomes that could be stained and studied under a microscope, and then somehow, when cell replication was through, merged back together into a baffling, ever-wriggling ball of chromatin — DNA wrapped in a protective packaging of histone proteins.

***

"We realized that in order to understand how genetic information is controlled, we had to figure out how DNA was folded in space,” said Bing Ren of the University of California, San Diego.

***

"Through chromosome conformation studies and related research, scientists have discovered the genome is organized into about 2,000 jurisdictions, and they are beginning to understand how these TADs operate.

"As with city neighborhoods, TADs come in a range of sizes, from tiny walkable zones a few dozen DNA subunits long to TADs that sprawl over tens of thousands of bases and you’re better off taking the subway. TAD borders serve as folding instructions for DNA. “They’re like the dotted lines on a paper model kit,” Dr. Dekker said.
TAD boundaries also dictate the rules of genetic engagement.

"Scientists have long known that protein codes are controlled by an assortment of genetic switches and enhancers — noncoding sequences designed to flick protein production on, pump it into high gear and muzzle it back down again. The new research indicates that switches and enhancers act only on those genes, those protein codes, stationed within their own precincts.

***

“'Genes and regulatory elements are like people,” Dr. Dekker said. “They care about and communicate with those in their own domain, and they ignore everything else.”

***

"Scientists are not entirely sure, but preliminary results indicate that the boundaries are DNA sequences that attract the attention of sticky, roughly circular proteins called cohesin and CTCF, which adhere thickly to the boundary sequences like insulating tape.

"Between those boundary points, those clusters of insulating proteins, the chromatin strand can loop up and over like the ribbon in a birthday bow, allowing genetic elements distributed along the ribbon to touch and interact with one another. But the insulating proteins constrain the movement of each chromatin ribbon, said Richard A. Young of the Whitehead Institute for Biomedical Research, and keep it from getting entangled with neighboring loops — and the genes and regulatory elements located thereon."

Comment: As I have commented in the past, only an understanding of DNA in 3-D will explain how it works to control gene expression. Only a brilliant mind can create a mechanism of code like DNA. God

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12297 views

If the mRNA has one methyl or two methyls determines how much protein is produced:

http://www.news.cornell.edu/stories/2016/12/research-reveals-codes-control-protein-expr...

"In their study, published Dec. 21 in Nature, Jaffrey and lead author Jan Mauer, a postdoctoral associate in pharmacology at Weill Cornell Medicine, found that chemical marks called methyl groups are responsible for influencing individual mRNA’s stability. At the beginning of all mRNAs are so-called cap structures, previously thought only to dock cellular machines called ribosomes that string together amino acids to form proteins.

"The researchers have discovered that additional methyl marks are present on those caps, and that the position and number of methyl marks encode information that determines how stable mRNAs will be, and in turn, how much protein they will produce. mRNA caps containing two methyl groups cause the mRNA to be highly stable and lead to increased protein production, while mRNA caps with only one methyl group cause normal mRNA stability and result in lower protein levels.

"The investigators discovered the methyl mark encoding process by examining adenine, one of the genetic building blocks of mRNA. Scientists have long known that a single methyl can attach to adenosine, creating N6-methyladenosine (m6A). However, if present at the cap, adenosine can also have two methyl marks, creating m6Am.

***

"Many of these mRNAs contained instructions for making proteins that support cellular metabolism, survival and growth, and these proteins are typically essential for cellular proliferation.

"The investigators also found that the methyl marks can be added or removed, allowing an mRNA to switch from a highly stable state to a less stable state. They identified an enzyme – a fat mass and obesity-associated protein, or FTO – that can remove the methyl marks of m6Am, helping to restore normal mRNA stability and translation.

"Additionally, researchers were able to control cellular levels of m6Am by increasing or decreasing FTO. “If you don’t have the right levels of m6Am, gene expression may go haywire and you get disease,” Jaffrey said.

Comments from uncommon descent ID folks:

http://www.evolutionnews.org/2017/01/cornell_researc103412.html

"Another player is involved in this coding scheme. It's called FTO ("fat mass and obesity associated protein"). This enzyme can remove methyl groups from the cap adenosines, but it mostly goes after the doubly methylated m6am forms. Because of this, FTO regulates the stability of mRNAs. The Cornell team found that FTO was 100 times more likely to remove a methyl tag from m6am than from m6a.

"And then there's another player: DCP2. This enzyme "decaps" mRNAs, facilitating their degradation. Once decapped, mRNAs are degraded by micro-RNAs. The m6am RNAs, however, are more resistant to decapping by DCP2. This new epigenetic code helps explain why some mRNAs are more robust against degradation than others.

***

"In their own words, the researchers consider this a coding system. "An internal code in cellular molecules called messenger RNA predetermines how much protein they will produce," Lindsey says. In the paper, the authors explicitly use the words code and information. In the Introduction, they say this:

"An emerging concept in gene expression regulation is that a diverse set of modified nucleotides is found internally within mRNA, and these modifications constitute an epitranscriptomic code.

And they repeat the concept in the concluding Discussion:

"Here we identify m6Am as a dynamic and reversible epitranscriptomic mark. In contrast to the concept that epitranscriptomic modifications are found internally in mRNA, we find that the 5′ cap harbours epitranscriptomic information that determines the fate of mRNA. The presence of m6Am in the extended cap confers increased mRNA stability, while Am is associated with baseline stability. m6Am has long been known to be a pervasive modification in a large fraction of mRNA caps in the transcriptome, making it the second most prevalent modified nucleotide in cellular mRNA. Dynamic control of m6Am can therefore influence a large portion of the transcriptome.

***

"the location of the modified nucleotide and the specific combination of methyl groups on adenosine residues encode distinct functional consequences on the mRNA.

"The essence of a "code" is that it bears information. This code resembles an "if-then" algorithm in software. Speaking mechanistically, there's nothing about a methyl group that should indicate, "keep this attached molecule stable against degradation." Instead, the coding system works because all the players recognize the convention.

"The methyltransferase enzyme has to "know" which mRNA needs a second methyl group to confer stability, because it has an essential role. The FTO enzyme "knows" to concentrate on demethylating one tag from the m6am forms, and to stay inside the nucleus unless stimulated to go after m6am RNAs in the cytoplasm. And DCP2 has to know to avoid uncapping the doubly-methylated m6am transcripts. Because the players know the signal, the cell produces the appropriate quantity of proteins corresponding to their importance."

Comment: Code carries information. The various molecules 'know' because they are guided by information. Too complex for chance. How much complexity before God is required?

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12295 views

In cell division the DNA must be unzipped, opened and divided accurately:

https://phys.org/news/2017-01-reveals-dna-helicase-replication-fork.html

"The latest study from long-time collaborators Huilin Li, Ph.D., and Michael O'Donnell, Ph.D., published today in the Proceedings of the National Academy of Sciences, elucidates the interaction between DNA and the eukaryotic enzyme CMG helicase, which opens the DNA double helix like the slider of a zipper and prepares the genetic code for copying.

"'Since discovery of the DNA double helix more than 50 years ago, helicase's activity in preparing DNA for replication has been poorly understood," says Li, professor at Van Andel Research Institute.

***

"Findings from the new study reverse a long-held assumption about the orientation of helicase around DNA. Images taken during DNA unwinding demonstrate that helicase's N-tier ring leads the C-tier motor ring and makes first contact with double-stranded DNA. Such orientation is opposite from the currently accepted polarity and has important implications in understanding the mechanism of replication.

"Helicase activity has long been recognized as a critical part of DNA replication, itself a fundamental process in the propagation of life. With the publication of this study, scientists have a more complete picture of how most advanced life on Earth proliferates.

"This study involved evaluation of CMG helicase purified from the baker's yeast Saccharomyces cerevisiae, an organism commonly used to model higher eukaryotes, including humans.

"The structure of the helicase on DNA was derived at Rockefeller University's cryo-electron microscopy (cryo-EM) core facility, leveraging a groundbreaking imaging technology that has revolutionized scientists' ability to visualize and understand the role of fundamental biological processes."

Comment: Here we see a giant molecule, an enzyme, following information/instructions to accurately divide DNA so two new cells ca form. Knowledge of the amazing complexity grows. Not by chance. Had to be part of the initial cells. Had to be a mechanism present in the first existing cells or life could not continue by cell division, as it did with the earliest bacteria. In other words life appeared with a mechanism to continue from the beginning.

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12361 views

DAVID'S comment: Here we see a giant molecule, an enzyme, following information/instructions to accurately divide DNA so two new cells ca form. Knowledge of the amazing complexity grows. Not by chance. Had to be part of the initial cells. Had to be a mechanism present in the first existing cells or life could not continue by cell division, as it did with the earliest bacteria. In other words life appeared with a mechanism to continue from the beginning.

Absolutely. A mechanism for replication had to be there from the start, and I would argue that in addition to its ability to divide itself accurately, the same mechanism must also have had the ability to produce variations. Without that ability, there could have been no evolution. For you, every variation had to be preprogrammed in this mechanism or personally manipulated by your God. I am suggesting (theistic version) that perhaps your God created the mechanism in such a way that it could provide its own variations.

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12253 views

DAVID'S comment: Here we see a giant molecule, an enzyme, following information/instructions to accurately divide DNA so two new cells ca form. Knowledge of the amazing complexity grows. Not by chance. Had to be part of the initial cells. Had to be a mechanism present in the first existing cells or life could not continue by cell division, as it did with the earliest bacteria. In other words life appeared with a mechanism to continue from the beginning.

dhw: Absolutely. A mechanism for replication had to be there from the start, and I would argue that in addition to its ability to divide itself accurately, the same mechanism must also have had the ability to produce variations. Without that ability, there could have been no evolution. For you, every variation had to be preprogrammed in this mechanism or personally manipulated by your God. I am suggesting (theistic version) that perhaps your God created the mechanism in such a way that it could provide its own variations.

If you accept the complexity of original life, that I've presented, and if you deny chance production of life, you have nothing left but a denial that a planning mind must exist to create life. Your 'theistic version' accepts that premise. Why not accept it fully?

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12293 views

dhw: Absolutely. A mechanism for replication had to be there from the start, and I would argue that in addition to its ability to divide itself accurately, the same mechanism must also have had the ability to produce variations. Without that ability, there could have been no evolution. For you, every variation had to be preprogrammed in this mechanism or personally manipulated by your God. I am suggesting (theistic version) that perhaps your God created the mechanism in such a way that it could provide its own variations.

DAVID: If you accept the complexity of original life, that I've presented, and if you deny chance production of life, you have nothing left but a denial that a planning mind must exist to create life. Your 'theistic version' accepts that premise. Why not accept it fully?

As I have explained many times before, not being able to believe in something is not the same as disbelieving it. I do not believe in chance, and I do not believe in a nebulous, all-powerful, universe-embracing, sourceless intelligence. I accept that one or other of these incredible hypotheses must be nearer the truth than the other, but that does not enable me to choose between them.

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12271 views

dhw:

"Nearer to the truth' is an interesting phrase. There must be a 'truth'. Is it other than your current list of possibilities? Can you suggest what that 'truth' might be?

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12292 views

Life cannot survive unless replication copy errors are quickly eliminated. The systems are in place:

http://casemed.case.edu/cwrumed360/news-releases/release.cfm?new"New research out of Case Western Reserve University School of Medicine describes a mechanism by which an essential quality control system in cells identifies and destroys faulty genetic material.

"In the new study, Baker and her team of researchers uncovered that ribosomes were stalled on mRNA at premature stop codons. This observation led to the discovery that one of proteins in the surveillance complex, UPF1, was important for interacting with the stalled ribosome and assisting with its release from the mRNA. The inability of UPF1 to properly communicate with the ribosome results in the failure of the mRNA to be targeted to rapid elimination and inactivates the whole surveillance system.
Moreover, Baker’s findings indicated that UPF1 harnesses energy found in adenosine triphosphate – a reserve for energy storage in the cell – to influence the function of the ribosome, and that this step in the cellular checkpoint is necessary for recognizing and destroying mRNA with premature stop codons."

http://www.nature.com/articles/ncomms14021

"Nonsense-mediated mRNA decay (NMD) represents a eukaryotic quality control pathway that recognizes and rapidly degrades transcripts harbouring nonsense mutations to limit accumulation of non-functional and potentially toxic truncated polypeptides. A critical component of the NMD machinery is UPF1, an RNA helicase whose ATPase activity is essential for NMD, but for which the precise function and site of action remain unclear. We provide evidence that ATP hydrolysis by UPF1 is required for efficient translation termination and ribosome release at a premature termination codon. UPF1 ATPase mutants accumulate 3′ RNA decay fragments harbouring a ribosome stalled during premature termination that impedes complete degradation of the mRNA. The ability of UPF1 to impinge on premature termination, moreover, requires ATP-binding, RNA-binding and NMD cofactors UPF2 and UPF3. Our results reveal that ATP hydrolysis by UPF1 modulates a functional interaction between the NMD machinery and terminating ribosomes necessary for targeting substrates to accelerated degradation."

http://www.pnas.org/content/early/2017/01/03/1615439114.short

"Cells must continuously repair inevitable DNA damage while avoiding the deleterious consequences of imprecise repair. Distinction between legitimate and illegitimate repair processes is thought to be achieved in part through differential recognition and processing of specific noncanonical DNA structures, although the mechanistic basis of discrimination remains poorly defined. Here, we show that Escherichia coli RecQ, a central DNA recombination and repair enzyme, exhibits differential processing of DNA substrates based on their geometry and structure. Through single-molecule and ensemble biophysical experiments, we elucidate how the conserved domain architecture of RecQ supports geometry-dependent shuttling and directed processing of recombination-intermediate [displacement loop (D-loop)] substrates. Our study shows that these activities together suppress illegitimate recombination in vivo, whereas unregulated duplex unwinding is detrimental for recombination precision. Based on these results, we propose a mechanism through which RecQ helicases achieve recombination precision and efficiency. "

Comment: Many more articles are presented in:

http://www.evolutionnews.org/2017/01/quality_control_3103426.html

Comment: There must be quality controls for all replication processes or life ceases. Further it must be present in the initial cells of life. Saltation by God.

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12241 views

dhw:

As I have explained many times before, not being able to believe in something is not the same as disbelieving it. I do not believe in chance, and I do not believe in a nebulous, all-powerful, universe-embracing, sourceless intelligence. I accept that one or other of these incredible hypotheses must be nearer the truth than the other, but that does not enable me to choose between them.

David: "Nearer to the truth' is an interesting phrase. There must be a 'truth'. Is it other than your current list of possibilities? Can you suggest what that 'truth' might be?

Not answered. what is your truth?

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12272 views

Dhw: As I have explained many times before, not being able to believe in something is not the same as disbelieving it. I do not believe in chance, and I do not believe in a nebulous, all-powerful, universe-embracing, sourceless intelligence. I accept that one or other of these incredible hypotheses must be nearer the truth than the other, but that does not enable me to choose between them.

DAVID: "Nearer to the truth' is an interesting phrase. There must be a 'truth'. Is it other than your current list of possibilities? Can you suggest what that 'truth' might be?

Chance is one possible ‘truth’, and a single mind (your God) is another, but if your single mind can be sourceless, so can multiple minds, and that is the panpsychist hypothesis that we have frequently discussed. If matter has a mental aspect, that mental dimension might evolve from the bottom upwards. No, I don’t believe it, but it is no more incredible than pure, mindless chance or your one sourceless mind that knows everything beforehand (top downwards). And for the record, I would regard that version of the panpsychist theory as closer to the chance theory than to the God theory.

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12220 views

DAVID: "Nearer to the truth' is an interesting phrase. There must be a 'truth'. Is it other than your current list of possibilities? Can you suggest what that 'truth' might be?

dhw: Chance is one possible ‘truth’, and a single mind (your God) is another, but if your single mind can be sourceless, so can multiple minds, and that is the panpsychist hypothesis that we have frequently discussed. If matter has a mental aspect, that mental dimension might evolve from the bottom upwards. No, I don’t believe it, but it is no more incredible than pure, mindless chance or your one sourceless mind that knows everything beforehand (top downwards). And for the record, I would regard that version of the panpsychist theory as closer to the chance theory than to the God theory.

Panpsychism is the theory that mind is present in everything. Since God is mind, I would think you would have placed panpsychism closer to the Gold theory.

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12214 views

DAVID: "Nearer to the truth' is an interesting phrase. There must be a 'truth'. Is it other than your current list of possibilities? Can you suggest what that 'truth' might be?

dhw: Chance is one possible ‘truth’, and a single mind (your God) is another, but if your single mind can be sourceless, so can multiple minds, and that is the panpsychist hypothesis that we have frequently discussed. If matter has a mental aspect, that mental dimension might evolve from the bottom upwards. No, I don’t believe it, but it is no more incredible than pure, mindless chance or your one sourceless mind that knows everything beforehand (top downwards). And for the record, I would regard that version of the panpsychist theory as closer to the chance theory than to the God theory.

DAVID: Panpsychism is the theory that mind is present in everything. Since God is mind, I would think you would have placed panpsychism closer to the Gold theory.

Most panpsychist theories do indeed lead to God (it underpins A.N. Whitehead’s process theology, though I believe his God - unlike yours - learns as he goes along), and that is why I am always careful to point out that mine is an individual version. It does not involve a single being, but billions and billions of rudimentary, autonomous intelligences, some of which developed sufficient awareness to begin the process of life and evolution. That is why it is “bottom up” and it is closer to chance than to God because there is no single directing power. Of course we have no idea how “sufficient awareness” could evolve, any more than we know how your God came by his awareness and knowledge – as glossed over by the meaningless philosophical escape route of First Cause.

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12217 views

DAVID: Panpsychism is the theory that mind is present in everything. Since God is mind, I would think you would have placed panpsychism closer to the Gold theory.

dhw; Most panpsychist theories do indeed lead to God (it underpins A.N. Whitehead’s process theology, though I believe his God - unlike yours - learns as he goes along), and that is why I am always careful to point out that mine is an individual version. It does not involve a single being, but billions and billions of rudimentary, autonomous intelligences, some of which developed sufficient awareness to begin the process of life and evolution. That is why it is “bottom up” and it is closer to chance than to God because there is no single directing power. Of course we have no idea how “sufficient awareness” could evolve, any more than we know how your God came by his awareness and knowledge – as glossed over by the meaningless philosophical escape route of First Cause.

Do you prefer a philosophic approach of no cause, just eternal existence of the universe?

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12153 views

DAVID: Panpsychism is the theory that mind is present in everything. Since God is mind, I would think you would have placed panpsychism closer to the Gold theory.

dhw: Most panpsychist theories do indeed lead to God (it underpins A.N. Whitehead’s process theology, though I believe his God - unlike yours - learns as he goes along), and that is why I am always careful to point out that mine is an individual version. It does not involve a single being, but billions and billions of rudimentary, autonomous intelligences, some of which developed sufficient awareness to begin the process of life and evolution. That is why it is “bottom up” and it is closer to chance than to God because there is no single directing power. Of course we have no idea how “sufficient awareness” could evolve, any more than we know how your God came by his awareness and knowledge – as glossed over by the meaningless philosophical escape route of First Cause.

DAVID: Do you prefer a philosophic approach of no cause, just eternal existence of the universe?

An eternal mindless universe IS a first cause. An eternal panpsychist universe IS a first cause. There are even those who claim that the first cause was some extraordinary form of nothing. The “first cause” is whatever you want it to be, which is why the term is philosophically meaningless.

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12083 views

DAVID: Do you prefer a philosophic approach of no cause, just eternal existence of the universe?

dhw: An eternal mindless universe IS a first cause. An eternal panpsychist universe IS a first cause. There are even those who claim that the first cause was some extraordinary form of nothing. The “first cause” is whatever you want it to be, which is why the term is philosophically meaningless.

The famous question by Leibiz, why is there anything carries weight:

http://spot.colorado.edu/~heathwoo/Phil100/leibniz.html

Basically I read it as saying if there is anything, it had a beginning which had a cause or force of creation.

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12104 views

DAVID: Do you prefer a philosophic approach of no cause, just eternal existence of the universe?

dhw: An eternal mindless universe IS a first cause. An eternal panpsychist universe IS a first cause. There are even those who claim that the first cause was some extraordinary form of nothing. The “first cause” is whatever you want it to be, which is why the term is philosophically meaningless.

The famous question by Leibiz, why is there anything carries weight:
http://spot.colorado.edu/~heathwoo/Phil100/leibniz.html
Basically I read it as saying if there is anything, it had a beginning which had a cause or force of creation.

The question carries enormous weight. But I’m afraid that for me the long-winded, nebulous answer Leibniz gives (“God” is just a name, not an explanation) carries no weight whatsoever, for the reasons I have given above.

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12089 views

DAVID: Do you prefer a philosophic approach of no cause, just eternal existence of the universe?

dhw: An eternal mindless universe IS a first cause. An eternal panpsychist universe IS a first cause. There are even those who claim that the first cause was some extraordinary form of nothing. The “first cause” is whatever you want it to be, which is why the term is philosophically meaningless.

The famous question by Leibiz, why is there anything carries weight:
http://spot.colorado.edu/~heathwoo/Phil100/leibniz.html
Basically I read it as saying if there is anything, it had a beginning which had a cause or force of creation.

The question carries enormous weight. But I’m afraid that for me the long-winded, nebulous answer Leibniz gives (“God” is just a name, not an explanation) carries no weight whatsoever, for the reasons I have given above.

I'm still in the same position. Something or someone started everything. I'll stick with God to name first cause

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12154 views

There are two methods to repair broken DNA, one of which employs enzymes:

https://www.sciencedaily.com/releases/2017/02/170202085851.htm

The results are significant for gene therapy procedures and for our understanding of cell transformation. A team of researchers has discovered that the processes for repairing DNA damage are far more complex than previously assumed. The ends of breaks in the double helix are not just joined, they are first changed in a meticulously choreographed process so that the original genetic information can be restored.

***

Over the course of evolution, ways to repair this DNA damage have developed, in which many enzymes work together to restore the genetic information with the maximum possible precision.

As it stands today, there are two main ways of repairing DNA double-strand breaks, which differ greatly in terms of their precision and complexity. The apparently simpler method, so-called non-homologous end joining, joins together the break ends as quickly as possible, without placing particular importance on accurately restoring the damaged genetic information. The second method of repair, homologous recombination, on the other hand, uses the exactly identical information present on a sister copy to repair the damaged DNA with great precision. However, such sister copies are only present in dividing cells, as the genetic information has to be duplicated before the cells divide. But most cells in the human body do not undergo division, which therefore assigns them to the apparently more inaccurate method of end joining.

***

We found it difficult to understand how it was that important genetic information could get lost during the non-homologous end joining repair process." As a result, the research teams examined the enzymatic processes occurring at the breaks before they join together -- with surprising results. In contrast to previous schools of thought, the break ends are not simply joining together, but are being changed by specific enzymes, so that the information that was lost as a result of the break could be identically repaired with the aid of a copy.

These changes at the break ends -- called "resection" in the lingo -- are highly reminiscent of the homologous recombination process, where a sister copy acts as a matrix for precise repair. It is just that in non-dividing cells, there is no sister copy of the DNA, so at present it is still unclear where the copy of the genetic information necessary for precise repair could actually come from. However, the new findings provide clear evidence that cells that do not divide also use copies of genetic information to repair DNA double-strand breaks.

Comment: DNA is an intricate code, beyond any invented by humans. There must be exac t copies as cells divide. The first cells of life had to copy exactly or life would not have lasted. The repair mechanism had to appear at the point of origin of the DNA code. An obvious saltation by a brilliant mind. Nothing else fits, does it?

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It is turning out to be a highly complex organic chemical process:

https://phys.org/news/2017-02-protein-chaperone-job.html

"For proteins, this would be the equivalent of the red-carpet treatment: each protein belonging to the complex machinery of ribosomes—components of the cell that produce proteins—has its own chaperone to guide it to the right place at the right time and protect it from harm.

***

"In all cells, genetic information is stored as DNA and transcribed into mRNAs that code for proteins. Ribosomes translate the mRNAs into amino acids, linking them together into polypeptide chains that fold into proteins. More than a million ribosomes are produced per day in an animal cell.

"Building ribosomes is a formidable undertaking for the cell, involving about 80 proteins that make up the ribosome itself, strings of ribosomal RNA, and more than 200 additional proteins that guide and regulate the process. "Ribosome assembly is a dynamic process, where everything happens in a certain order. We are only now beginning to elucidate the many steps involved," says Hoelz.

"To make matters more complex, the proteins making up a ribosome are first synthesized outside the nucleus of a cell, in the cytoplasm, before being transported into the nucleus where the initial stages of ribosome assembly take place.

"Chaperone proteins help transport ribosomal proteins to the nucleus while also protecting them from being chopped up by a cell's protein shredding machinery. The components that specifically aim this machinery at unprotected ribosomal proteins, ....ensures that equal numbers of the various ribosomal proteins are available for building the massive structure of a ribosome.

***

"...a ribosomal protein called L4 is bound by a chaperone called "Assembly chaperone of RpL4," or Acl4. The chaperone ushers L4 through the nucleus, protecting it from harm, and delivers it to a developing ribosome at a precise time and location.

***

"Hoelz says that the structure was a surprise because it was not known previously that chaperones hold on to their ribosomal proteins so tightly. He says they want to study other chaperones in the future to see if they function in a similar fashion to tightly guard ribosomal proteins."

Comment: In living biochemistry the actions of the genome are demonstrably extremely complex, defying simple chance creation. Saltation by a brilliant mind is the only answer to the origin that seems correct.

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Researchers have found new tiny organelles on stem cells which provide controls of cell division and outcomes of cell types. Another layer of genome complexity:

https://www.sciencedaily.com/releases/2017/02/170210165948.htm

"When it divides, a stem cell has a choice: produce more stem cells or turn into the specific types of cells that compose skin, muscle, brain, or other tissue. New experiments in skin show this decision can be altered if tiny organs within cells aren't positioned and divvied up properly.

***

"'In order for the body's tissues to develop properly and maintain themselves, renewal and differentiation must be carefully balanced," says senior author Elaine Fuchs, the Rebecca C. Lancefield Professor and head of the Robin Chemers Neustein Laboratory of Mammalian Cell Biology and Development. "Our experiments suggest an unexpected role for the positioning and inheritance of cellular organelles, in this case enzyme-filled peroxisomes, in controlling this intricate balance."

***

"The outer section of the skin, the epidermis, provides a protective barrier for the body, and stem cells reside deep within it. During development, these cells divide so that one renewing stem cell daughter remains inward while the other daughter differentiates and moves outward to become part of the epidermis' outer layers. First author Amma Asare, a graduate student in the lab, wanted to know how skin cells first emerge and begin this transition.

"Looking in developing mouse skin, Asare devised an approach to identify genes that help guide the balance between new cells that either stay stem-like or differentiate. One particular protein, Pex11b, caught her attention. It is associated with the membrane that surrounds the peroxisome, an organelle that helps to free energy from food.

"Asare showed that the protein seems to work by making sure the organelles are in the right locations so they can be divided between the daughter cells. In cells that lacked Pex11b, peroxisomes weren't divvied up evenly -- in some cases, one daughter cell ended up with all of the peroxisomes and the other didn't get any at all. And for those cells whose peroxisome distribution was disrupted, cell division took longer, and the mitotic spindle, the structure that separates the daughters' genetic material, didn't align correctly.

"The net result of depleting skin stem cells of Pex11b, Asare found, was that fewer daughter cells were able to differentiate into mature skin cells.

"The researchers next moved peroxisomes around in the cell using a sophisticated laboratory technique, and the effect was the same. "If the peroxisomes are in the wrong positions during cell division, no matter how they get there, that slows down the process," Asare says.

"The effect for the whole organism was dramatic: If peroxisome positioning was disrupted in the stem cells, the mice embryos could no longer form normal skin.
"While some evidence already suggested the distribution of organelles, including energy-producing mitochondria, can influence the outcome of cell division, we have shown for the first time that this phenomenon is essential to the proper behavior of stem cells and formation of the tissue," says Fuchs."

Comment: Here again the development of this embryological process cannot have developed stepwise. It involves the little organelles, peroxisomes, which contain enzymes, and the protein Pex11b. The enzymes, Pex11b, and the positioning of the peroxisomes all must work together from the start. Only saltation can do this. God at work.

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A new study finds a different level of epigenetic controls than methylation or acetyl markings:

https://phys.org/news/2017-03-proteins-domesticated-genomes.html

"EPFL scientists have carried out a genomic and evolutionary study of a large and enigmatic family of human proteins, to demonstrate that it is responsible for harnessing the millions of transposable elements in the human genome. The work reveals the largely species-specific gene-regulatory networks that impact all of human biology, in both health and disease.

"The human genome contains millions of sequences derived from so-called transposable elements, genetic units that "jump" around the entire genome. Long considered as junk DNA, transposable elements are now recognized as influencing the expression of genes. However, the extent of this regulation and how it is harnessed were so far unknown. EPFL scientists have now taken the first extensive look at a family of ~350 human proteins, showing that they establish a complex interplay with transposable elements to create largely human-specific gene regulatory networks.

***

" The lab of Didier Trono at EPFL revealed a few years ago that a protein serving as cofactor to many KZFPs (KRAB-containing zinc-finger proteins) was involved in silencing transposable elements during the first few days of embryogenesis. Now he and his collaborators have carried out an extensive analysis of human KZFPs, retracing their evolutionary history and identifying their genomic targets.

***

"Trono's team then mapped out the genomic targets of most human KZFPs, finding that the greatest fraction recognizes transposable elements. "The vast majority of KZFPs binds to specific motifs in transposable elements," says Trono. "For each KZFP we were able to assign one subset of transposable elements, and also found that one transposable element can often interact with several KZFPs. It is a highly combinatorial and versatile system."

"'After emerging some 420 million years ago, KZFPs evolved rapidly in a lineage-specific fashion, parallel to the invasion of host genomes by transposable elements," says Trono. "This co-evolution resulted in shaping human gene regulatory networks that are largely proper to our species or at least primate-restricted—the farther away in evolution, the fewer the similarities."

"The data from the study demonstrate that KZFP partner up with transposable elements to create what the authors call "a largely species-restricted layer of epigenetic regulation". Epigenetics refers to biological processes—mostly biochemical modifications of the DNA and its associated proteins—that condition the expression or repression of genes. As a field, epigenetics has come into prominence in recent years, revealing a previously unimagined complexity and elegance in genetics.

"'KZFPs contribute to make human biology unique," says Trono. "Together with their genomic targets, they likely influence every single event in human physiology and pathology, and do so by being largely species-specific—the general system exists in many vertebrates, but most of its components are different in each case." (my bold)

"'This paper lifts the lid off something that had been largely unsuspected: the tremendous species-specific dimension of human gene regulation", says Trono. "It has profound implications for our understanding of human development and physiology,"(my bold)

Comment: Note the bolded areas! This is a whole newly discovered level of epigenetic control of gene expression control, and shows us the probable genetic area where God could drive human development from the apes! Remember this: over the past eight million years the only major evolutionary drive we see is in human development, nothing else!

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Stress is passed on by definite genetic molecular RNA actions:

https://www.sciencenews.org/article/how-dad-stress-changes-sperm

"Sperm from stressed-out dads can carry that stress from one generation to another. “But one question that really hasn’t been addressed is, ‘How do dad’s experiences actually change his germ cell?’” Jennifer Chan, a neuroendocrinologist at the University of Pennsylvania.

"The researchers focused on the part of the male reproductive tract called the caput epididymis, a place where sperm cells mature. Getting rid of a stress-hormone sensor there called the glucocorticoid receptor stopped the transmission of stress, the researchers found. When faced with an alarming predator odor, offspring of chronically stressed mice dads overproduce the stress hormone corticosterone. But mice dads that lacked this receptor in the epididymis had offspring with normal hormonal responses.

"Earlier work has shown that epididymis cells release small packets filled with RNA that can fuse to sperm and change their genetic payload. Experiments on cells in dishes revealed that chronic exposure to corticosterone changed the RNA in these vesicles. The results offer an explanation of how stress can change sperm: By activating the glucocorticoid receptor, stress tweaks the RNA in epididymis vesicles. Then, those vesicles deliver their altered contents to sperm, passing stress to the next generation.

"Similar vesicles are present in human seminal fluid, even after ejaculation. Chan and colleagues are testing whether humans carry similar signs of stress in these RNA-loaded vesicles by studying college students’ semen samples. Exam schedules will be used as a stress indicator, she said."

Comment: Not intelligence but simple automatic molecular reactions drive epigenetics in this experimental exhibition.

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Precise control of chromosome size and shape:

https://phys.org/news/2022-12-unwinding-chromosomes-unique-perspective-chromosomal.html

"Mitosis, chromosomes ensure that genetic material is equally divided among the daughter cells. Interestingly, the dimensions and degree of DNA condensation in mitotic chromosomes vary from organism to organism. How this is regulated—i.e., what factor governs mitotic chromosomal formation and dimensions—remains a mystery.

***

"During mitosis, DNA undergoes significant compaction to form chromosomes. A large protein ring complex called condensin plays a key role in the compaction process. It binds at specific sites on DNA and compresses it by forming loops. So, scientists know that condensin is crucial for DNA compaction, which is closely related to chromosomal dimensions—with thicker chromosomes being more compacted. They also know that the pattern of condensin-binding sites is species-specific. But the exact role of condensin and chromatin contacts in determining chromosomal dimensions is, as yet, unclear.

"The researchers explored various facets of condensin and chromatin contacts to address the questions at hand. They employed Hi-C and super-resolution microscopy to analyze the correlation between mitotic chromatin contacts and chromosomal arm length in both budding and fission yeasts, S. cerevisiae and S. pombe, respectively.

"Conclusive evidence was found indicating that the distance between chromatin contacts is directly proportional to arm length in both interphase and mitosis. Hence, shorter arms have short range contacts and longer arms have long range contacts. This was found to be species-specific. (my bold)

"Now, longer distances of chromatin contacts lead to larger chromatin loops, both of which are indicators of wider chromosomal arms. The authors thus investigated both budding and fission yeasts to conclude that within a species, longer chromosomal arms were always wider. Motivated by the successful observation in the yeasts, they extended their study to human cells, to find the same correlations.

"'We made the unexpected discovery that longer chromosomal arms are always thicker throughout eukaryotic species, which helps us understand how mitotic chromosomes form during cell divisions," explains Kakui. Their study would be the first to conclusively establish that chromosomal arm length determines mitotic chromosome width."

Comment: these precise requirements in all species require design. How this is controlled is yet to be found.

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Mother's contribution controls very early development:

https://phys.org/news/2022-12-developmental-genetics-germ-cells-cord.html

"For the first cell to develop into an entire organism, genes, RNA molecules and proteins have to work together in a complex way. At first, this process is indirectly controlled by the mother. At a certain point in time, the protein GRIF-1 ensures that the offspring cut themselves off from this influence and start their own course of development.

"When a new organism starts to develop, the mother calls the shots. During fertilization, the egg cell and sperm fuse to form a single new cell. However, the course of cell division, and thus how a new living being forms, is initially determined by the mother cell.

"Regardless of the organism, cell division is initially pre-programmed by the mother," explains geneticist Professor Christian Eckmann from MLU. The mother's cell provides a developmental starter set that includes the first proteins as well as the RNA molecules that serve as blueprints for further proteins. All this is necessary to jump start cell division and an organism's development.

"During this initial period, cells have no access to its own genetic material, something which restricts its own development. "As important as this maternal contribution is for the new organism, at a certain point these components have to be removed. Only then can it fully utilize its own genetic material and pursue its own course of development," says Eckmann.

"This process starts much later in germ cells, the precursors to gametes, than in somatic cells, which develop into all of the body's other cells. "Cells have a lot of options for killing things off. Longevity has to be earned," says Eckmann. In germ cell precursors, so called poly-A polymerases provide the mother's short-lived RNA molecules a kind of protective cap to ensure they live longer.

"In experiments with the model organism C. elegans, Eckmann's team discovered how the cord cutting process works at a molecular level in germ cells. At a certain stage, cells start producing the protein GRIF-1. The instructions for this process come from the maternal RNA. As soon as the protein is built, it starts looking for the maternal poly-A polymerases, binds to them, and attaches to them a kind of marker. "It's like a flag which GRIF-1 uses to mark which maternal proteins are to be degraded," says Eckmann.

"This sets off a chain reaction: once the poly-A polymerases are destroyed, they can no longer attach new protective caps to maternal RNA molecules, which would protect them from degradation and thus, no new maternal proteins can be built. "Eventually, all maternal RNA molecules and proteins are eliminated. The germ cell gains full access to its genetic material and can continue to develop on its own," concludes Eckmann. It remains unclear how the cell knows that it has to produce GRIF-1 and that it has to activate its own genetic material. (my bold)

"Incidentally, this long maternal control process is there for a reason: the genetic material in the germ cells is passed on to the offspring via the sperm or egg. Therefore, it must be preserved as completely and as error-free as possible. Eckmann's researchers artificially prevented this degradation process from happening in the laboratory in C. elegans. "A disruption to this process causes a lot problems. The germline cannot develop robustly and the worms' offspring become more infertile with each generation," says Eckmann." (my bold)

Comment: note the bold, reasons come from brains. A Darwinian slip of the tongue. What is seen in this study is the overall mechanism, while my bold notes the underlying complexity of controls is yet to be found. This system is so dependent on timing and parts it is irreducibly complex. All sexual reproduction is irreducibly complex.

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The bacterial Crispr defense system is further explained in that it immediately attacks invading viruses:

https://phys.org/news/2017-03-microbes-viruses-fast-response-defense.html

"The Rockefeller University reveals how microbes act quickly to fend off the incoming threat using CRISPR, a bacterial immune system that also serves as a powerful tool for editing genomes.

"The discovery, described in Nature on March 29, answers a long-standing question as to how CRISPR works.

Scientists already knew the basics: When a bacterial cell is invaded by viral DNA, its CRISPR system captures snippets of it and catalogs those DNA pieces. Should the same virus show up again, the system will quickly recognize it.

"'For about a decade, we've known that CRISPR works by acquiring pieces of viral DNA, but it's been a mystery exactly when this key step in CRISPR immunity occurs during an infection," says Luciano A. Marraffini, head of the Laboratory of Bacteriology, who studies CRISPR systems in their native bacteria.

"Experiments in his lab revealed that CRISPR springs into action early on, when the virus is injecting itself into the cell.

"To pinpoint the timing, the research team designed an experiment to stop the viral life cycle at different points. Joshua W. Modell, a postdoc, and Wenyan Jiang, a graduate student, then examined the CRISPR systems to see when and how they acquired spacers from the virus.

"Just any DNA won't do for CRISPR; previous research has shown it favors spacers from the loose ends of DNA. This preference narrows the options, since viral DNA takes linear form only during certain points in the infection; the rest of the time its two ends stick together, creating a circle.

"The team halted the infection at three points. But regardless of when they stopped it, CRISPR continued to acquire spacers, indicating it picks them up at the beginning, around when the virus injects its genome—as a strand—into the cell.

"This timing matters. By taking spacers from the first part of the virus to enter the cell, CRISPR ensures it will attack the virus as soon as it shows up next time. When the researchers altered CRISPR systems to contain spacers that matched sequences at the end of the viral genome, the last part to be injected, the microbes struggled to proliferate. (my bold)

"'It turns out that the CRISPR system is very clever," says Modell. "It takes advantage of a nuance of the viral infection cycle to halt an infection as early as possible.'"

Comment: The Crispr system is a series of enzymes that break down foreign DNA. It is difficult to imagine that this defense system took time to develop. If stepwise there would be only dead bacteria, as the virus attacker would always win. Looks like a saltation to me.

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Research has uncovered proteins that can modify RNA control of gene expression in embryology:

https://phys.org/news/2017-04-reveals-multitasking-secrets-rna-binding-protein.html

"Researchers from Princeton University and the National Institute of Environmental Health Sciences have discovered how a fruit fly protein binds and regulates two different types of RNA target sequence.

***

"There are hundreds of RNA-binding proteins in the human genome that together regulate the processing, turnover and localization of the many thousands of RNA molecules expressed in cells. These proteins also control the translation of RNA into proteins. RNA-binding proteins are crucial for maintaining normal cellular function, and defects in this family of proteins can lead to disease.

***

"Gavis and colleagues are particularly interested in a protein called Glorund (Glo), a type of RNA-binding protein that performs several functions in fruit fly development. This protein was originally identified due to its ability to repress the translation of an RNA molecule called nanos to protein in fly eggs. By binding to a stem structure formed by uracil and adenine nucleotides in the nanos RNA, Glo prevents the production of Nanos protein at the front of the embryo, a step that enables the fly's head to form properly.

"Like many other RNA-binding proteins, however, Glo is multifunctional. It regulates several other steps in fly development, apparently by binding to RNAs other than nanos. The mammalian counterparts of Glo, known as heterogeneous nuclear ribonucleoprotein (hnRNP) F/H proteins, bind to RNAs containing stretches of guanine nucleotides known as G-tracts, and, rather than repressing translation, mammalian hnRNP F/H proteins regulate processes such as RNA splicing, in which RNAs are rearranged to produce alternative versions of the proteins they encode.

"To understand how Glo might bind to diverse RNAs and regulate them in different ways, Gavis and graduate student Joel Tamayo collaborated with Traci Tanaka Hall and Takamasa Teramoto from the National Institute of Environmental Health Sciences to generate X-ray crystallographic structures of Glo's three RNA-binding domains. As expected, the three domains were almost identical to the corresponding domains of mammalian hnRNP F/H proteins. They retained, for example, the amino acid residues that bind to G-tract RNA, and the researchers confirmed that, like their mammalian counterparts, each RNA-binding domain of Glo can bind to this type of RNA sequence.

"However, the researchers also saw something new. "When we looked at the structures, we realized that there were also some basic amino acids that projected from a different part of the RNA-binding domains that could be involved in contacting RNA," Gavis explained.

"The researchers found that these basic amino acids mediate binding to uracil-adenine (U-A) stem structures like the one found in nanos RNA. Each of Glo's RNA-binding domains therefore contains two distinct binding surfaces that interact with different types of RNA target sequence. "While there have been examples previously of RNA-binding proteins that carry more than one binding domain, each with a different specificity, this represents the first example of a single domain harboring two different specificities," said Howard Lipshitz, a professor of molecular genetics at the University of Toronto who was not involved in the study.

***

"The researchers discovered that, as well as binding the U-A stem in the nanos RNA, Glo also recognized a nearby G-tract sequence. But Glo's ability to regulate other RNAs at different developmental stages only depended on the protein's capacity to bind G-tracts.

"'We think that the binding mode may correlate with Glo's activity towards a particular RNA," said Gavis. "If it binds to a G-tract, Glo might promote RNA splicing. If it simultaneously binds to both a G-tract and a U-A stem, Glo acts as a translational repressor."

"The RNA-binding domains of mammalian hnRNP F/H proteins probably have a similar ability to bind two different types of RNA, allowing them to regulate diverse target RNAs within the cell..... "Since these proteins are evolutionarily conserved from fruit flies to humans, experiments of this type tell us a lot about how their human versions normally work or can go wrong.'"

Comment: Like the Crispr mechanisms in bacteria, mentioned previously, this level of complexity insists that these arrangements are designed. God had to do this. This is certainly the way embryology works to create a new organism with a complex body plan. Layer upon layer of controls carefully planned.

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My last three entries in this line of research clearly show how God's hand in planning during evolution:

Genome complexity: newly found epigenetic controls - David Turell, 2017-03-08, 18:54
Genome complexity: Explaining Crispr - David Turell, 2017-03-29, 23:38
Genome complexity: modifying RNA controls of genes - David Turell, 2017-04-04, 19:54

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DAVID: My last three entries in this line of research clearly show how God's hand in planning during evolution:

I can’t pretend to understand the details, but the complexities are undeniable, and this for me is where the grounds for belief in a designer are as firm as they can possibly be. Together with psychic experiences, they seem to me to represent an insurmountable obstacle to atheism. My problem, of course, is that there are equally insurmountable obstacles to theism! And that means I am wrong one way or the other.

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In cephalopods there are RNA editing sites that control the genetics, not seen so far in other parts of the bush of life:

http://www.the-scientist.com/?articles.view/articleNo/49153/title/Cephalopod-Genomes-Co...

"RNA editing sites are rarely found in the coding regions of most animals’ genomes. But according to a study published today (April 6) in Cell, the genomes of squid, octopus, and cuttlefish contain hundreds of thousands of editing sites, many of which are found in coding regions and are evolutionarily conserved.

"The authors showed that recoding events—in which RNA’s adenosine (A) is post-transcriptionally converted to inosine (I), resulting in incorporation of a new amino acid—are often adaptive and contribute to diversity in the animals’ proteomes. And sequence conservation of regions surrounding editing sites has slowed down genome evolution in behaviorally complex coleoid cephalopods.

"Coleoid cephalopods “change the amino acid code, so you have a big diversification of the proteome, which you don’t see in any other animals,” Marie Öhman, who studies RNA editing in the mammalian brain at Stockholm University in Sweden and did not participate in the work, told The Scientist. “That it’s so extensive is really amazing.”

“'When we started looking into this we really didn’t know if this massive recoding was more of a bug or more of a feature,” said coauthor Noa Liscovitch-Brauer, a postdoc at Tel Aviv University in Israel. “What we show here is that it is probably advantageous, and this is something special that only they do.”

"Most organisms have very few functional [editing] sites in coding regions,” said coauthor Eli Eisenberg of Tel Aviv University. “This is why we find it so unusual and surprising that in squid, octopus, and cuttlefish, we see exactly the opposite.”

***

"The team found evidence of positive selection in genomic regions immediately adjacent to editing sites. These regions had fewer mutations than sequences far from editing sites. And because there are so many editing sites and thus sequences under positive selection, the cumulative constraints have slowed down coleoid genome evolution.

“'There are lots of [editing] sites that are highly conserved between octopus and squid,” coauthor Joshua Rosenthal of the Marine Biological Laboratory in Woods Hole, Massachusetts, told The Scientist. “They’re going so far as to dampen genomic evolution in order to maintain it.” (my bold)

“'The editing is very pervasive, particularly the recoding events,” said Jin Billy Li, who studies RNA editing at Stanford University in Palo Alto, California, and was not involved in the study. “It’s a striking finding, but it’s also a first step. There are just so many questions to ask . . . How does this happen? And what’s the functional consequence?”

***

“'The cephalopods will offer a gold mine in terms of understanding the mechanisms that they’ve adopted to generate this [behavioral] complexity,” said Rosenthal. “I’m certainly not suggesting that editing is the only answer. I think it’s part of the equation, and I think looking how organisms solve problems differently is invaluable.'”

Comment: Note my bold. This appears to be a mechanism to sustain current phenotypes, not advancing evolution in this group. This is opposite to the recent report on how human evolution proceeded: Wednesday, March 08, 2017, 18:54, which was not seen in the rest of the primate group. From the report:

"'This paper lifts the lid off something that had been largely unsuspected: the tremendous species-specific dimension of human gene regulation", says Trono. "It has profound implications for our understanding of human development and physiology,"(my bold)

This suggests that genome controls complexity is broadly different across the bush of life. If common descent is true, the genome mechanisms should be similar across the bush. Since it isn't perhaps God is actively seen to be monkeying with the works. This seems to be direct evidence of dabbles!

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Another article on cephalopods and RNA editing:

https://www.scientificamerican.com/article/curiouser-and-curiouser-octopuss-evolution-i...

"Not so for cephalopods—at least not entirely. A new study published in Cell reports these aquarium oddities can modify the proteins found in their bodies without having to change the basic sequence of their DNA blueprint. As a result, it looks as if cephalopods have changed very slowly over the eons of their existence. The findings also suggest that octopuses and their tentacled cousins may be a lot older than previously thought.

"The new paper reports on a process called “RNA editing,” which involves enzymes swapping out one RNA base (or nitrogen-based “letter” in the RNA/DNA alphabet) for another, presumably in the interest of an organism adapting to its environment. RNA editing is rarely employed in most animals. Among the 20,000 or so genes found in humans, for example, only a few dozen sites are thought to change their RNA so that it no longer matches the original DNA template.

"Yet previous work, in part by the same authors, suggested the process is employed rather frequently by octopuses and squid to respond to changes in ocean water temperature. The new study looked at DNA sequences, RNA sequences and proteomes—meaning all of the proteins encoded in a particularly cell or tissue—of multiple cephalopod species to determine how common RNA editing really is. Very, it turns out.

"Squid also have around 20,000 genes, a whopping 11,000 of which code for RNA that in some cases undergoes editing. A similar degree of editing was found in two species of octopus and the common cuttlefish. Far lower levels of RNA-editing were seen in the nautilus—a more primitive cephalopod—and in a non-cephalopod control, a mollusk called a sea hare. RNA editing was especially high in the cephalopod nervous system, including in genes coding for ion channels that facilitate electrical communication between neurons.

"What’s more, such extensive RNA editing seems to have helped to minimize changes in the cephalopod DNA over the eons that they have been around. Unlike most animal species, whose genomes are riddled with millions of years of mutations that have helped them adapt to a volatile world, cephalopod adaption appears to have been more a result of RNA editing.

***

“'If a squid and octopus want to edit a base, they must preserve the underlying RNA structure,” Rosenthal says, “This means that the RNA structure can’t evolve. If it collects mutations as a result of DNA mutations, it would no longer be recognized by the editing enzymes. We normally think of mutations as the currency of evolution. But in this case their accumulation is suppressed.”

***

"No one knows why cephalopods are so keen on RNA editing. Perhaps it is a faster, easier way to adapt to their environment than waiting for a random mutation to occur. Or maybe it better suits their relatively short life spans.

"Cephalopods grow up fast and die young . Most live only for a few years and they only breed once. Ragsdale feels RNA editing may help them navigate what are often lonesome, fleeting lives. “This may explain why they’re such good problem solvers. No one’s around to show them how to figure out the world!” Ragsdale says, “How to make their dens. How to camouflage themselves and attack prey. They’re on their own, and fortunately for them they have big brains and can sort matters out.”
(my bold)

***

" If RNA editing allows changes in the cephalopod's DNA to occur at a markedly slower rate than is normally assumed, the animals most likely arose many millions of years earlier than current time lines suggest. In other words, the DNA mutations they do harbor would have taken a lot longer to crop up.

“'This may mean that our molecular clock estimates of when different cephalopod lineages arose and diverged might be too recent,” Ragsdale says. “The Nobel Prize–winning biologist Sydney Brenner once said that octopi were the first intelligent beings on Earth. This could prove he was right.'”

Comment: Note my bold. Is this a big brain running the genome, or is this a God dabble in setting up a genetic action which is different than all other evolutionary genomes? Then not common descent, but possibly differing descents are present in evolution? Raises new questions about Darwin's so-called common descent.

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QUOTE: "The new paper reports on a process called “RNA editing,” which involves enzymes swapping out one RNA base (or nitrogen-based “letter” in the RNA/DNA alphabet) for another, presumably in the interest of an organism adapting to its environment. (dhw’s bold)
QUOTE: No one’s around to show them how to figure out the world!” Ragsdale says, “How to make their dens. How to camouflage themselves and attack prey. They’re on their own, and fortunately for them they have big brains and can sort matters out.” (David’s bold)

DAVID’s comment: Note my bold. Is this a big brain running the genome, or is this a God dabble in setting up a genetic action which is different than all other evolutionary genomes? Then not common descent, but possibly differing descents are present in evolution? Raises new questions about Darwin's so-called common descent.

Once you accept that cells are intelligent beings, and that all multicellular organisms consist of cell communities cooperating and responding to the requirements or opportunities arising from environmental change, you have a clear explanation for all these adaptations and possibly for all innovations as well. Different cell communities (the authors here emphasize the cell community that makes up the brain) work out different ways of responding. Since as far as we know life began with single cells, this whole process of cellular cooperation makes for a logical progression of common descent that encompasses all organisms, including cephalopods – they all stem from cells/cell communities responding intelligently but differently to environmental conditions.

I would disagree profoundly with Sydney Brenner’s suggestion that octopi were the first intelligent beings on earth, but perhaps we need to know what he meant by “intelligence”.

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dhw: Since as far as we know life began with single cells, this whole process of cellular cooperation makes for a logical progression of common descent that encompasses all organisms, including cephalopods – they all stem from cells/cell communities responding intelligently but differently to environmental conditions.

Certain genomes have certainly branched off, mechanisms not proven to be this or that.

dhw: I would disagree profoundly with Sydney Brenner’s suggestion that octopi were the first intelligent beings on earth, but perhaps we need to know what he meant by “intelligence”.

You have forgotten this entry about octopi:

Natures wonders: the mind of the octopus (Introduction)
by David Turell , Tuesday, December 13, 2016, 00:47

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I would disagree profoundly with Sydney Brenner’s suggestion that octopi were the first intelligent beings on earth, but perhaps we need to know what he meant by “intelligence”.

Perhaps Brenner is saying that octopi were the first intelligent "beings" to be formed from organisms and bacteria?

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dhw: I would disagree profoundly with Sydney Brenner’s suggestion that octopi were the first intelligent beings on earth, but perhaps we need to know what he meant by “intelligence”.

DAVID: You have forgotten this entry about octopi:
Natures wonders: the mind of the octopus (Introduction)
by David Turell , Tuesday, December 13, 2016, 00:47

Thank you. I have reread it and it is indeed fascinating. There are degrees of intelligence, and obviously the octopus comes high on the scale. That does not make him the first intelligent being.

BBELLA: Perhaps Brenner is saying that octopi were the first intelligent "beings" to be formed from organisms and bacteria?

Some scientists tell us that bacteria themselves are intelligent beings. This observation underlies my hypothesis that evolution may be driven by the (perhaps God-given) intelligence of cells/cell communities.

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dhw: I would disagree profoundly with Sydney Brenner’s suggestion that octopi were the first intelligent beings on earth, but perhaps we need to know what he meant by “intelligence”.

DAVID: You have forgotten this entry about octopi:
Natures wonders: the mind of the octopus (Introduction)
by David Turell , Tuesday, December 13, 2016, 00:47

Thank you. I have reread it and it is indeed fascinating. There are degrees of intelligence, and obviously the octopus comes high on the scale. That does not make him the first intelligent being.

BBELLA: Perhaps Brenner is saying that octopi were the first intelligent "beings" to be formed from organisms and bacteria?

dhw: Some scientists tell us that bacteria themselves are intelligent beings. This observation underlies my hypothesis that evolution may be driven by the (perhaps God-given) intelligence of cells/cell communities.

The Octopus intelligence article was fascinating and their antics in labs was featured in the movie "Finding Nemo". But cells which have a brilliant set of instructions in their genomes will fool outsiders into thinking they are innately intelligent.

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dhw: I would disagree profoundly with Sydney Brenner’s suggestion that octopi were the first intelligent beings on earth, but perhaps we need to know what he meant by “intelligence”.

DAVID: You have forgotten this entry about octopi:
Natures wonders: the mind of the octopus (Introduction)
by David Turell , Tuesday, December 13, 2016, 00:47

Thank you. I have reread it and it is indeed fascinating. There are degrees of intelligence, and obviously the octopus comes high on the scale. That does not make him the first intelligent being.

BBELLA: Perhaps Brenner is saying that octopi were the first intelligent "beings" to be formed from organisms and bacteria?

Some scientists tell us that bacteria themselves are intelligent beings. This observation underlies my hypothesis that evolution may be driven by the (perhaps God-given) intelligence of cells/cell communities.

I agree, dhw, that bacteria themselves are intelligent beings, but think this scientist believes something has to be big enough to be seen by the naked eye to be an actual being. Would that be considered "being chauvinism"?

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DAVID: The Octopus intelligence article was fascinating and their antics in labs was featured in the movie "Finding Nemo". But cells which have a brilliant set of instructions in their genomes will fool outsiders into thinking they are innately intelligent.

Clear choice then: a) they ARE innately intelligent (and their intelligence may have been given to them by your God); b) 3.8 billion years ago your God preprogrammed every decision they take; c) your (hidden) God has always made and is currently making every decision for them. Please tell us which of these you think is most likely.

BBELLA: Perhaps Brenner is saying that octopi were the first intelligent "beings" to be formed from organisms and bacteria?

Dhw: Some scientists tell us that bacteria themselves are intelligent beings. This observation underlies my hypothesis that evolution may be driven by the (perhaps God-given) intelligence of cells/cell communities.

BBELLA: I agree, dhw, that bacteria themselves are intelligent beings, but think this scientist believes something has to be big enough to be seen by the naked eye to be an actual being. Would that be considered "being chauvinism"?

It’s what James A. Shapiro, a champion of bacterial intelligence, calls “large organisms chauvinism”. The perfect description.

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DAVID: The Octopus intelligence article was fascinating and their antics in labs was featured in the movie "Finding Nemo". But cells which have a brilliant set of instructions in their genomes will fool outsiders into thinking they are innately intelligent.

dhw: Clear choice then: a) they ARE innately intelligent (and their intelligence may have been given to them by your God); b) 3.8 billion years ago your God preprogrammed every decision they take; c) your (hidden) God has always made and is currently making every decision for them. Please tell us which of these you think is most likely.

Choice 'b' is correct in my thinking. They are programmed to run their lives automaticaly, and that makes them look intelligent.

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dhw: Clear choice then: a) they ARE innately intelligent (and their intelligence may have been given to them by your God); b) 3.8 billion years ago your God preprogrammed every decision they take; c) your (hidden) God has always made and is currently making every decision for them. Please tell us which of these you think is most likely.

DAVID: Choice 'b' is correct in my thinking. They are programmed to run their lives automaticaly, and that makes them look intelligent.

QUOTE (under “Dolphin eats octopus”): "Octopus shaking and tossing is yet another example that illustrates how intelligent and adaptable these charismatic marine predators are."
DAVID’s comment: Bigger brains can think and find solutions.

“Large organisms chauvinism”! I wonder where you draw the line. Insects have smaller brains, and appear to think and find solutions. Bacteria have no brains, but appear to think and find solutions. One might argue that if organisms appear to think and find solutions, maybe they do think and find solutions. Alternatively, if smaller ones have been preprogrammed to look as if they think but they don’t, maybe bigger ones have been preprogrammed to look as if they think but they don’t. Your God can do anything, so if bacteria are mere automatons, why not you and me, brother?

I’ll be very bold here. It seems to me that if organisms behave as if they are intelligent - i.e. they are able to solve problems, take decisions, respond to their surroundings and adapt their behaviour accordingly – the least one can do is allow for the possibility that they ARE intelligent.

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DAVID’s comment: Bigger brains can think and find solutions.

dhw: “Large organisms chauvinism”! I wonder where you draw the line. Insects have smaller brains, and appear to think and find solutions. Bacteria have no brains, but appear to think and find solutions. One might argue that if organisms appear to think and find solutions, maybe they do think and find solutions. Alternatively, if smaller ones have been preprogrammed to look as if they think but they don’t, maybe bigger ones have been preprogrammed to look as if they think but they don’t. Your God can do anything, so if bacteria are mere automatons, why not you and me, brother?

I’ll be very bold here. It seems to me that if organisms behave as if they are intelligent - i.e. they are able to solve problems, take decisions, respond to their surroundings and adapt their behaviour accordingly – the least one can do is allow for the possibility that they ARE intelligent.

Yes be bold. Use your writer's imagination to become a bacteria in your mind. What is your life like? What are your everyday duties and accomplishments? To find food and eat. To expel waste. To avoid predators. To reproduce by using a standardized mechanism to split in two. To shift from one metabolic pathway to another available one to adapt to local environmental changes. Not like a dolphin, or a human. Bacteria live within one cubic millimeter their entire lives, extreme or not. Bacteria live extremely limited life styles, which allows for my contention they are automatons. Please try your imagination.

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Dhw: I’ll be very bold here. It seems to me that if organisms behave as if they are intelligent - i.e. they are able to solve problems, take decisions, respond to their surroundings and adapt their behaviour accordingly – the least one can do is allow for the possibility that they ARE intelligent.

DAVID: Yes be bold. Use your writer's imagination to become a bacteria in your mind. What is your life like? What are your everyday duties and accomplishments? To find food and eat. To expel waste. To avoid predators. To reproduce by using a standardized mechanism to split in two. To shift from one metabolic pathway to another available one to adapt to local environmental changes. Not like a dolphin, or a human. Bacteria live within one cubic millimeter their entire lives, extreme or not. Bacteria live extremely limited life styles, which allows for my contention they are automatons. Please try your imagination.

Use your imagination. Become a refugee in your mind, fleeing from the horrors of war. What are your everyday duties and accomplishments? To find food and eat. To expel waste. To avoid predators – especially those on two legs like yourself. To reproduce by using a standardized mechanism of sperm and egg. The name of the game is survival, and you use your intelligence to find ways of fulfilling all these basic needs, according to the environment in which you find yourself. Nobody is claiming that when bacteria have fulfilled all their basic needs, they begin to philosophize, to paint pictures and write symphonies, to explore the universe. All forms of life live extremely limited life styles, but some are more limited than others. That does not make them automatons. The appearance of intelligence, no matter how limited, may well denote the existence of intelligence.

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dhw: Nobody is claiming that when bacteria have fulfilled all their basic needs, they begin to philosophize, to paint pictures and write symphonies, to explore the universe. All forms of life live extremely limited life styles, but some are more limited than others. That does not make them automatons. The appearance of intelligence, no matter how limited, may well denote the existence of intelligence.

Your point is well-taken, but the simplicity of bacterial lifestyle which you have tried to equate to our lifestyle doesn't work. Bacterial lives are so simple, full genome directions can give the appearance of intelligent action when it is simply intelligent design of controls and responses..

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dhw: Nobody is claiming that when bacteria have fulfilled all their basic needs, they begin to philosophize, to paint pictures and write symphonies, to explore the universe. All forms of life live extremely limited life styles, but some are more limited than others. That does not make them automatons. The appearance of intelligence, no matter how limited, may well denote the existence of intelligence.

DAVID: Your point is well-taken, but the simplicity of bacterial lifestyle which you have tried to equate to our lifestyle doesn't work. Bacterial lives are so simple, full genome directions can give the appearance of intelligent action when it is simply intelligent design of controls and responses.

My post pointed out that all the basic needs you had listed are shared by humans. I did not equate basterial lifestyle with ours, as should be clear from the passage you have quoted. The fact that some organisms lead simpler lives than others does not mean your God has had to preprogramme or personally direct every single decision they make. However, taken to its logical conclusion, your argument can be applied to every form of life. Perhaps we are all variations of the Stepford wives and don’t know it.

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dhw: My post pointed out that all the basic needs you had listed are shared by humans. I did not equate basterial lifestyle with ours, as should be clear from the passage you have quoted. The fact that some organisms lead simpler lives than others does not mean your God has had to preprogramme or personally direct every single decision they make. However, taken to its logical conclusion, your argument can be applied to every form of life. Perhaps we are all variations of the Stepford wives and don’t know it.

You cannot get around the fact that seemingly intelligent activity can be the result of intelligent controls offered by well-designed DNA.

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DNA is six feet long and packed into a tiny nucleus. Knotting would create a mess. Preventing them is only partially understood:

http://www.nature.com/news/dna-s-secret-weapon-against-knots-and-tangles-1.21838?spUser...

“'It's a dynamic process of motors constantly extruding loops!” says Mirny, a biophysicist here at the Massachusetts Institute of Technology in Cambridge.

"Mirny's excitement isn't about keeping computer accessories orderly. Rather, he's talking about a central organizing principle of the genome — how roughly 2 metres of DNA can be squeezed into nearly every cell of the human body without getting tangled up like last year's Christmas lights.

"He argues that DNA is constantly being slipped through ring-like motor proteins to make loops. This process, called loop extrusion, helps to keep local regions of DNA together, disentangling them from other parts of the genome and even giving shape and structure to the chromosomes.

"Scientists have bandied about similar hypotheses for decades, but Mirny's model, and a similar one championed by Erez Lieberman Aiden, a geneticist at Baylor College of Medicine in Houston, Texas, add a new level of molecular detail at a time of explosive growth for research into the 3D structure of the genome. The models neatly explain the data flowing from high-profile projects on how different parts of the genome interact physically — which is why they've garnered so much attention.

"But these simple explanations are not without controversy. Although it has become increasingly clear that genome looping regulates gene expression, possibly contributing to cell development and diseases such as cancer, the predictions of the models go beyond what anyone has ever seen experimentally.

"For one thing, the identity of the molecular machine that forms the loops remains a mystery. If the leading protein candidate acted like a motor, as Mirny proposes, it would guzzle energy faster than it has ever been seen to do. “As a physicist friend of mine tells me, 'This is kind of the Higgs boson of your field',” says Mirny; it explains one of the deepest mysteries of genome biology, but could take years to prove.

"And although Mirny's model is extremely similar to Lieberman Aiden's — and the differences esoteric — sorting out which is right is more than a matter of tying up loose ends. If Mirny is correct, “it's a complete revolution in DNA enzymology”, says Kim Nasmyth, a leading chromosome researcher at the University of Oxford, UK. What's actually powering the loop formation, he adds, “has got to be the biggest problem in genome biology right now”.

***

"The Hi-C snapshots that Dekker and his collaborators had taken revealed distinct compartmentalized loops, with interactions happening in discrete blocks of DNA between 200,000 and 1 million letters long5.

"These 'topologically associating domains', or TADs, are a bit like the carriages on a crowded train. People can move about and bump into each other in the same carriage, but they can't interact with passengers in adjacent carriages unless they slip between the end doors. The human genome may be 3 billion nucleotides long, but most interactions happen locally, within TADs.

***

"they were careful to describe the model in terms of a generic “loop-extruding factor”. But the paper didn't shy away from speculating as to its identity: cohesin was the driving force behind the looping process for cells not in the middle of dividing, when chromosomes are loosely packed6. Condensin, they argued in a later paper, served this role during cell division, when the chromosomes are tightly wound.

"A key clue was the protein CTCF, which was known to interact with cohesin at the base of each loop of uncondensed chromosomes. For a long time, researchers had assumed that loops form on DNA when these CTCF proteins bump into one another at random and lock together. But if any two CTCF proteins could pair, why did loops form only locally, and not between distant sites?

"Mirny's model assumes that CTCFs act as stop signs for cohesin. If cohesin stops extruding DNA only when it hits CTCFs on each side of a growing loop, it will naturally bring the proteins together.

***

"David Rudner, a bacterial cell biologist at Harvard Medical School in Boston, Massachusetts, and his colleagues made time-lapse Hi-C maps of the bacterium Bacillus subtilis that reveal SMC zipping along the chromosome and creating a loop at a rate of more than 50,000 DNA letters per minute. This tempo is on par with what researchers estimate would be necessary for Mirny's model to work in human cells as well.

"Rudner hasn't yet proved that SMC uses ATP to make that happen. But, he says, he's close — and he would be “shocked” if cohesin worked differently in human cells."

Comment: Much complex debate left out. Only careful mental planning can produce this 3-D arrangement for gene control and knot protection. Never by chance.

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QUOTE: “The models neatly explain the data flowing from high-profile projects on how different parts of the genome interact physically — which is why they've garnered so much attention.
"But these simple explanations are not without controversy. Although it has become increasingly clear that genome looping regulates gene expression, possibly contributing to cell development and diseases such as cancer, the predictions of the models go beyond what anyone has ever seen experimentally.
“For one thing, the identity of the molecular machine that forms the loops remains a mystery.” (My bold)

This article is far too specialized for me to follow in detail, but I would like to ask a straightforward question: could this unidentified “molecular machine” be the equivalent of the cell’s brain?

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QUOTE: “The models neatly explain the data flowing from high-profile projects on how different parts of the genome interact physically — which is why they've garnered so much attention.
"But these simple explanations are not without controversy. Although it has become increasingly clear that genome looping regulates gene expression, possibly contributing to cell development and diseases such as cancer, the predictions of the models go beyond what anyone has ever seen experimentally.
“For one thing, the identity of the molecular machine that forms the loops remains a mystery.” (My bold)

dhw: This article is far too specialized for me to follow in detail, but I would like to ask a straightforward question: could this unidentified “molecular machine” be the equivalent of the cell’s brain?

Cells run a myriad of biochemical processes which act as if they are 'brainy'. This specific molecular machine which controls the 3-D placement of DNA will be found eventually by complex research. It will prove that cells are too complex to have been a result of chance formation.

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A set of three letters (a codon) denotes an amino acid. Now researchers that there may be more complex relationships between groups of codons:

https://www.evolutionnews.org/2017/04/genetic-code-complexity-just-tripled/

"The so-called central dogma of molecular biology states the process for turning genetic information into proteins that cells can use. “DNA makes RNA,” the dogma says, “and RNA makes protein.” Each protein is made of a series of amino acids, and each amino acid is coded for by sets of “triplets,” which are sets of three informational DNA units, in the genetic code.

"University of Utah biologists now suggest that connecting amino acids to make proteins in ribosomes, the cell’s protein factories, may in fact be influenced by sets of three triplets – a “triplet of triplets” that provide crucial context for the ribosome.

***

"Neo-Darwinian evolution is supposed to work by mutating DNA codons, either making them “synonymous” with the prior codon (i.e., yielding the same amino acid), or “non-synonymous” (i.e., putting a different amino acid in its place, potentially affecting the resulting protein). If codons could be treated as independent entities acted on by natural selection, Darwinians at least understood the challenge before them. If these researchers are correct, the stakes just skyrocketed.

***

"The authors of the PNAS paper, Hughes and Chevance, describe what drove them to examine the context for each triplet codon. They were playing with the genes for a component of the bacterial flagellum named FlgM when they noticed something interesting:

"Changing the codon on one side of the defective codon resulted in a 10-fold increase in FlgM protein activity. Changing the codon on the other side resulted in a 20-fold decrease. And the two changes together produced a 35-fold increase. “We realized that these two codons, although separated by a codon, were talking to each other,” Hughes says. “The effective code might be a triplet of triplets.”

***

"The “triplet of triplets” problem helps explain why you can’t easily get the same expression pattern by substituting a plant or animal protein in a bacterium, a lab procedure called heterologous expression. One doesn’t just tinker with a particular codon and expect to get the same result in a different organism that has a different expression context. The particular codon used affects downstream factors, including tRNA modifications, which the authors say are extensive in every organism.

***

"The difficulty for natural selection would be in finding codon optimization for a given gene. If the speed through a codon is dependent on the 5′ and 3′ flanking codons, and the flanking codons are dependent on their 5′ and 3′ flanking codons, then selection pressure on a single codon is exerted over five successive codons, which represent 615 or 844,596,301 codon combinations. If modified tRNAs interact with bases in a codon context-dependent manner that differs among species depending on differences in tRNA modifications, ribosome sequences, and ribosomal and translation factor proteins, it is easy to understand why many genes are poorly expressed in heterologous expression systems in which codon use is the primary factor in the design of coding sequences for foreign protein expression. The potential impact of differences in tRNA modifications represents a significant challenge in designing genes for maximal expression whether by natural selection or in the laboratory.

***

"Data presented here support a model in which the evolutionary selection pressure on a single codon is over five successive codons, including synonymous codons.

"The more that natural selection has to “think” about (if you’ll pardon the expression), the less able it will be to get things right. More accurately, it’s going to take a lot more of what David Berlinski calls “sheer dumb luck” to find a beneficial change. If there are 844,596,301 codon combinations to worry about, it’s like having to get many more numbers right in Powerball than you thought when you bought your lottery ticket.

***

"The tRNA modifications vary throughout the three kingdoms of life and could affect codon–anticodon pairing. The differences in tRNA modifications could account for differences in synonymous codon biases and for the effects of codon context (the ability to translate specific triplet bases relative to specific neighboring codons) on translation among different species. Here, using in vivo genetic systems of Salmonella, we demonstrate that the translation of a specific codon depends on the nature of the codons flanking both the 5′ and 3′ sides of the translated codon, thus generating higher-order genetic codes for proteins that can include codon pairs and codon triplets."

Comment: It is not surprising to find more complexity. The original dogma re' DNA and RNA was much too simple to explain how the code runs life. This coding system did not arise by chance.

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The lysosome was thought to be a minor organelle as a garbage collector. its not. it exhibits major cellular controls:

https://www.quantamagazine.org/20170425-lysosomes-gene-regulation-signaling/?utm_source...

"Lysosomes first drew attention in the 1950s, when the Belgian biochemist Christian de Duve stumbled across the saclike intracellular structures while trying to purify a protein found in rat livers. He named the previously unknown sacs after the Greek for “digestive body” because their contents were highly acidic and filled with enzymes that break down virtually any biomolecule that’s set before them.

***

"A critical clue came when the team tracked the protein’s movements within cells. When cells were bathed in amino acid-free media, mTOR seemed to spread evenly throughout the cytoplasm. But if the media contained amino acids, within minutes mTOR moved into distinct clusters at specific locations inside the cell, shepherded there by other proteins called Rag GTPases.

***

"In a healthy, well-fed cell, lysosomes have a cornucopia of proteins to break down to their amino acid components, and those amino acids work with proteins on the lysosome surface to anchor mTORC1 and activate it. The mTORC1 in turn keeps cytoplasmic TFEB out of the nucleus. When a cell becomes starved or stressed, mTORC1 drops away from the lysosome and TFEB is freed to bind its targets on the nuclear DNA. Acting as a master sensor of lysosomal function, TFEB turns on genes for more lysosomal enzymes.

***

"And the focus on deficiencies inside lysosomes had shifted to the lysosomal membrane and the ways in which it enlists TFEB, mTOR and roughly 200 other identified proteins in a conversation with the rest of the cell.

***

"Lysosomes may once have seemed like garbage bins that were “boring on the outside,” Nixon says, but they are increasingly appreciated as regulated signal platforms crucial to cellular health. And as perspectives on the lysosome change, views of the associated biology shift, too. Perera notes that cancer researchers have long wanted to know more about the signals that let malignant cells grow and multiply nonstop, and about how the cells co-opt nutrients. The new view of lysosomes, she says, reveals that these are “all different aspects of the same problem.'”

Comment: this essay shows how a self-contained cell must work. We take out the garbage and the garbage can doesn't care. The can simply takes what we give it. But the organelle that handles cellular garbage can't do that. It has to carefully control when and how it receives garbage to handle it properly. Note how intricate this system is. It has to be designed. It cannot develop stepwise or cells would not survive. It must be in place all at once. Cells are highly active protein factories with byproducts and waste products that cannot be allowed to pile up. Logically, this system had to exist at the start of life or single-celled animals would not survive. Only a planning mind can do this: God.

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If mitochondrial DNA is damaged it can be repaired quickly:

https://www.sciencedaily.com/releases/2017/04/170428145549.htm

"The five-year study led by scientists at the University of Sheffield, published in Science Advances, reveals how the enzyme TDP1 -- which is already known to have a role in repairing damaged DNA in the cell's nucleus -- is also responsible for repairing damage to mitochondrial DNA (mtDNA).
'
"Mitochondria are the powerhouses of cells, they generate the energy required for all cellular activity and have their own DNA -- the genetic material which they rely upon to produce important proteins for their function.

"During the process of energy production and making proteins, a large amount of rogue reactive oxygen species are produced which constantly attack the DNA in the mitochondria. These attacks break their DNA, however the new findings show mitochondria have their very own repair toolkits which are constantly active to maintain their own DNA integrity.

***

"Each mitochondria repair toolkit has unique components -- enzymes -- which can cut, hammer and seal the breaks. The presence of these enzymes is important for energy production.

***

"The team further identified a mechanism through which mtDNA can be damaged and then fixed, via a protein called TOP1, which is responsible for untangling coils of mtDNA. When the long strands become tangled, TOP1 breaks and quickly repairs the strands to unravel the knots. If free radicals are also attacking the mitochondrial DNA, then TOP1 proteins can become trapped on the mitochondrial DNA strands, making repair even more difficult."

Comment: Since mitchondria supply the energy for cells to keep working in production, once mitochondria were part of the cell this repair mechanism had to be in place, from the beginning. That is not a problem. Mitochondria were originally independent organisms according to accepted theory. They had the repair mechanism on board. But carry the thought further. Any independent single-celled animal had to have repair mechanisms from the very first time DNA was formed, or the cells would not have survived. The lesson is the only way life started in cellular form, it had to have a complete set of functions: energy, production of product, disposal of byproduct garbage, the ability to reproduce by splitting, and constant accurate repair. And each of these processes use giant molecules called enzymes, which are specific for each reaction to make it happen and quickly. Bacteria reproduce themselves about every 20 minutes. Since they never die, as sexual animals do, today's bacteria represent direct vestige's of original life. Which had to appear all at once!! Only a designing mind could create this: God

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This aphid seems to be able to adapt to any plant to pestify:

http://www.the-scientist.com/?articles.view/articleNo/49219/title/Uncovering-the-Secret...

"While most aphids are only able to colonize one or a few plant species, the green peach aphid (Myzus persicae) isn’t picky about its food. The polyphagous, or generalist, pest can feed on more than 100 species from around 40 different plant families. “Polyphagous insects always have a host somewhere, so they can keep going and can become massive pests,” says Saskia Hogenhout.

***

"Hogenhout, Mathers, and colleagues recently set out to see what gave M. persicae its remarkable ability to colonize such a huge variety of plants. To do so, they first sequenced M. persicae’s genome and compared it to that of the pea aphid, Acyrthosiphon pisum, a specialist that only occupies a few host plant species.

"Much to the authors’ surprise, A. pisum had a genome nearly double the size of M. persicae’s. “[This] is very surprising and counterintuitive,” You might expect that this aphid, with its very large host range, has a larger complement of genes that might allow it to feedsays Chris Bass, a University of Exeter professor who was not involved in the work. says Chris Bass, a University of Exeter professor who was not involved in the work. “You might expect that this aphid, with its very large host range, has a larger complement of genes that might allow it to feed on a different number of hosts—but it looks like the opposite is actually the case.”

"The group then investigated the transcriptional changes that occurred when M. persicae colonizes a new host. From this analysis, they found that gene expression changes in two gene families, cathepsin B and RR-2 cuticular protein, occurred rapidly—a mere two days after the aphids were transferred to a new plant host. When the researchers generated transgenic plants that could knock down cathepsin B gene expression in the insects, the aphids’ ability to survive and reproduce on a new host was significantly reduced.

"The team also discovered that the genes involved in host-switching were older gene duplicates that arose during aphid evolution. “It was as if Myzus persicae was able to take pre-existing genetic diversity in the genome and then just fine-tune the expression of those genes to be able to colonize a new host, rather than having more duplicated genes to colonize these different plant species,” Mathers says.

***

"According to Hogenhout, it’s possible that the ability to transfer rapidly between hosts helps M. persicae develop resistance to pesticides as well. If a pesticide is applied to a crop, these aphids can quickly move away to another crop after only experiencing sublethal doses of pesticides. A few years ago, a group at Imperial College London reported evidence for this type of mechanism."

Comment: This insect is a champion of epigenetic gene expression/transcription changes. Did it develop this ability by itself or was it given this ability? It is still the same species. Closely related species do not this ability. It is hard to explain by a blind evolutionary process.

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Scientists are finding that neurons in the brain have many different DNA patterns. To me this is not surprising. As a person grows up from childhood, each personality will use their brain differently and the brain will respond with a 'use pattern' in which different neurons will be used differently. I don't know why the scientist are surprised at their findings:

https://www.scientificamerican.com/article/scientists-surprised-to-find-no-two-neurons-...

"Accepted dogma holds that—although every cell in the body contains its own DNA—the genetic instructions in each cell nucleus are identical. But new research has now proved this assumption wrong. There are actually several sources of spontaneous mutation in somatic (nonsex) cells, resulting in every individual containing a multitude of genomes—a situation researchers term somatic mosaicism....There are reasons to think somatic mosaicism may be particularly important in the brain, not least because neural genes are very active.

***

"Somatic mutations can occur in multiple circumstances. They may emerge during DNA replication or from DNA damage (caused by free radicals or environmental stresses) combined with imperfect repair machinery. In addition to SNVs, mutations known as “indels,” involving insertions and deletions of small DNA sequences (typically tens of nucleotides), also occur frequently. Larger, rarer mutations include structural changes in chromosomes, either in the form of gains or losses of whole chromosomes or copy number variants (CNVs), in which the number of repetitions of long chunks of DNA (covering multiple genes) is altered. Within genomes there are also “mobile genetic elements” that act almost like parasites, jumping around or making copies of themselves and inserting themselves elsewhere in the genome, seemingly to ensure their survival. These strange entities are an active field of research in their own right: they are important here because they can cause somatic mutations, including a type known as mobile genetic element insertions, or MEIs. They are switched on in the same way as genes involved in producing new neurons, making them especially active in the brain during development.

***

"There are also plans to collaborate with other NIMH initiatives including BrainSpan, which maps gene expression during brain development, and psychENCODE, which is mapping the brain epigenome (environmentally driven modifications of DNA that influence gene activity without changing the genetic code)."

Comment: DNA is the same throughout the body to start with, but in each organ it is modified to set up the machinery for that organ. In the brain use must cause changes, and since neurons last for life, they must be able to change and adapt. this paper describes the start of this new research into this aspect of brain function.

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Another review on the same subject:

https://www.cell.com/cell/fulltext/S0092-8674(17)30344-6

"Unlike other taxa, cephalopods diversify their proteomes extensively by RNA editing
•
Extensive recoding is specific to the behaviorally complex coleiods
•
Unlike mammals, cephalopod recoding is evolutionarily conserved and often adaptive
•
Transcriptome diversification comes at the expense of slowed-down genome evolution

"Summary

RNA editing, a post-transcriptional process, allows the diversification of proteomes beyond the genomic blueprint; however it is infrequently used among animals for this purpose. Recent reports suggesting increased levels of RNA editing in squids thus raise the question of the nature and effects of these events. We here show that RNA editing is particularly common in behaviorally sophisticated coleoid cephalopods, with tens of thousands of evolutionarily conserved sites. Editing is enriched in the nervous system, affecting molecules pertinent for excitability and neuronal morphology. The genomic sequence flanking editing sites is highly conserved, suggesting that the process confers a selective advantage. Due to the large number of sites, the surrounding conservation greatly reduces the number of mutations and genomic polymorphisms in protein-coding regions. This trade-off between genome evolution and transcriptome plasticity highlights the importance of RNA recoding as a strategy for diversifying proteins, particularly those associated with neural function."

Another discussion:

https://www.sciencealert.com/it-s-official-octopus-and-squid-evolution-is-weirder-than-...

"It's true that coleoid cephalopods are exceptionally intelligent. There are countless riveting octopus escape artist stories out there, not to mention evidence of tool use, and that one eight-armed guy at a New Zealand aquarium who learned to photograph people. (Yes, really.)

"So it's certainly a compelling hypothesis that octopus smarts might come from their unconventionally high reliance on RNA edits to keep the brain going.

"There is something fundamentally different going on in these cephalopods," said Rosenthal.

"But it's not just that these animals are adept at fixing up their RNA as needed - the team found that this ability came with a distinct evolutionary tradeoff, which sets them apart from the rest of the animal world.

"In terms of run-of-the-mill genomic evolution (the one that uses genetic mutations, as mentioned above), coleoids have been evolving really, really slowly. The researchers claimed that this has been a necessary sacrifice - if you find a mechanism that helps you survive, just keep using it.

"The conclusion here is that in order to maintain this flexibility to edit RNA, the coleoids have had to give up the ability to evolve in the surrounding regions - a lot," said Rosenthal.

"As the next step, the team will be developing genetic models of cephalopods so they can trace how and when this RNA editing kicks in.

"It could be something as simple as temperature changes or as complicated as experience, a form of memory," said Rosenthal."

Comment: An amazing side branch on the bush of life. They have ganglions of neurons in each leg helping to run the show in each leg.

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Studies in two bacteria show more complexity:

https://phys.org/news/2019-08-scientists-uncover-mystery-dna-methylation.html

"All species mark their DNA with methyl groups. This is done to regulate gene expression, distinguish indigenous DNA from foreign DNA, or to mark old DNA strands during replication. Methylation is carried out by certain enzymes called methyltransferases, which decorate DNA with methyl groups in certain patterns to create an epigenetic layer on top of DNA.

"Until now, scientists have not been struggling to tell which enzymes are responsible for which patterns. But in a new study, recently published in Nature Communications, scientists from The Novo Nordisk Foundation Center for Biosustainability (DTU Biosustain) at Technical University of Denmark have coupled enzymes with specific methylation patterns in two bacteria.

***

"The goal was to find out, which enzymes are responsible for which patterns. In order to uncover this, the researchers constructed DNA-rings (plasmids) containing one of the methyltransferases and "cassettes" holding multiple copies of certain DNA patterns. These DNA-patterns, called motifs, are the targets for methyltransferases. By coupling the two, the methyltransferase expressed by the plasmid would mark the DNA in a specific way, thus, revealing the enzyme's methylation pattern.

"This was done for all methyltransferases. Afterwards, all the plasmids (in a pool) were read using a sequencing method designed to reveal methyl groups. This gave the researchers a "library" of enzyme-to-motif couplings.

***

"This quick method of identifying methyltransferase methylation patterns holds great promise to other researchers struggling with DNA degradation, according to the research team.
To validate the method, the scientists analysed the genomes of the temperature resistant bacterium M. thermoacetica as well as the bacterium A. woodii. Both bacteria are hosts with great potential for industrial applications and substantially modified genomes.

"In total, the two bacterial organisms hold 23 methyltranstransferase genes, but only show modification on 12 different DNA-motifs on their genomes, meaning that not all methyltransferases are active.

"The team assessed all of the 23 methyltransferases, looking for those being active on the genomes. For 11 of the 12 motifs, they were able to couple activity to specific methyltransferases gene."

Comment: Epigenetic changes are controlled by specific enzymes. Not by chance.

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More work on m6A on RNA's:

https://phys.org/news/2019-08-mysterious-m6a-rna-yield-secrets.html

"Modifications called N6–methyladenosine, or m6A marks, are made by enzymes on the RNA transcripts of some human genes under certain conditions, but the functions of these marks have been largely mysterious. The research team, in a study that appeared online in Nature on July 10, found that m6A marks can cause m6A-containing RNAs to be stored in special, droplet-like compartments in cells. Normally these RNAs would be translated into proteins by the cells' protein-making machinery, but their sequestration in the droplet-like compartments effectively blocks protein production. The scientists found evidence that one important context for this RNA-sequestering action is when a cell is being damaged or otherwise stressed.

"'Our findings suggest that a major function of m6A marks is to induce the storage of certain RNAs during cellular stress," said senior author Dr. Samie Jaffrey, the Greenberg-Starr Professor of Pharmacology at Weill Cornell Medicine. "A lot of these m6A-marked RNAs encode cellular repair proteins, so it appears that cellular repair processes are suppressed in this way during stress, but then un-repressed when the damage has stopped and it becomes appropriate for repairs to start."

***

"[They]began their new study by examining three proteins called YTHDF proteins, which naturally bind to m6A marks on RNAs. The scientists found that the YTHDF proteins have properties that make them tend to stick together when multiple copies are present on m6A-marked RNAs. This clustering causes the YTHDF proteins and their attached m6A-containing RNAs to sequester themselves in droplet-like compartments within the cell—effectively shutting down production of the proteins the RNAs encode.

"Scientists have known that droplets of sequestered RNAs can form in cells, for example during conditions of cellular stress. The droplet-like compartments formed under these conditions are called "stress granules." The discovery by Dr. Jaffrey and colleagues shows that m6A marks are one trigger that causes mRNAs to be placed into stress granules."

Comment: Of course the genome will have built-in protections. This degree of complexity requires design.

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Surprise! Epigenetic mechanisms are different in prokaryotes and eukaryotes according to this review article: - http://www.la-press.com/the-evolution-of-epigenetics-from-prokaryotes-to-humans-and-its... - Abstract: - "The evolution process includes genetic alterations that started with prokaryotes and now continues in humans. A distinct difference between prokaryotic chromosomes and eukaryotic chromosomes involves histones. As evolution progressed, genetic alterations accumulated and a mechanism for gene selection developed. It was as if nature was experimenting to optimally utilize the gene pool without changing individual gene sequences. This mechanism is called epigenetics, as it is above the genome. Curiously, the mechanism of epigenetic regulation in prokaryotes is strikingly different from that in eukaryotes, mainly higher eukaryotes, like mammals. In fact, epigenetics plays a significant role in the conserved process of embryogenesis and human development. Malfunction of epigenetic regulation results in many types of undesirable effects, including cardiovascular disease, metabolic disorders, autoimmune diseases, and cancer. This review provides a comparative analysis and new insights into these aspects. - *** - "...the eukaryotic genome differs from prokaryotes because it is located within a membrane bound nucleus and the DNA contains histones. This histone complex consists of an octamer of histone proteins, two each of H2A, H2B, H3, and H4, along with a single H1 protein (Fig. 2). DNA strands wind around the histone complex to form nucleosomes that are used to condense DNA into a tightly coiled and compact chromosome. In eukaryotes (and certain species of Archaea), gene expression may be regulated by modification to these histones, in addition to DNA. - *** - "Epigenetics, including DNA methylation and histone modification, plays a significant role from the start of fertilization, during embryogenesis, and throughout development. Essentially, modifications in histones determine open or closed chromatin conformation in specific regions, depending mainly on the acetylation- deacetylation of lysine residues on histone tails. More specific modifications are methylation and demethylation of lysine or arginine residues, which determines the conformational identity of a gene and its ability to be transcribed. (my bold) - *** - "Thus, the process from fertilization to tissue development is tightly synchronized under control of epigenetic regulation. Aberration of this epigenetic balance in any developed tissue or organ may create an imbalance that may lead to disorders and diseases." - Comment: the main point of this very technical article is that the difference in handling DNA in the two types of organisms results in very different ways of applying epigenetic changes. The main point for me is going from unicellular organisms to multicellular is a giant step for evolution to have accomplished, and that step is no more explained than the origin of life itself. The origin of life, multicellularity, and the Cambrian explosion have no explanation in the Darwin theory. - The paragraph in bold points out that epigenetics play a huge role in early fetal formation, an interesting point for me.

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Up-to-date review of epignetic studies from Reznick onward:

http://www.the-scientist.com/?articles.view/articleNo/49258/title/Evolution-s-Quick-Pac...

"Here was evolution—genetic change at the population level—happening right before Reznick’s eyes.

“'People thought, if we want to understand the process of evolution, we look at the fossil record,” says Reznick, now a biology professor at the University of California, Riverside. But by averaging phenotypic change across tens of thousands or millions of years, the fossil record underestimates rates of change on shorter timescales, so “for a very long time, people were looking at a biased image of how evolution happens.”

***

"As Reznick was puddle-jumping across Trinidad, famed husband-and-wife evolutionary biologists Peter and Rosemary Grant in the Galápagos Islands were documenting changes in the size and shape of finch beaks following environmental fluctuations.

***

"Within evolutionary biology there really has been an unheralded paradigm shift between 1980 and now,” says Reznick. “Most evolutionary biologists consider it routine to think of evolution as a contemporary process.”

"The concept, appropriately termed contemporary evolution, is now well accepted, agrees Stephen Ellner, an ecologist and evolutionary biologist at Cornell University. “At this point, there’s a general understanding that this is happening, and it’s happening all over.” The research has now shifted from documenting this phenomenon to studying its consequences.

***

"The literature on “rapid evolution” is now 30 years deep. Using what are known as common garden experiments—raising animals from different populations in the same controlled environment (as Reznick did with the guppies)—researchers have observed some astonishing rates. In 1997, Reznick and his colleagues calculated rates of change in his guppy experiments of “up to seven orders of magnitude greater than rates inferred from the paleontological record,” the authors wrote in Science.6 That same year, Harvard University’s Jonathan Losos, then at Washington University in St. Louis, and collaborators published a Nature paper documenting the differentiation of anole populations over a decade and a half following the release of the lizards onto 14 small islands in the Bahamas in 1977 and 1981.

***

"In 2011, for example, Reznick worked in collaboration with Martin Turcotte’s group at the University of Pittsburgh to demonstrate that evolving field populations of green peach aphids grew significantly faster and reached higher densities than control populations that could not evolve because they harbored no genetic variation. In 2014, Tim Farkas, a postdoc at the University of Connecticut, reported similar dynamics in experimental populations of stick insects, where the relative fitness of two morphs—equally represented at the outset—varied according to the density of the founding populations.

***

"Uusi-Heikkilä knows without more solid fieldwork there’s still a steep hill to climb to convince skeptics; laboratory studies alone just won’t cut it. “I have to be very careful when I mention zebrafish and fisheries in the same sentence,” she admits. “But what we are able to do with this model system and experimental studies is disentangle the plastic and evolutionary effects to show that it is possible. Because I think previously people didn’t even believe this is possible. I mean, evolution can’t happen in a few generations, it’s something that takes millions of years.'”

Comment: Once again we are looking at adaptations, not species change. The fossil record suggests that it happens quickly since we don't find intermediate forms. Is speciation always by saltation? Is there more evolution to come or is the process at an end?

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DAVID’s comment: Once again we are looking at adaptations, not species change. The fossil record suggests that it happens quickly since we don't find intermediate forms. Is speciation always by saltation? Is there more evolution to come or is the process at an end?

It’s not often that I agree with your comments, but we can shake hands on this one. Although we can’t always draw a clear line between adaptation and innovation (I’m thinking of the transition from water to land), it is misleading to say that these relatively minor adaptations prove how fast evolution can work when the mystery is innovation, which nobody has observed. My own hypothesis of (possibly God-given) inventive intelligence allows for saltation. Your final question of course refers to your theory that humans are the end point. My answer is that I do not for one second believe that the world will be the same in a million, let alone a billion years’ time, and if the end point (prior to the disappearance of Planet Earth) proves to be bacteria, that will also be part of the evolutionary process.

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dhw: It’s not often that I agree with your comments, but we can shake hands on this one. Although we can’t always draw a clear line between adaptation and innovation (I’m thinking of the transition from water to land), it is misleading to say that these relatively minor adaptations prove how fast evolution can work when the mystery is innovation, which nobody has observed. My own hypothesis of (possibly God-given) inventive intelligence allows for saltation. Your final question of course refers to your theory that humans are the end point. My answer is that I do not for one second believe that the world will be the same in a million, let alone a billion years’ time, and if the end point (prior to the disappearance of Planet Earth) proves to be bacteria, that will also be part of the evolutionary process.

Humans are now doing more than watchi.ng evolution. We are doing active genetic engineering. Will the natural process continue under this kind of assault?

https://cosmosmagazine.com/biology/benefits-and-dangers-in-altering-our-evolutionary-tr...

"The paper’s lead author, Ary Hoffman of the University of Melbourne’s Bio21 Institute, says the technology “has enormous potential to control disease, increase agricultural productivity and to improve quality of life, particularly for those living in developing countries”.

"It’s a powerful technology, with the capacity to alter the evolutionary trajectory of species and to warp the web of ecological relations in an unprecedented way.

"With that power comes risk and uncertainty. As the report notes, “no synthetic gene drives have yet been released into wild populations,” so much remains untested.

"The authors nonetheless express confidence the benefits outweigh the risks and have called for further research to be conducted in highly secure laboratories. Multiple containment, reversal and vaccination methods have been devised in the event of an uncontrolled release into wild populations.

"Importantly, any future decisions on release of gene drives would be carried out on a case-by-case basis, taking into account environmental, ecological and evolutionary concerns.

"The academy seems to be taking a cautious approach to getting it right.
As its president, Andrew Holmes, has said, “once gene drives are released into wild populations in other countries, they will inevitably reach Australia”.

"One way or another, genes drives will be reality soon, and we best be prepared."

Comment: The best laid plans of man can and will go awry.

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DAVID: Humans are now doing more than watching evolution. We are doing active genetic engineering. Will the natural process continue under this kind of assault?
https://cosmosmagazine.com/biology/benefits-and-dangers-in-altering-our-evolutionary-tr...

QUOTE: "Importantly, any future decisions on release of gene drives would be carried out on a case-by-case basis, taking into account environmental, ecological and evolutionary concerns.
"The academy seems to be taking a cautious approach to getting it right.

"One way or another, genes drives will be reality soon, and we best be prepared."

David’s comment: The best laid plans of man can and will go awry.

Once again, we are in agreement. Even if the academy is trying to get it right, the time is sure to come when someone will get it wrong. Human attempts to improve on Nature are sometimes wonderfully successful, but they are fraught with danger.

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DAVID: Humans are now doing more than watching evolution. We are doing active genetic engineering. Will the natural process continue under this kind of assault?
https://cosmosmagazine.com/biology/benefits-and-dangers-in-altering-our-evolutionary-tr...

QUOTE: "Importantly, any future decisions on release of gene drives would be carried out on a case-by-case basis, taking into account environmental, ecological and evolutionary concerns.
"The academy seems to be taking a cautious approach to getting it right.

"One way or another, genes drives will be reality soon, and we best be prepared."

David’s comment: The best laid plans of man can and will go awry.

dhw: Once again, we are in agreement. Even if the academy is trying to get it right, the time is sure to come when someone will get it wrong. Human attempts to improve on Nature are sometimes wonderfully successful, but they are fraught with danger.

If humans are fiddling with DNA, is evolution over?

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David’s comment: The best laid plans of man can and will go awry.

dhw: Once again, we are in agreement. Even if the academy is trying to get it right, the time is sure to come when someone will get it wrong. Human attempts to improve on Nature are sometimes wonderfully successful, but they are fraught with danger.

DAVID: If humans are fiddling with DNA, is evolution over?

Whatever takes place in life’s history, including humans fiddling with DNA, is part of the evolutionary process. Do you really think the Earth and its inhabitants will be the same in a thousand million years’ time?

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DAVID: If humans are fiddling with DNA, is evolution over?

dhw: Whatever takes place in life’s history, including humans fiddling with DNA, is part of the evolutionary process. Do you really think the Earth and its inhabitants will be the same in a thousand million years’ time?

I think evolution is over now, but I'm sure humans will not be here in a billion years, having destroyed ourselves.

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DAVID: If humans are fiddling with DNA, is evolution over?

dhw: Whatever takes place in life’s history, including humans fiddling with DNA, is part of the evolutionary process. Do you really think the Earth and its inhabitants will be the same in a thousand million years’ time?

DAVID: I think evolution is over now, but I'm sure humans will not be here in a billion years, having destroyed ourselves.

That doesn’t mean evolution is over now. You seem to think evolution means nothing but the production of humans! Evolution simply means that all life forms descend from earlier life forms, and we do not have a clue what life forms will exist in a billion years time.

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DAVID: I think evolution is over now, but I'm sure humans will not be here in a billion years, having destroyed ourselves.

dhw: That doesn’t mean evolution is over now. You seem to think evolution means nothing but the production of humans! Evolution simply means that all life forms descend from earlier life forms, and we do not have a clue what life forms will exist in a billion years time.

The correct interpretation of what I have written is humans are here and evolution is over. Humans were the goal of evolution. Yes, all forms are descended from earlier forms by a totally unknown process.

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DAVID: I think evolution is over now, but I'm sure humans will not be here in a billion years, having destroyed ourselves.

dhw: That doesn’t mean evolution is over now. You seem to think evolution means nothing but the production of humans! Evolution simply means that all life forms descend from earlier life forms, and we do not have a clue what life forms will exist in a billion years time.

DAVID: The correct interpretation of what I have written is humans are here and evolution is over. Humans were the goal of evolution. Yes, all forms are descended from earlier forms by a totally unknown process.

You are of course entitled to your belief that humans were the goal of evolution and that every form (broad sense of species) that descended from earlier forms, plus every lifestyle and natural wonder extant and instinct, was specially designed by your God for that single purpose. However, I am delighted by your last sentence, as you are no longer insisting that your God either preprogrammed all those forms and lifestyles and wonders 3.8 billion years ago, or popped in to do a direct dabble. Recognition that certain things are “totally unknown” is the first step towards open-mindedness in relation to other hypotheses.

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DAVID: The correct interpretation of what I have written is humans are here and evolution is over. Humans were the goal of evolution. Yes, all forms are descended from earlier forms by a totally unknown process.

dhw: You are of course entitled to your belief that humans were the goal of evolution and that every form (broad sense of species) that descended from earlier forms, plus every lifestyle and natural wonder extant and instinct, was specially designed by your God for that single purpose. However, I am delighted by your last sentence, as you are no longer insisting that your God either preprogrammed all those forms and lifestyles and wonders 3.8 billion years ago, or popped in to do a direct dabble. Recognition that certain things are “totally unknown” is the first step towards open-mindedness in relation to other hypotheses.

Of course speciation is entirely unknown as a process. We all make judgments as to how it might proceed. Darwin's method of tiny progressive chance changes is obviously false. To make major body plan changes requires a complex plan before the changes can occur. Only a planning mind can do this. I've not changed my mind that it must be God.

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dhw: You are of course entitled to your belief that humans were the goal of evolution and that every form (broad sense of species) that descended from earlier forms, plus every lifestyle and natural wonder extant and instinct, was specially designed by your God for that single purpose. However, I am delighted by your last sentence, as you are no longer insisting that your God either preprogrammed all those forms and lifestyles and wonders 3.8 billion years ago, or popped in to do a direct dabble. Recognition that certain things are “totally unknown” is the first step towards open-mindedness in relation to other hypotheses.

In all our discussions on evolution, I have been putting on my theist’s hat, because I am challenging your hypothesis that your God either preprogrammed or dabbled every single species (broad sense), lifestyle and natural wonder extant and extinct throughout the history of life in order eventually to produce humans. We needn’t go over all the illogicalities yet again. My point here is that since the process is totally unknown, and nobody has ever observed speciation, you should not reject the hypothesis of a perhaps God-given AUTONOMOUS inventive mechanism (i.e. intelligence operating without divine “guidance”), as you keep doing, on the grounds that the mechanism has not been found. Your 3.8-billion-year-old computer programme has not been found, and nobody has ever seen your God dabbling.

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DAVID: Of course speciation is entirely unknown as a process. We all make judgments as to how it might proceed. Darwin's method of tiny progressive chance changes is obviously false. To make major body plan changes requires a complex plan before the changes can occur. Only a planning mind can do this. I've not changed my mind that it must be God.

dhw: In all our discussions on evolution, I have been putting on my theist’s hat, because I am challenging your hypothesis that your God either preprogrammed or dabbled every single species (broad sense), lifestyle and natural wonder extant and extinct throughout the history of life in order eventually to produce humans. We needn’t go over all the illogicalities yet again. My point here is that since the process is totally unknown, and nobody has ever observed speciation, you should not reject the hypothesis of a perhaps God-given AUTONOMOUS inventive mechanism (i.e. intelligence operating without divine “guidance”), as you keep doing, on the grounds that the mechanism has not been found. Your 3.8-billion-year-old computer programme has not been found, and nobody has ever seen your God dabbling.

I feel you are talking around my argument but never addressing it. The complexity of living matter was not discussed in the above comment by you. I constantly present new studies into the complexity, and you generally ignore them. The key to my argument is COMPLEXITY. It cannot occur by chance. It requires planning, which means it occurs from mentation. This statement is not some wooly concept. It comes from our human experience. This is why I follow the concept of a universal consciousness with its mental capacity. That is how I visualize God. I have never seen your consciousness. I can only experience mine. I have faith you have one. I can have the same faith in God's. How God manages evolution is just guess work on my part and on your part. It fills much of our discussions, but it is totally beside the point. One must address the complexity of the living mechanisms, and it's source cannot be bottom up.

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DAVID: Of course speciation is entirely unknown as a process. We all make judgments as to how it might proceed. Darwin's method of tiny progressive chance changes is obviously false. To make major body plan changes requires a complex plan before the changes can occur. Only a planning mind can do this. I've not changed my mind that it must be God.
dhw: My point here is that since the process is totally unknown, and nobody has ever observed speciation, you should not reject the hypothesis of a perhaps God-given AUTONOMOUS inventive mechanism (i.e. intelligence operating without divine “guidance”), as you keep doing, on the grounds that the mechanism has not been found. Your 3.8-billion-year-old computer programme has not been found, and nobody has ever seen your God dabbling.
DAVID: I feel you are talking around my argument but never addressing it. The complexity of living matter was not discussed in the above comment by you. I constantly present new studies into the complexity, and you generally ignore them. The key to my argument is COMPLEXITY. It cannot occur by chance. It requires planning, which means it occurs from mentation.

I have ALWAYS accepted and acknowledged the complexity argument against chance. Even in the “brief guide” I included among the design arguments “the hugely complex nature of all the organs that we know of” (the others being origins, heredity and adaptability). I did so again as recently as 4 May at 12.12 under “Biological complexity”. You wrote: “It is more than reasonable to conclude that only design by a planning mind is the source of the beginning of life.” I replied: “Perfectly reasonable. And alongside a variety of psychic experiences, the complexity of the cell is the major reason why I cannot embrace atheism.”

DAVID: […] How God manages evolution is just guess work on my part and on your part. It fills much of our discussions, but it is totally beside the point. One must address the complexity of the living mechanisms, and it's source cannot be bottom up.

You are yet again conflating two separate issues. One is the existence of your God, and I have repeatedly explained why I cannot reject or accept the God hypothesis. The second issue is IF God does exist, what might be his purpose, his methods and his nature? These are not “beside the point”. If God exists, they are a point in themselves, as you insist when constantly harping on about his purposefulness. My proposal that he may have given organisms the intelligence to do their own designing (with the option of an occasional dabble) seems to me at least as reasonable as your proposal that he preprogrammed or dabbled everything (including today’s Diplostomum pseudospathaceum and sexy orchid - thank you for two more amazing examples of Nature’s wonders) in order to keep life going until he could design the one thing he actually wanted to design (humans), which is the only hypothesis you have come up with.

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DAVID: […] How God manages evolution is just guess work on my part and on your part. It fills much of our discussions, but it is totally beside the point. One must address the complexity of the living mechanisms, and it's source cannot be bottom up.

dhw: You are yet again conflating two separate issues. One is the existence of your God, and I have repeatedly explained why I cannot reject or accept the God hypothesis. The second issue is IF God does exist, what might be his purpose, his methods and his nature? These are not “beside the point”. If God exists, they are a point in themselves, as you insist when constantly harping on about his purposefulness.

I understand that you divide the God issue into two parts. Lets simply accept that I am convinced God exists and you aren't. Fine. As to the second issue, I see humans as His purpose, nothing more. His method is evolution. He does that with the development of the universe, of Earth, and with life. That history is quite clear. I do not know how He manages speciation, but it is obvious to me He does handle speciation. As for His nature, religions have discussed it for two millennia with no conclusions but many suggestions. I'm not inclined to bother with it as an issue.

dhw: My proposal that he may have given organisms the intelligence to do their own designing (with the option of an occasional dabble) seems to me at least as reasonable as your proposal that he preprogrammed or dabbled everything (including today’s Diplostomum pseudospathaceum and sexy orchid - thank you for two more amazing examples of Nature’s wonders) in order to keep life going until he could design the one thing he actually wanted to design (humans), which is the only hypothesis you have come up with.

Thank you for mentioning the current natures wonders. They bring up the major point I make. In creating a lifestyle or a new species, the designer or planner must have a mental vision of the future before beginning to design the jump to the next step in a developing evolution. That vision of the future will not be possible in bacteria which lack the consciousness to see a picture of a future arrangement as multicellular organisms, as one clear example of my viewpoint. To jump the gaps in the fossil record the organisms must visualize what is wanted or needed in the future in order to set up the design. Currently the only organisms we know of that have that capacity are humans, or at a different level, God!

We have round and round about how God runs evolution. I am convinced He guides each speciation and His goal is humans with a smidgen of His consciousness. I don't need any more than the statements I have just given. It is you who refuses to accept the necessity for mental planning to accomplish the appearance of life and its subsequent evolution to humans.

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David: I understand that you divide the God issue into two parts. Lets simply accept that I am convinced God exists and you aren't. Fine. As to the second issue, I see humans as His purpose, nothing more. His method is evolution. He does that with the development of the universe, of Earth, and with life. That history is quite clear.

No, it is not “quite clear”. There is no clear line of development between the countless species, lifestyles and natural wonders and what you believe to be the sole purpose of evolution, which is humans. You gloss this over with the illogical argument that your God – who in your most recent version has unlimited powers – chose to preprogamme or personally design all of these organisms and wonders (epitomized by the weaverbird’s nest) in order to keep life going until he could design the one and only thing he wanted to design.

DAVID: I do not know how He manages speciation, but it is obvious to me He does handle speciation.

Once again, don’t forget the specially designed lifestyles and natural wonders (which today include the selection of queen bees). Nobody “knows”, but you have persistently proposed a 3.8-billion-year-old computer programme or direct divine intervention, and you reject any other suggestion.

DAVID: Thank you for mentioning the current natures wonders. They bring up the major point I make. In creating a lifestyle or a new species, the designer or planner must have a mental vision of the future before beginning to design the jump to the next step in a developing evolution.

A good diversion from the above dislocated anthropocentrism, but you are making assumptions here. Lifestyles and wonders and even species may all be the consequence not of planning but of intelligent, inventive responses to environmental conditions which represent either a threat or an opportunity. This is crystal clear when we actually observe organisms changing their structure in order to adapt. No planning – simply a direct response. The (perhaps God-given) mechanism for change is there. Extend the principle to lifestyle: the climate becomes a threat to the organism, and so the only solution is migration. Extend it to natural wonders: maybe by chance two organisms hit upon a scenario that is of mutual benefit, and this becomes the wonder of symbiosis. Extend it to speciation: an aquatic organism discovers an abundance of food on land, and its body adapts to the new opportunities, with fins in due course becoming legs etc. All of these depend on the creative response of cell communities to new conditions, and not on planning. You are sceptical that cell communities have the intelligence to go beyond the process of minor adaptation and achieve all these complexities. You may be right. But nobody knows. Just like your divine preprogramming and dabbling, it is a hypothesis.

DAVID: That vision of the future will not be possible in bacteria which lack the consciousness to see a picture of a future arrangement as multicellular organisms, as one clear example of my viewpoint. To jump the gaps in the fossil record the organisms must visualize what is wanted or needed in the future in order to set up the design. Currently the only organisms we know of that have that capacity are humans, or at a different level, God!

Bacteria clearly know the advantages of joining together to form a community, since this is how they solve many of the problems they are confronted with. And once we have multicellular communities, “currently” who knows how much their intelligence is capable of as they respond to (as opposed to planning for) the challenges and opportunities provided by changing conditions?

DAVID: We have round and round about how God runs evolution. I am convinced He guides each speciation and His goal is humans with a smidgen of His consciousness.

Your being convinced that he guides each speciation AND lifestyle AND natural wonder provides no evidence (a) that he does, or (b) that he does so with the sole purpose of producing humans, and your conviction does not make these dislocated ideas any more coherent.

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David: I understand that you divide the God issue into two parts. Lets simply accept that I am convinced God exists and you aren't. Fine. As to the second issue, I see humans as His purpose, nothing more. His method is evolution. He does that with the development of the universe, of Earth, and with life. That history is quite clear.

dhw: No, it is not “quite clear”. There is no clear line of development between the countless species, lifestyles and natural wonders and what you believe to be the sole purpose of evolution, which is humans.

I thought you agreed that life evolved in common descent. That is all I referred to.

dhw:You gloss this over with the illogical argument that your God – who in your most recent version has unlimited powers – chose to preprogamme or personally design all of these organisms and wonders (epitomized by the weaverbird’s nest) in order to keep life going until he could design the one and only thing he wanted to design.

Illogical to only you.

DAVID: I do not know how He manages speciation, but it is obvious to me He does handle speciation.

dhw: Nobody “knows”, but you have persistently proposed a 3.8-billion-year-old computer programme or direct divine intervention, and you reject any other suggestion.

Remember I think God did all of it, and see no reason to change.

DAVID: In creating a lifestyle or a new species, the designer or planner must have a mental vision of the future before beginning to design the jump to the next step in a developing evolution.

dhw: This is crystal clear when we actually observe organisms changing their structure in order to adapt. No planning – simply a direct response.

Structural changes require coordinated planning. You show none.

dhw The (perhaps God-given) mechanism for change is there. Extend the principle to lifestyle: the climate becomes a threat to the organism, and so the only solution is migration.

Migration is not evolutionary phenotypic change, which is my point.

dhw: Extend it to natural wonders: maybe by chance two organisms hit upon a scenario that is of mutual benefit, and this becomes the wonder of symbiosis. Extend it to speciation: an aquatic organism discovers an abundance of food on land, and its body adapts to the new opportunities, with fins in due course becoming legs etc.

Requires mental planning.

dhw:All of these depend on the creative response of cell communities to new conditions, and not on planning.

Denying the obvious need for advanced planning.

DAVID: That vision of the future will not be possible in bacteria which lack the consciousness to see a picture of a future arrangement as multicellular organisms, as one clear example of my viewpoint. To jump the gaps in the fossil record the organisms must visualize what is wanted or needed in the future in order to set up the design. Currently the only organisms we know of that have that capacity are humans, or at a different level, God!

dhw: Bacteria clearly know the advantages of joining together to form a community, since this is how they solve many of the problems they are confronted with.

Agreed but quite simple

dhw: And once we have multicellular communities, “currently” who knows how much their intelligence is capable of as they respond to (as opposed to planning for) the challenges and opportunities provided by changing conditions?

You can't simply assume bacterial communities are really multicellular. 'Responding to' like the guppies is not planning. Large or small is not body type change. You keep avoiding the problem I present.

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dhw: There is no clear line of development between the countless species, lifestyles and natural wonders and what you believe to be the sole purpose of evolution, which is humans.
DAVID: I thought you agreed that life evolved in common descent. That is all I referred to.

You referred to humans as his purpose and evolution as his method of achieving that purpose.The history of how every specially designed species, lifestyle etc. served/serves the purpose of producing humans is a million miles away from being clear.

DAVID: In creating a lifestyle or a new species, the designer or planner must have a mental vision of the future before beginning to design the jump to the next step in a developing evolution.
dhw: [Intelligent response] is crystal clear when we actually observe organisms changing their structure in order to adapt. No planning – simply a direct response.
DAVID: Structural changes require coordinated planning. You show none.

I am contrasting structural with behavioural adaptation, i.e. changes in the anatomy enabling resistance to toxins, camouflage, longer or different coloured fur. And it is your “planning” that I am questioning. These changes require intelligent coordination between the cell communities, and they occur as a RESPONSE to changes in the environment.

dhw Extend the principle to lifestyle: the climate becomes a threat to the organism, and so the only solution is migration.
DAVID: Migration is not evolutionary phenotypic change, which is my point.

But you don’t confine your God’s planning to phenotypes – you insist that only he could have planned the monarch’s migration and designed the weaverbird’s nest, all for the sake of humans. It is the whole package put together that is so illogical. Or are you now backtracking on lifestyles and natural wonders?

dhw: Extend it to speciation: an aquatic organism discovers an abundance of food on land, and its body adapts to the new opportunities, with fins in due course becoming legs etc.
DAVID: Requires mental planning.

It requires intelligent (= mental) and physical cooperation between cell communities to coordinate their response. Planning requires prior knowledge. In my hypothetical example, you therefore seem to be suggesting that your God gave the fish animal legs and lungs, then put lots of food onto dry land and told the fish to leave the water. And presumably he designed the monarch’s metamorphoses and navigational apparatus before changing the climate and forcing the butterfly to emigrate (in order to keep life going before he designed the only thing he wanted to design – homo sapiens).

dhw: And once we have multicellular communities, “currently” who knows how much their intelligence is capable of as they respond to (as opposed to planning for) the challenges and opportunities provided by changing conditions?
DAVID: You can't simply assume bacterial communities are really multicellular.

I am pointing out that communities can produce greater intelligence than individuals.

DAVID: 'Responding to' like the guppies is not planning. Large or small is not body type change. You keep avoiding the problem I present.

We don’t know how the major body changes of speciation occur, but minor adaptations give us a possible clue. I find it difficult to accept the idea that evolution depends on reversing the known process of adaptation, with your God making all the structural changes before creating all the new local and/or global environments which require or allow such changes, as opposed to new environments triggering the structural changes.

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dhw: [Intelligent response] is crystal clear when we actually observe organisms changing their structure in order to adapt. No planning – simply a direct response.
DAVID: Structural changes require coordinated planning. You show none.

dhw: I am contrasting structural with behavioural adaptation, i.e. changes in the anatomy enabling resistance to toxins, camouflage, longer or different coloured fur. And it is your “planning” that I am questioning. These changes require intelligent coordination between the cell communities, and they occur as a RESPONSE to changes in the environment.

Resistance to toxins is epigenetic using alternative pathways that are available. Camouflage in butterflies is structural as probably is change in fur color. Require planning.

dhw Extend the principle to lifestyle: the climate becomes a threat to the organism, and so the only solution is migration.
DAVID: Migration is not evolutionary phenotypic change, which is my point.

dhw: But you don’t confine your God’s planning to phenotypes – you insist that only he could have planned the monarch’s migration and designed the weaverbird’s nest, all for the sake of humans. It is the whole package put together that is so illogical. Or are you now backtracking on lifestyles and natural wonders?

You are correct, migration requires planning. I was referring to body type changes in speciation. Your cell committees are incapable of future planning to accomplish species change.

dhw: Extend it to speciation: an aquatic organism discovers an abundance of food on land, and its body adapts to the new opportunities, with fins in due course becoming legs etc.
DAVID: Requires mental planning.

dhw: It requires intelligent (= mental) and physical cooperation between cell communities to coordinate their response. Planning requires prior knowledge. In my hypothetical example, you therefore seem to be suggesting that your God gave the fish animal legs and lungs, then put lots of food onto dry land and told the fish to leave the water. And presumably he designed the monarch’s metamorphoses and navigational apparatus before changing the climate and forcing the butterfly to emigrate (in order to keep life going before he designed the only thing he wanted to design – homo sapiens).

Perfectly acceptable scenario.

dhw: I am pointing out that communities can produce greater intelligence than individuals.

True.

DAVID: 'Responding to' like the guppies is not planning. Large or small is not body type change. You keep avoiding the problem I present.

dhw: We don’t know how the major body changes of speciation occur, but minor adaptations give us a possible clue. I find it difficult to accept the idea that evolution depends on reversing the known process of adaptation, with your God making all the structural changes before creating all the new local and/or global environments which require or allow such changes, as opposed to new environments triggering the structural changes.

I have made the point that environmental changes never pushed the drive to humans. apes are still apes. Environment is only one of many factors that drive evolution. Darwin used that argument, but his entire theory is weak, as we know.

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Have you ever constructed a shed or small building? I have several times. It requires planning the structure and then using materials you already have or getting new materials. This is how evolution makes a new species. Note these two articles which show the implied purpose behind the development of this jaw bone structure:

http://www.nature.com/nature/journal/v545/n7653/full/545158d.html?WT.ec_id=NATURE-20170...

"The tuatara of New Zealand (Sphenodon punctatus; pictured), formerly thought to be a lizard, was recognized 150 years ago this month as the only living member of its own reptile group — Rhynchocephalia (A. Günther Phil. Trans. R. Soc. 157, 595–629; 1867).

"The tuatara's ancestors separated from those of lizards and snakes (Squamata) around 240 million years ago. The frame-like skull of S. punctatus, long believed to be an archaic feature, is in fact a specialization for supporting its powerful jaws (D. I. Whiteside Phil. Trans. R. Soc. Lond. B 312, 379–430; 1986).

"The animal's taxonomic isolation has turned it into a flagship species for studies of evolution, biodiversity and conservation (see, for example, A. Cree Tuatara Canterbury Univ. Press; 2014)."

Abstract:

"The skull and lower jaw of a new sphenodontid reptile Diphydontosaurus avonis is described from disarticulated bones. The fossils were recovered from a detrital limestone of Rhaetian age deposited within solutional and tectonically formed fissures within the Carboniferous Limestone of Tytherington quarry near Bristol. The bone remains, numbering over 1000, are exquisitely preserved with intact facets. Diphydontosaurus was the smallest member of an insular fauna, was primarily insectivorous, and probably formed locally high-density populations. Uniquely for a sphenodontid, Diphydontosaurus had pleurodont teeth on the premaxilla and on the anterior regions of the dentary and maxilla. However, Diphydontosaurus also has the series of acrodont teeth alternating in size on the maxilla and dentary which is characteristic of the Sphenodontidae and particularly Sphenodon. An analysis of 49 synapomorphs in the Diapsida emphasises the sphenodontid nature of Diphydontosaurus. A study of these synapomorphs among the other Triassic sphenodontids Clevosaurus and Planocephalosaurus and the eosuchian Gephyrosaurus suggests that the lack of a quadrate-quadratojugal conch and the complete lower temporal bar are secondarily derived in the `living fossil' Sphenodon punctatus. The tuatara is therefore much less archaic than hitherto proposed. Functional reasons are advocated for the loss of the conch and the regrowth of a complete lower temporal bar. Transformation series are described which could have led to the shape of the maxilla, dentary, premaxilla, palatine and to the loss of the lacrimal in Sphenodon."

Comment: Of course there are 'functional reasons' for changes. They require planning. The big black box in our discussions is our lack of knowledge. We can tell which genes control what function or what appears in embryogenesis but we have no idea how the controls work, how the gene actually does its direction through chemical action. Until we have this knowledge, if it is possible to find, we will have no idea how speciation occurs. A fluffy nod to intelligence in cells tells us nothing of what we need to know. What is obvious is the need for prior planning, which only a competent mind can provide.

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David’s comment : Of course there are 'functional reasons' for changes. They require planning. The big black box in our discussions is our lack of knowledge. We can tell which genes control what function or what appears in embryogenesis but we have no idea how the controls work, how the gene actually does its direction through chemical action. Until we have this knowledge, if it is possible to find, we will have no idea how speciation occurs. A fluffy nod to intelligence in cells tells us nothing of what we need to know. What is obvious is the need for prior planning, which only a competent mind can provide.

A fluffy nod to an unknown sourceless mind tells us nothing of what we need to know. Adaptation suggests that organisms can respond to conditions without “prior planning”. There are some scientists who have concluded from their tests and observations that cells ARE intelligent, so the suggestion that they may be intelligent enough to invent as well as to adapt is not as fluffy as you would like it to be. After all, intelligence seen from the outside might actually be intelligence.

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David’s comment : Of course there are 'functional reasons' for changes. They require planning. The big black box in our discussions is our lack of knowledge. We can tell which genes control what function or what appears in embryogenesis but we have no idea how the controls work, how the gene actually does its direction through chemical action. Until we have this knowledge, if it is possible to find, we will have no idea how speciation occurs. A fluffy nod to intelligence in cells tells us nothing of what we need to know. What is obvious is the need for prior planning, which only a competent mind can provide.

dhw: A fluffy nod to an unknown sourceless mind tells us nothing of what we need to know. Adaptation suggests that organisms can respond to conditions without “prior planning”. There are some scientists who have concluded from their tests and observations that cells ARE intelligent, so the suggestion that they may be intelligent enough to invent as well as to adapt is not as fluffy as you would like it to be. After all, intelligence seen from the outside might actually be intelligence.

Yes, the whale series was all done by cell committees.

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David Comment: Of course there are 'functional reasons' for changes. They require planning. The big black box in our discussions is our lack of knowledge. We can tell which genes control what function or what appears in embryogenesis but we have no idea how the controls work, how the gene actually does its direction through chemical action.

Here is an article, very long, on gene networks and the fact that we know very little about how it all results in functions, traits, even free will and consciousness. We do have a few specifics:

https://aeon.co/essays/dna-is-the-ruling-metaphor-of-our-age?utm_source=Aeon+Newsletter...

"Sounds simple enough, but what if we need to predict the specific outcome of a large number of such flips, somewhat like the challenge we face in predicting, from a person’s genotype, the risk of life events such as a heart attack or diabetes? Each of us has a unique set of variants in perhaps hundreds of different genes that separately contribute to the probability of disease. What will each one do? Will they flip as ‘illness’ or ‘health’? Is that even a realistic question?

***

"What role do genes play in non-physical traits such as behavior, or even the ultimate questions of consciousness and free will? Here, the metaphoric replacement of ‘soul’ by ‘gene’ works in a different way. How much of our feelings, thoughts and behavior is actually determined from the moment we are conceived, and could in principle be read like a computer program from our genome?

"The extent to which we have free will is a fundamental aspect of how we view our ‘selves’, and for many religions, relates to whether we can be held responsible for our moral behavior. The scientific view, on the other hand, goes something like this: we live in a totally material world made of matter, energy, and the forces that connect them. Since genes are the fundamental causal elements of life, it would seem inevitable that, if we knew enough, we could predict everything about all of us — our health, our behavior, and our ideas. The alternative would seem to be mysticism — invoking some sort of immaterial something-or-other that we can’t measure but that affects who and what we are.

***

"Evolutionary determinism was the first thread of the gene metaphor. Natural selection preserves only what is inherited from the successful organisms in the past.....Mendel identified a pattern of inheritance that provided perhaps the most powerful tool for research design in the history of science. The genetic research that followed eventually led to the identification of the nature of DNA, the locations and structure of genes in DNA, and the understanding of how they code for proteins. But that same Mendelian thinking made us conceptual prisoners of the deterministic, law-like interpretation of genetic function.

***

"Genomic studies searching for causal genes have grown ever larger and more expensive, but commensurately important results have yet to roll in. Most of the estimated overall genetic influence on the traits or diseases of interest is still unidentified. What we’re finding instead is ‘polygenic’ causation, that is, that many different parts of the genome contribute mainly trivial individual effects.

***

"Instead of the widespread view of life as raw, relentless Darwinian competition leading to a single ‘fittest’ way to be, a far better way to see it is in terms of cooperation. By cooperation we do not necessarily mean the social, emotional variety. Cooperation describes the way in which a trait is produced by many factors, the countless genes and lifestyle aspects that contribute to the trait.

***

"... genes are molecules and hence fundamental causal agents of life, yet their effects are highly probabilistic and very hard to pin down or predict.

***

"conceptually, we have not advanced very much in our understanding of what are deeply puzzling aspects of the way the cosmos — including life — works.

***
"that is perhaps why the metaphor of the gene as the atom of causation in life is so easy to absorb, and its subtleties so easy to overlook. We are made very uneasy by things that are only probabilistic unless, as in coin-flipping, we can sense what’s going on. When we can’t see it, and causation is many-to-many, that is far too much for our minds to deal with easily. Yet that seems to be the reality of the world."

Comment: Very long article worth reading. We know so little. Like quantum theory.

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DAVID: Here is an article, very long, on gene networks and the fact that we know very little about how it all results in functions, traits, even free will and consciousness. We do have a few specifics:
https://aeon.co/essays/dna-is-the-ruling-metaphor-of-our-age?utm_source=Aeon+Newsletter...

QUOTE: "What role do genes play in non-physical traits such as behavior, or even the ultimate questions of consciousness and free will? Here, the metaphoric replacement of ‘soul’ by ‘gene’ works in a different way. How much of our feelings, thoughts and behavior is actually determined from the moment we are conceived, and could in principle be read like a computer program from our genome?
"The extent to which we have free will is a fundamental aspect of how we view our ‘selves’, and for many religions, relates to whether we can be held responsible for our moral behavior. The scientific view, on the other hand, goes something like this: we live in a totally material world made of matter, energy, and the forces that connect them. Since genes are the fundamental causal elements of life, it would seem inevitable that, if we knew enough, we could predict everything about all of us — our health, our behavior, and our ideas. The alternative would seem to be mysticism — invoking some sort of immaterial something-or-other that we can’t measure but that affects who and what we are."

DAVID’s comment: Very long article worth reading. We know so little. Like quantum theory.

Huge thanks yet again not only for telling us about the article, but also for selecting these quotes. (I’m afraid I don’t have time at the moment to read it all.) The quote above provides a good summary of some of the questions we keep asking, and it doesn’t look as if the author has any answers!

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DAVID: Here is an article, very long, on gene networks and the fact that we know very little about how it all results in functions, traits, even free will and consciousness. We do have a few specifics:
https://aeon.co/essays/dna-is-the-ruling-metaphor-of-our-age?utm_source=Aeon+Newsletter...

QUOTE: "What role do genes play in non-physical traits such as behavior, or even the ultimate questions of consciousness and free will? Here, the metaphoric replacement of ‘soul’ by ‘gene’ works in a different way. How much of our feelings, thoughts and behavior is actually determined from the moment we are conceived, and could in principle be read like a computer program from our genome?
"The extent to which we have free will is a fundamental aspect of how we view our ‘selves’, and for many religions, relates to whether we can be held responsible for our moral behavior. The scientific view, on the other hand, goes something like this: we live in a totally material world made of matter, energy, and the forces that connect them. Since genes are the fundamental causal elements of life, it would seem inevitable that, if we knew enough, we could predict everything about all of us — our health, our behavior, and our ideas. The alternative would seem to be mysticism — invoking some sort of immaterial something-or-other that we can’t measure but that affects who and what we are."

DAVID’s comment: Very long article worth reading. We know so little. Like quantum theory.

dhw: Huge thanks yet again not only for telling us about the article, but also for selecting these quotes. (I’m afraid I don’t have time at the moment to read it all.) The quote above provides a good summary of some of the questions we keep asking, and it doesn’t look as if the author has any answers!

The old idea that was called dogma, DNA simply coded for proteins, is dead. The enormous complexity of genome control of life is still unfolding. Only more complexity will be found. It obviously represents mental planning.

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DAVID: Resistance to toxins is epigenetic using alternative pathways that are available. Camouflage in butterflies is structural as probably is change in fur color. Require planning.

Resistance to toxins has to be a physical as opposed to a behavioural process. I suggest that all of these processes come as a RESPONSE to the environment. Planning requires knowledge of the future. Please tell us about adaptations that have been observed BEFORE the relevant environmental changes took place.

DAVID: Migration is not evolutionary phenotypic change, which is my point.
dhw: But you don’t confine your God’s planning to phenotypes – you insist that only he could have planned the monarch’s migration and designed the weaverbird’s nest, all for the sake of humans. It is the whole package put together that is so illogical. Or are you now backtracking on lifestyles and natural wonders?
DAVID: You are correct, migration requires planning. I was referring to body type changes in speciation. Your cell committees are incapable of future planning to accomplish species change.

I am not suggesting that my cell committees plan for future changes in the environment. I am suggesting that they respond to changes as they happen. In your scenario, speciation, lifestyles and natural wonders all require God’s preprogramming or dabbling in order to keep life going for the sake of humans. Once again: are you now backtracking on your insistence that God also designed all the lifestyles and natural wonders for the same purpose?

dhw: […] you therefore seem to be suggesting that your God gave the fish animal legs and lungs, then put lots of food onto dry land and told the fish to leave the water. And presumably he designed the monarch’s metamorphoses and navigational apparatus before changing the climate and forcing the butterfly to emigrate (in order to keep life going before he designed the only thing he wanted to design – homo sapiens).
DAVID: Perfectly acceptable scenario.

Just to make it clear: we now have evolution as a process in which God creates new species, lifestyles and natural wonders, and then creates the conditions in which they are able to live, as opposed to new environments triggering the structural changes.

DAVID: I have made the point that environmental changes never pushed the drive to humans. apes are still apes. Environment is only one of many factors that drive evolution. Darwin used that argument, but his entire theory is weak, as we know.

We have both made the point over and over again that environmental changes never pushed the drive to multicellularity as a whole, since bacteria are still with us. That is why over and over again I have suggested that all advances beyond bacteria, including humans, can be attributed to the drive for survival and/or improvement. Darwin argued that environmental factors, random mutations, competition for survival and natural selection drove evolution. We both reject random mutations, I suggest cellular intelligence (perhaps God-given) instead, and would add cooperation to competition. I don’t know how any of this supports your thesis that God created new species, lifestyles etc. before creating the conditions that demanded or allowed them.

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dhw: Resistance to toxins has to be a physical as opposed to a behavioural process. I suggest that all of these processes come as a RESPONSE to the environment. Planning requires knowledge of the future. Please tell us about adaptations that have been observed BEFORE the relevant environmental changes took place.

My point is that in seeing a future body type requires mentation and planning. See the whale series as shown in the video of today. As you know and see below about apes, many species appear without any environmental change.

dhw: I am not suggesting that my cell committees plan for future changes in the environment. I am suggesting that they respond to changes as they happen. In your scenario, speciation, lifestyles and natural wonders all require God’s preprogramming or dabbling in order to keep life going for the sake of humans. Once again: are you now backtracking on your insistence that God also designed all the lifestyles and natural wonders for the same purpose?

The primary purpose of evolution is humans. You are reverting to pure Darwin. Speciation can occur without environmental changes.

dhw: Just to make it clear: we now have evolution as a process in which God creates new species, lifestyles and natural wonders, and then creates the conditions in which they are able to live, as opposed to new environments triggering the structural changes.

I repeat:

DAVID: I have made the point that environmental changes never pushed the drive to humans. apes are still apes. Environment is only one of many factors that drive evolution. Darwin used that argument, but his entire theory is weak, as we know.

dhw: We have both made the point over and over again that environmental changes never pushed the drive to multicellularity as a whole, since bacteria are still with us. That is why over and over again I have suggested that all advances beyond bacteria, including humans, can be attributed to the drive for survival and/or improvement. Darwin argued that environmental factors, random mutations, competition for survival and natural selection drove evolution.

Again pure Darwin: natural selection is a passive judge, not a driver. Competition and environmental changes may not have driven evolution. A drive to complexity os an obvious component.

dhw: We both reject random mutations, I suggest cellular intelligence (perhaps God-given) instead, and would add cooperation to competition. I don’t know how any of this supports your thesis that God created new species, lifestyles etc. before creating the conditions that demanded or allowed them.

My thesis is based on many more factors than the ones you list. They are in two books and the entries here. The evolution of the conditions on Earth and the evolution of life obviously co-evolved. God prefers evolutionary processes to achieve His goals. I've agreed elsewhere that it might be a way God can experiment, if He wishes, but that is a big IF.

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dhw: Planning requires knowledge of the future. Please tell us about adaptations that have been observed BEFORE the relevant environmental changes took place.
DAVID: My point is that in seeing a future body type requires mentation and planning. See the whale series as shown in the video of today. As you know and see below about apes, many species appear without any environmental change.

The pre-whale did change its environment, from land to water. This required adaptation, and the final result of the adaptations was a new species.(We can't always draw a clear line between adaptation and innovation.) Please tell me now about adaptations observed before the relevant environmental changes took place.

dhw: I am not suggesting that my cell committees plan for future changes in the environment. I am suggesting that they respond to changes as they happen. In your scenario, speciation, lifestyles and natural wonders all require God’s preprogramming or dabbling in order to keep life going for the sake of humans. Once again: are you now backtracking on your insistence that God also designed all the lifestyles and natural wonders for the same purpose?

DAVID: The primary purpose of evolution is humans. You are reverting to pure Darwin. Speciation can occur without environmental changes.

So are you backtracking on your insistence that only God could have designed all the lifestyles and natural wonders, and did so in order to keep life going until he could produce humans? We have no idea how speciation takes place, but I would draw your attention to your own comment: “The evolution of the conditions on Earth and the evolution of life obviously co-evolved.” Yes, it’s obvious. However, according to you God creates new species, lifestyles and natural wonders, and afterwards creates the conditions in which they are able to live, as opposed to new environments triggering structural changes.

dhw: We have both made the point over and over again that environmental changes never pushed the drive to multicellularity as a whole, since bacteria are still with us. That is why over and over again I have suggested that all advances beyond bacteria, including humans, can be attributed to the drive for survival and/or improvement. Darwin argued that environmental factors, random mutations, competition for survival and natural selection drove evolution.

DAVID: Again pure Darwin: natural selection is a passive judge, not a driver. Competition and environmental changes may not have driven evolution. A drive to complexity is an obvious component.

We have been over this umpteen times. Your drive to complexity is my drive to improvement. “Pure" Darwin? You have split my comments Here is the continuation:

dhw: We both reject random mutations, I suggest cellular intelligence (perhaps God-given) instead, and would add cooperation to competition. I don’t know how any of this supports your thesis that God created new species, lifestyles etc. before creating the conditions that demanded or allowed them.
DAVID: My thesis is based on many more factors than the ones you list. They are in two books and the entries here. The evolution of the conditions on Earth and the evolution of life obviously co-evolved. God prefers evolutionary processes to achieve His goals. I've agreed elsewhere that it might be a way God can experiment, if He wishes, but that is a big IF.

Since we both believe evolution happened, then clearly if God exists, he used evolutionary methods to achieve his goals. However, the goal that you impose on him (the production of humans) does not fit in with the higgledy-piggledy history of evolution, and there is no evidence that the evolutionary processes he prefers are a 3.8-billion-year-old programme and/or dabbling not only for every single innovation, lifestyle and natural wonder, but also for every single change in the environment – local and global – that apparently followed on after he had designed the organism that was to live in the new environment. Apart, that is, from the pre-whale, which apparently had to be designed and then redesigned over and over again AFTER it had entered the water. (Or do you believe it only entered the water after God had fiddled with its nostrils?)

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DAVID: The primary purpose of evolution is humans. You are reverting to pure Darwin. Speciation can occur without environmental changes.

dhw: So are you backtracking on your insistence that only God could have designed all the lifestyles and natural wonders, and did so in order to keep life going until he could produce humans? We have no idea how speciation takes place, but I would draw your attention to your own comment: “The evolution of the conditions on Earth and the evolution of life obviously co-evolved.” Yes, it’s obvious. However, according to you God creates new species, lifestyles and natural wonders, and afterwards creates the conditions in which they are able to live, as opposed to new environments triggering structural changes.

My point is my ape/human comparison. They both lived in exactly the same environment, but only humans involved to something much more complex and improved.

dhw: Since we both believe evolution happened, then clearly if God exists, he used evolutionary methods to achieve his goals. However, the goal that you impose on him (the production of humans) does not fit in with the higgledy-piggledy history of evolution, and there is no evidence that the evolutionary processes he prefers are a 3.8-billion-year-old programme and/or dabbling not only for every single innovation, lifestyle and natural wonder, but also for every single change in the environment – local and global – that apparently followed on after he had designed the organism that was to live in the new environment.

We continue to disagree on the reasons for the bush of life, but you do keep agreeing that energy is needed for a long term evolutionary process, and then that agreement disappears when you face the issue of humans as the goal. Darwin theory does not predict the arrival of humans. Apes are still apes.

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DAVID: The primary purpose of evolution is humans. You are reverting to pure Darwin. Speciation can occur without environmental changes.
dhw: So are you backtracking on your insistence that only God could have designed all the lifestyles and natural wonders, and did so in order to keep life going until he could produce humans? We have no idea how speciation takes place, but I would draw your attention to your own comment: “The evolution of the conditions on Earth and the evolution of life obviously co-evolved.” Yes, it’s obvious. However, according to you God creates new species, lifestyles and natural wonders, and afterwards creates the conditions in which they are able to live, as opposed to new environments triggering structural changes.
DAVID: My point is my ape/human comparison. They both lived in exactly the same environment, but only humans involved to something much more complex and improved.

There are lots of species that live in the same environment, and they all find their “niche” as you call it. We don’t know how they evolved from their common ancestors, but it can only have been through individuals that diverged while others remained the same. Not all fish came out onto dry land. Not all ape ancestors evolved into humans. Once a life form diverges (perhaps through the drive for improvement) and is successful, it survives. If its contemporaries are still OK in their niche, they will also survive. Meanwhile, once again: are you backtracking on your theory that God designed all lifestyles and natural wonders to provide the energy for life to continue until he designed humans, and are you still sticking to your theory that when environmental change was involved, your God designed them (along with innovations) before he changed their environment?

DAVID: We continue to disagree on the reasons for the bush of life, but you do keep agreeing that energy is needed for a long term evolutionary process, and then that agreement disappears when you face the issue of humans as the goal. Darwin theory does not predict the arrival of humans. Apes are still apes.

And bacteria are still bacteria. See above re apes. I have never disagreed that energy is needed for life and evolution, long term or short term, but it has nothing whatsoever to do with your insistence that your God’s purpose in creating life and evolution was the production of humans. Darwin’s theory could hardly predict the arrival of humans since humans had already arrived! :-) His contribution was to tell us that we and apes sprang from a common ancestor, and that all species sprang from a few forms or just one. I don’t know why you keep bringing Darwin into it when what is under the microscope is your own attempt to impose your anthropocentrism on the entire history of life.

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DAVID: My point is my ape/human comparison. They both lived in exactly the same environment, but only humans involved to something much more complex and improved.

dhw: Meanwhile, once again: are you backtracking on your theory that God designed all lifestyles and natural wonders to provide the energy for life to continue until he designed humans, and are you still sticking to your theory that when environmental change was involved, your God designed them (along with innovations) before he changed their environment?

I haven't changed. Humans arrived with no obvious environmental change and against all odds. The bush of life supplies energy for evolution to continue, since it took a long time.

DAVID: We continue to disagree on the reasons for the bush of life, but you do keep agreeing that energy is needed for a long term evolutionary process, and then that agreement disappears when you face the issue of humans as the goal. Darwin theory does not predict the arrival of humans. Apes are still apes.

dhw: Darwin’s theory could hardly predict the arrival of humans since humans had already arrived! His contribution was to tell us that we and apes sprang from a common ancestor, and that all species sprang from a few forms or just one. I don’t know why you keep bringing Darwin into it when what is under the microscope is your own attempt to impose your anthropocentrism on the entire history of life.

We agree on common descent. Beyond that I'm sure the rest of Darwin's thoughts do not apply. I bring up his theory when you seem to be implying some of them, those trying to explain common descent.

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dhw: Meanwhile, once again: are you backtracking on your theory that God designed all lifestyles and natural wonders to provide the energy for life to continue until he designed humans, and are you still sticking to your theory that when environmental change was involved, your God designed them (along with innovations) before he changed their environment?

DAVID: I haven't changed. Humans arrived with no obvious environmental change and against all odds. The bush of life supplies energy for evolution to continue, since it took a long time.

That is not what I keep asking. With my theist’s hat on, I have even agreed that your God might have produced humans with a dabble, and we have long since agreed that life and evolution require energy. Neither of these observations means that he personally designed every lifestyle and natural wonder for the sake of humans. But at least under “whale changes” you appear to have now jettisoned your theory that your God “planned” every structure, lifestyle etc. before he changed the environment. One answer given, and one still to come.

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DAVID: I haven't changed. Humans arrived with no obvious environmental change and against all odds. The bush of life supplies energy for evolution to continue, since it took a long time.

dhw: That is not what I keep asking. With my theist’s hat on, I have even agreed that your God might have produced humans with a dabble, and we have long since agreed that life and evolution require energy. Neither of these observations means that he personally designed every lifestyle and natural wonder for the sake of humans. But at least under “whale changes” you appear to have now jettisoned your theory that your God “planned” every structure, lifestyle etc. before he changed the environment. One answer given, and one still to come.

I 'appear' to you in strange ways. Why shouldn't He plan all of evolution to produce humans? I see that as His purpose. The bush of life provides us with many resources that we now manage. Show me why history of evolution tells us humans were required. They weren't. As for whales the only way it can work is if He designs all eight stages. Envirnomental change is simple. We see the animals move from land to water as changed mammals, but still mammals, in a new environment with overall environment the same.

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DAVID: I 'appear' to you in strange ways. Why shouldn't He plan all of evolution to produce humans? I see that as His purpose. The bush of life provides us with many resources that we now manage. Show me why history of evolution tells us humans were required. They weren't.

Nor was the duck-billed platypus. You don’t even know why the whale was “required”. The history of evolution tells us that once bacteria were on earth, nothing else was “required”, since they have survived from the beginning. But I have fallen over backwards to offer you the possibility that your God may have experimented in his efforts to create a being similar to himself (that was “off the reservation” until you decided it was a possibility), or that the idea for humans came late on in the process (rejected), and that he might have dabbled (though that raises the question of why he had to dabble the different hominids and hominins before he got to sapiens, not to mention the question of why he had to design the vast bush with its 99% failure rate if he could dabble humans without any difficulty).

DAVID: As for whales the only way it can work is if He designs all eight stages. Envirnomental change is simple. We see the animals move from land to water as changed mammals, but still mammals, in a new environment with overall environment the same.

And why did he have to design it in eight stages if he knew what he wanted (though you don’t know why he wanted it)? I don’t know what you mean by a new environment with overall environment the same. The whole point of the changes was to enable the whale to live in a new environment – water not land. And yet you see no link between speciation and the environment.

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DAVID: As for whales the only way it can work is if He designs all eight stages. Envirnomental change is simple. We see the animals move from land to water as changed mammals, but still mammals, in a new environment with overall environment the same.

dhw: And why did he have to design it in eight stages if he knew what he wanted (though you don’t know why he wanted it)? I don’t know what you mean by a new environment with overall environment the same. The whole point of the changes was to enable the whale to live in a new environment – water not land. And yet you see no link between speciation and the environment.

Water and land environments differ but I was referring to overall environmental alterations, not that specific difference in where to live.

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DAVID: As for whales the only way it can work is if He designs all eight stages. Envirnomental change is simple. We see the animals move from land to water as changed mammals, but still mammals, in a new environment with overall environment the same.

dhw: And why did he have to design it in eight stages if he knew what he wanted (though you don’t know why he wanted it)? I don’t know what you mean by a new environment with overall environment the same. The whole point of the changes was to enable the whale to live in a new environment – water not land. And yet you see no link between speciation and the environment.

DAVID: Water and land environments differ but I was referring to overall environmental alterations, not that specific difference in where to live.

I don’t think anyone would claim that every instance of speciation was triggered by a global change in the environment. Speciation has to take place in individuals or groups, and individuals and groups live in local environments. It makes perfect sense to me that a change in local conditions might trigger changes in certain organisms, and if they are successful they will flourish and spread. And I still don’t see how conditions and life can “co-evolve” and yet there is no link between speciation and the environment.

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dhw: I don’t think anyone would claim that every instance of speciation was triggered by a global change in the environment. Speciation has to take place in individuals or groups, and individuals and groups live in local environments. It makes perfect sense to me that a change in local conditions might trigger changes in certain organisms, and if they are successful they will flourish and spread. And I still don’t see how conditions and life can “co-evolve” and yet there is no link between speciation and the environment.

There is a link in adaptations. We don't know how they might lead to speciation, since there is no Darwin-desired step by step fossil pattern.

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dhw: I don’t think anyone would claim that every instance of speciation was triggered by a global change in the environment. Speciation has to take place in individuals or groups, and individuals and groups live in local environments. It makes perfect sense to me that a change in local conditions might trigger changes in certain organisms, and if they are successful they will flourish and spread. And I still don’t see how conditions and life can “co-evolve” and yet there is no link between speciation and the environment.

DAVID: There is a link in adaptations. We don't know how they might lead to speciation, since there is no Darwin-desired step by step fossil pattern.

As on the “whale” thread, yet again: nobody knows what causes speciation, and we can only offer our hypotheses. However, taking your favourite example of the whale, if a land mammal changed its environment, moved into the water, and became a different species,how can you then claim that there is no link between speciation and the environment?

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DAVID: There is a link in adaptations. We don't know how they might lead to speciation, since there is no Darwin-desired step by step fossil pattern.

dhw: As on the “whale” thread, yet again: nobody knows what causes speciation, and we can only offer our hypotheses. However, taking your favourite example of the whale, if a land mammal changed its environment, moved into the water, and became a different species,how can you then claim that there is no link between speciation and the environment?

As I've explained today the link is the other way around than your thought: prior speciation allows the animal to enter a new environment.

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The Sherpa's have adapted their total metabolism to high altitude:

https://cosmosmagazine.com/biology/sherpas-use-oxygen-more-efficiently-to-thrive-at-hig...

"What makes the Sherpa people, who have lived in the Himalayan mountains for thousands of years, so well-adapted to the high-altitude life, able to function on levels of oxygen that mean incapacity or even death for others, has inspired plenty of investigation. Past studies point to Sherpas having fewer red blood cells but higher levels of nitric oxide, which open up blood vessels and keep blood flowing.

"The finding comes from research by a team led by scientists from the University of Cambridge who, to better understand the biological differences between the Sherpas and “lowlanders” monitored two separate groups (one comprising Sherpas, the other lowlanders) as they made a gradual ascent up to Everest Base Camp, 5,300 metres above sea level. For most people hypobaric hypoxia (insufficient supply of oxygen due to low air pressure) begins to set in at about 3,000 metres. The peak of Everest is 8,848 metres, with the part above 8,000 metres known as “the death zone”.

"Using parallel molecular, biochemical, physiological and genetic approaches to study the difference between the groups, the researchers report that Sherpas demonstrated a lower capacity for fatty acid oxidation in skeletal muscles, along with more efficient use of oxygen, improved muscle energetics, and protection against oxidative stress.

"At a mitochondrial level – which is to say, at the level of power generation within cells – the Sherpas used oxygen more efficiently to produce the energy required to power their bodies.

"As well as converting oxygen and nutrients more efficiently into adenosine triphosphate (ATP, the principal chemical powering the body), Sherpas also showed higher levels of phosphocreatine, an energy reserve that acts as a buffer to help muscles contract in the absence of ATP. After two months at high altitude, phosphocreatine levels crashed in the lowlanders but increased in the Sherpas.

"These metabolic adaptations, the researchers write in Proceedings of the National Academy of Sciences (PNAS), appear to be related to an enriched gene known as the peroxisome proliferator-activated receptor A (PPARA).

"The study was part of Xtreme Everest, a project that aims to improve outcomes for people who become critically ill by understanding how our bodies respond to the extreme altitude on the world's highest mountain. This year marks 10 years since the group's first expedition to Everest.

"The researchers note that the Sherpas’ adaptations provide an advantage even in the womb, since “fetal growth at altitude [is] poorer in Lowlander populations than in many native highlanders, including Tibetans and Sherpas'”.

Comment: this research shows the extent of epigenetic changes to humans at high altitude. A marked change in environment, but they are still humans.

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This discovery finds a gene that works in two opposite ways for DNA damage:

http://www.the-scientist.com/?articles.view/articleNo/49223/title/Noncoding-RNA-Helps-C...

"Scientists discover transcripts from the same gene that can express both proteins and noncoding RNA.

The paper
L. Williamson et al., “UV irradiation induces a non-coding RNA that functionally opposes the protein encoded by the same gene,” Cell, doi:10.1016/j.cell.2017.01.019, 2017.

"Damaged DNA
When its DNA is damaged, a cell activates genes to repair the lesion and slows down the transcription of many others. According to Jesper Svejstrup of the Francis Crick Institute, researchers have known about this response for a few decades. However, “that was the extent of what we knew,” he says.

"Two for one
Last year, Svejstrup and colleagues identified factors associated with transcription-related changes after UV-induced DNA damage, including the transcription of ASCC3, which encodes a protein involved in regulating gene expression (Cell Rep, 15:1597-1610, 2016). In their latest study using sequencing analysis, they discovered that normally long ASCC3 transcripts became much shorter after damage.

"Functional see-saws
Knocking down the short ASCC3 transcript produced after UV exposure prevented the cell from recovering normal levels of transcription. “Without the short isoform of ASCC3, you can no longer respond correctly to DNA damage, and cells die,” Svejstrup explains. Blocking the long version, on the other hand, increased transcription levels after UV irradiation. “It’s interesting because the same gene, ASCC3, is producing two opposed [functions],” says Alberto Kornblihtt, a molecular biologist at the University of Buenos Aires who was not involved in the work. “If the protein is made from the long pre-mRNA, then global transcription is repressed. But if the short RNA is made, it helps recover transcription hours after damage.”

"Uncovering mechanisms
How the short isoform aids repair remains unknown. “The most logical, simple explanation is that the [noncoding RNA] counteracts the protein encoding form,” Svejstrup says. “Perhaps [it] binds to ASCC3 protein—but we haven’t been able to get clear evidence for that [yet].'”

Comment: Not fully elucidated yet, but it seems like a clever mechanism to get the DNA back to full function quickly after injury to prevent cell death. UV light was certainly present at the start of life. This suggests the mechanism must go back to the beginning of life to protect the single-celled bacteria from exposure. However, if life began deep in the ocean, protected from UV light, the mechanism had to appear immediately upon life surfacing into sunlight. Again stronly suggests saltation.

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The controls for RNA survival is now found:

https://phys.org/news/2017-06-rna-lifespan-transcription.html

"Control of RNA lifespan is vital for the proper functioning of our cells. Marc Bühler's group at the Friedrich Miescher Institute for Biomedical Research (FMI) has discovered a novel mechanism determining the fate of RNA in mammalian cells: two proteins involved in RNA interference - Dgcr8 and Drosha - together with a methyltransferase, Mettl3, mark nascent RNAs for degradation as they are transcribed. This mechanism allows RNA transcripts to "remember" the conditions under which they were synthesized.

"Life of an RNA is never easygoing. Its formation, processing, lifespan and degradation are all tightly regulated. This stringent control of RNA metabolism ensures that genes become active at the right time and place, safeguarding cell functions.

***

"the scientists showed that two well known mammalian RNAi factors interact with chromatin: both Dgcr8 (an RNA-binding protein) and Drosha (an RNase) bind to nascent transcripts, thereby silencing genes co-transcriptionally. First author Philip Knuckles, an NCCR-funded postdoctoral fellow in Bühler's lab, explains: "In multicellular organisms, Dgcr8 and Drosha form a complex called the microprocessor (MP). This complex does not exist in yeast, but our results suggest that it takes over the function of the yeast RNAi protein Dicer. The principle is conserved, but the players differ slightly."

"The FMI scientists also showed that an enzyme known as Mettl3 is involved in the degradation of nascent RNAs. Mettl3 transfers methyl groups to adenosine residues in RNA, a mark that also influences RNA stability. Knuckles says: "In our experiments, we showed that Mettl3 binds to chromatin while RNA is being transcribed, and that this Mettl3 association stimulates Dgcr8 binding."

"The MP/Mettl3 system allows the cell to react rapidly to changing growth conditions. Bühler explains: "During a stress situation induced by high temperature, the heat-shock RNA transcripts produced are concomitantly tagged by adenosine methylation. This marks these RNAs for subsequent degradation, enabling a swift but time-limited response to stress." According to Bühler, both the fast stress response and the rapid clearance of heat-shock transcripts and proteins are important for cells: "The accumulation of stress response proteins is detrimental to the cell and is often observed in cancer."

Comment: The knowledge of complexity of the genome increases constantly. Concentrations of living biochemicals are always controlled by feedback loops, which are always held in tight defined limits of concentration. This arrangement cannot be found by chance hunt and peck. It must work from the beginning.

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Controlled by two genes who cross talk with each other:

https://phys.org/news/2017-06-genetic-cross-talk-key-cell.html

"Competing regulatory genes "talk" to each other to maintain balance of cell state, according to new research from the Stowers Institute for Medical Research.

"Stowers scientists Bony De Kumar, Ph.D., and Robb Krumlauf, Ph.D., provide evidence of direct cross-regulatory feedback, or cross-talk, between Nanog and Hox genes.

"Nanog and Hox genes regulate cell pluripotency and differentiation, respectively. When cells are pluripotent, they have the capacity to self-renew and the potential to change into any of a number of cell types. And when cells differentiate, they become a more specialized cell type, like heart, brain, or skin cells.

"In adult organisms, striking a balance between these two states is important to keep many tissues in equilibrium. The blood supply, for example, has cells that are differentiating, dying, or being repaired, and a reserve population of blood-producing adult stem cells is needed to help replace them.

"The Stowers study suggests that balance between pluripotency and differentiation hinges in part on regulatory communication involving inhibition between Nanog and Hox genes. Krumlauf compares this cross-talk to parents giving their children instructions.

***

"Both positive and negative instructions are important. Nanog and Hox genes each have their own distinct jobs and by inhibiting each other they work together to direct the proper balance of cell states by helping the cell avoid wrong turns and stay on course.

"'Differentiation and pluripotency are well-studied processes," says first author De Kumar. "This paper actually links the processes together. Before, we did not know that these pathways were talking to each other. It was pretty surprising for us."

"The researchers made the discovery while studying Hox genes in the early stages of mouse embryonic stem cell differentiation. These "architect genes" control the layout of a developing embryo and play a key role in the establishment of the basic body plan and craniofacial development.

***

"'Over the past 10 to 20 years, biologists have shown that cells are actively assessing their environment, and that they have many fates they can choose. The regulatory loops we've found show how the dynamic nature of cells is being maintained," says Krumlauf, who was recently inducted into the National Academy of Sciences for his seminal work on Hox genes.
The work provides important insight into the basic processes of tissue formation"

The article abstract:

http://www.pnas.org/content/early/2017/05/30/1610612114

"Homeobox a1 (Hoxa1) is one of the most rapidly induced genes in ES cell differentiation and it is the earliest expressed Hox gene in the mouse embryo. In this study, we used genomic approaches to identify Hoxa1-bound regions during early stages of ES cell differentiation into the neuro-ectoderm. Within 2 h of retinoic acid treatment, Hoxa1 is rapidly recruited to target sites that are associated with genes involved in regulation of pluripotency, and these genes display early changes in expression. The pattern of occupancy of Hoxa1 is dynamic and changes over time. At 12 h of differentiation, many sites bound at 2 h are lost and a new cohort of bound regions appears. At both time points the genome-wide mapping reveals that there is significant co-occupancy of Nanog (Nanog homeobox) and Hoxa1 on many common target sites, and these are linked to genes in the pluripotential regulatory network. In addition to shared target genes, Hoxa1 binds to regulatory regions of Nanog, and conversely Nanog binds to a 3′ enhancer of Hoxa1. This finding provides evidence for direct cross-regulatory feedback between Hoxa1 and Nanog through a mechanism of mutual repression. Hoxa1 also binds to regulatory regions of Sox2 (sex-determining region Y box 2), Esrrb (estrogen-related receptor beta), and Myc, which underscores its key input into core components of the pluripotential regulatory network. We propose a model whereby direct inputs of Nanog and Hoxa1 on shared targets and mutual repression between Hoxa1 and the core pluripotency network provides a molecular mechanism that modulates the fine balance between the alternate states of pluripotency and differentiation. "

Comment: Just more evidence of the interlocking feedback loops of balanced controls by genes as they automatically build an embryo. They contain information to do this. No innate intelligence required, even though they are acting intelligently.

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The mechanism is now somewhat understood:

https://www.sciencedaily.com/releases/2017/06/170608073251.htm

"An international scientific consortium including the Freiburg plant biologist Prof. Dr. Thomas Laux has discovered a regulatory pathway that turns plants' ordinary somatic cells into germ cells for sexual reproduction.

"the germ cells of plants are established de novo from somatic cells in the floral reproductive organs, the stamens and carpels. To this end, the selected cells switch their cell division mode from mitosis, cell proliferation maintaining the chromosome number, to meiosis, the division that reduces the number of chromosomes and where genetic recombination occurs. Plants have therefore evolved strategies to enable somatic cells to switch to germline fate and to do so in the right place and at the right time.

"Laux and colleagues have identified multiple genes in the model organism Arabidopsis thaliana that give the start signal for switching from mitose to meiose. The starting point for the findings presented in Science are mutants that create multiple germ cells instead of a singular one in each ovule. Key of the newly discovered pathway is the limitation of activity of the transcription factor WUSCHEL, which Laux's team had identified several years ago as an important regulator of pluripotent stem cells that are able to develop into every cell type in the organism. The involvement of WUSCHEL in creating germ cells is a discovery that provides molecular evidence for the longstanding hypothesis derived from paleobotanical studies that the reproductive ovules and the shoot meristem have evolved from the same precursor organ in ancient plants. The newly discovered regulatory mechanism shows how plants are able to limit switching to the germ cell program so that only a single germ cell emerges, while the surrounding cells take on other tasks."

Comment: how this developed is not fully understood, but it is clearly an automatic molecular process. Sexual reproduction aids in a diverse evolution, but is a much more complex process than simply using the bacterial system of cell splitting. Did God introduce sex as a means of advancing evolution?

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It also involves a specialized protein:

https://www.sciencedaily.com/releases/2017/06/170608123648.htm

"Drexel University and Georgia Institute of Technology researchers have discovered how the Rad52 protein is a crucial player in RNA-dependent DNA repair. The results of their study, published in Molecular Cell, reveal a surprising function of the homologous recombination protein Rad52. They also may help to identify new therapeutic targets for cancer treatment.

***

"Alexander Mazin, PhD, a professor at Drexel University's College of Medicine, and Francesca Storici, PhD, an associate professor at Georgia Tech, have dedicated their research to studying mechanisms and proteins that promote DNA repair.

"In 2014, Storici and Mazin made a major breakthrough when they discovered that RNA can serve as a template for the repair of a DNA double-strand break in budding yeast, and Rad52, a member of the homologous recombination pathway, is an important player in that process.
"We provided evidence that RNA can be used as a donor template to repair DNA and that the protein Rad52 is involved.'"

"In their current study, the research team uncovered the unusual, important role of Rad52: It promotes "inverse strand exchange" between double-stranded DNA and RNA, meaning that the protein has a novel ability to bring together homologous DNA and RNA molecules. In this RNA-DNA hybrid, RNA can then be used as a template for accurate DNA repair.

"It appeared that this ability of Rad52 is unique in eukaryotes, as otherwise similar proteins do not possess it.

"'Strikingly, such inverse strand exchange activity of Rad52 with RNA does not require extensive processing of the broken DNA ends, suggesting that RNA-templated repair could be a relatively fast mechanism to seal breaks in DNA," Storici said.

"As a next step, the researchers hope to explore the role of Rad52 in human cells."

Comment: Once again a complex protective mechanism to maintain DNA integrity. Must have been present since the origin of life as reproducibility of accurate DNA copies is ital. for life to continue once originated.

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A video of how DNA replicates changes all the concepts of how it works:

http://www.sciencealert.com/dna-replication-has-been-filmed-for-the-first-time-and-it-s...

"Here's proof of how far we've come in science - in a world-first, researchers have recorded up-close footage of a single DNA molecule replicating itself, and it's raising questions about how we assumed the process played out.

"The real-time footage has revealed that this fundamental part of life incorporates an unexpected amount of 'randomness', and it could force a major rethink into how genetic replication occurs without mutations.

***

"The new genetic material that's attached to each one during the replication process is an exact match to what was on its original partner.

"So as the leading strand detaches, the enzymes add bases that are identical to those on the original lagging stand, and as the lagging strand detaches, we get material that's identical to the original leading strand.

"Scientists have long assumed that the DNA polymerases on the leading and lagging strands somehow coordinate with each other throughout the replication process, so that one does not get ahead of the other during the unravelling process and cause mutations.

"But this new footage reveals that there's no coordination at play here at all - somehow, each strand acts independently of the other, and still results in a perfect match each time.

***

"The team found that on average, the speed at which the two strands replicated was about equal, but throughout the process, there were surprising stops and starts as they acted like two separate entities on their own timelines.

"Sometimes the lagging strand stopped synthesising, but the leading strand continued to grow. Other times, one strand could start replicating at 10 times its regular speed - and for seemingly no reason.

"'We've shown that there is no coordination between the strands. They are completely autonomous," Kowalczykowski says.

"The researchers also found that because of this lack of coordination, the DNA double helix has had to incorporate a 'dead man's switch', which would kick in and stop the helicase from unzipping any further so that the polymerase can catch up.

"The question now is that if these two strands "function independently" as this footage suggests, how does the unravelling double helix know how to keep things on track and minimise mutations by hitting the brakes or speeding up at the right time?

"Hopefully that's something more real-time footage like this can help scientists figure out. And it's also an important reminder that while we humans love to assume that nature has a 'plan' or a system, in reality, it's often a whole lot messier."

Comment: Accurate DNA replication is the key to life continuing, and it looks messy. But we know it can't be. All of this appeared on a rocky Earth by an unknown process. Logically, only planning by a mind can do this. I choose God.

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11486 views

All four DNA code amino acids protect themselves from u-v light. Thiss protects DNA from u-v light damage:

https://phys.org/news/2017-06-electron-tiny-molecular-sunscreen-response.html

"In experiments at the Department of Energy's SLAC National Accelerator Laboratory, scientists were able to see the first step of a process that protects a DNA building block called thymine from sun damage: When it's hit with ultraviolet light, a single electron jumps into a slightly higher orbit around the nucleus of a single oxygen atom.

"This infinitesimal leap sets off a response that stretches one of thymine's chemical bonds and snaps it back into place, creating vibrations that harmlessly dissipate the energy of incoming ultraviolet light so it doesn't cause mutations.

***

"Thymine and the other three DNA building blocks also strongly absorb ultraviolet light, which can trigger mutations and skin cancer, yet these molecules seem to get by with minimal damage. In 2014, a team led by Markus Guehr – then a SLAC senior staff scientist and now on the faculty of the University of Potsdam in Germany – reported that they had found the answer: The stretch-snap of a single bond and resulting energy-dissipating vibrations, which took place within 200 femtoseconds, or millionths of a billionth of a second after UV light exposure.

"But what made the bond stretch? The team knew the answer had to involve electrons, which are responsible for forming, changing and breaking bonds between atoms. So they devised an ingenious way to catch the specific electron movements that trigger the protective response.

***

"For this new experiment, the scientists hit thymine molecules with a pulse of UV laser light and tuned the energy of the LCLS X-ray laser pulses so they would home in on the response of the oxygen atom that's at one end of the stretching, snapping bond.

"The energy from the UV light excited one of the atom's electrons to jump into a higher orbital. This left the atom in a sort of tippy state where just a little more energy would boost a second electron into a higher orbital; and that second jump is what sets off the protective response, changing the shape of the molecule just enough to stretch the bond.

"The first jump, which was previously known to happen, is difficult to detect because the electron winds up in a rather diffuse orbital cloud, Guehr said. But the second, which had never been observed before, was much easier to spot because that electron ended up in an orbital with a distinctive shape that gave off a big signal.

"'Although this was a very tiny electron movement, the signal kind of jumped out at us in the experiment," Guehr said. "I always had a feeling this would be a strong transition, just intuitively, but when we saw this come in it was a special moment, one of the best moments an experimentalist can have."

"Study lead author Thomas Wolf, an associate staff scientist at SLAC, said the results should settle a longstanding debate about how long after UV exposure the protective response kicks in: It happens 60 femtoseconds after UV light hits. This time span is important, he said, because the longer the atom spends in the tippy state between the first jump and the second, the more likely it is to undergo some sort of reaction that could damage the molecule."

Comment: we see plastics denature when outside in sunlight. DNA can do the same, but the amino acids in DNA can respond very quickly. Did God arrange this protection? The only way to look into the point is to test the other 16 essential amino acids in living matter to see if they are as quick in response. By the way the article doesn't mention uracil which is in RNA and probably is just as fast in response.

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11487 views

DNA is six feet long and other than in bacteria must be packed into a nucleus. This is how it is accomplished:

https://cosmosmagazine.com/biology/how-your-body-packs-a-metre-of-dna-inside-every-cell

"Human cells that carry a full complement of DNA range in volume from a very tiny 130 cubic micrometres for a white blood cell to a comparatively massive 600,000 cubic micrometres for a fat cell.

"But even at the top end of the scale, cells are very tiny things. A micrometre, after all, is just one millionth of a metre.

"Yet here’s the thing: every cell in the body (bar sperm, eggs, and red blood cells) contains a whole metre of DNA.

***

"To do that, they looked closely at the nucleosome, the most basic building block of chromosomes – the rigid framework that holds the DNA.

"The team identified a target protein, known as linker histone H1 – or H1, for short – which the scientists suspected played a key role in inducing chromosomes to be inflexible and compact.

"Hayes recruited fellow researchers in France and Japan to take high-magnification X-ray images of H1 and other DNA proteins in an effort to better understand the mechanisms involved. The resulting images were useful, but the resolution was insufficient to enable unambiguous interpretation.

"To the rescue came co-author Amber Cutter, who conducted a series of test-tube experiments using a range of DNA proteins. The result, added to the information obtained through the X-rays, was clear: with H1, chromosomes were tight and strong; without it, they were long and floppy.

"Apart from its use as a storage enabler, Hayes and his team suggest the protein may have a protective effect, buffering DNA from deforming pressure, and shielding it from physical damage."

Comment: Not only is DNA a complex code. It's storage is carefully designed. Not by chance.

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11443 views

Telomeres protect the ends of chromosomes and shorten as cells an individuals age. The feedback mechanism that controls them is now understood as proteins are identified:

https://www.sciencedaily.com/releases/2017/06/170630105013.htm

"Researchers have further uncovered the secrets of telomeres, the caps that protect the ends of our chromosomes. They discovered that an RNA molecule called TERRA helps to ensure that very short (or broken) telomeres get fixed again. The work,, provides new insights into cellular processes that regulate cell senescence and survival in ageing and cancer.

"Telomeres protect the ends of our chromosomes, much like the plastic cap at the end of a shoelace that prevents the lace from unravelling. Over a cell's lifetime, telomeres get gradually shorter with each cell division and therefore the protective cap becomes less and less effective. If they get too short, it is a signal for the cell that its genetic material is compromised and the cell stops dividing. Telomere shortening and reduced cell division are considered a hallmark of ageing and likely contribute to the ageing process. However, telomere shortening is also a defense mechanism against cancer because highly proliferative cells can only divide when their telomeres do not shorten. Therefore, telomere shortening is a double-edged sword and has to be carefully regulated to strike a balance between ageing and cancer prevention. When a telomere accidentally gets cut short early in a cell's lifetime, it needs to be fixed so that the cell doesn't become senescent too early.

***

"In their recent paper, published in the journal Cell, Luke and his group have shown that one of the keys to understanding this problem is TERRA. TERRA is an RNA species that accumulates specifically at the ends of critically short telomeres by binding directly to the DNA and signals to the cell that these telomeres should be repaired, allowing the cell to carry on dividing.

"We already knew that short telomeres play a key role in determining the onset of cellular senescence, but we didn't really understand which features of short telomeres were important. What we have found with TERRA is an intricate regulatory system that explains how short telomeres are identified by the cell," said Luke.

"The paper is actually the result of two different research projects on telomeres in the Luke lab. Diego Bonetti was looking into the regulation of TERRA in the cell cycle and found that TERRA levels were different at different stages of the cell cycle. Meanwhile, Arianna Lockhart and Marco Graf were investigating the accumulation of TERRA at short telomeres. When they discovered that the pattern of cyclic TERRA accumulation was different between short and long telomeres, they knew they were on to something and joined forces for this project.

"Their joint work led them to realize that TERRA actually accumulates at all telomeres, but at long telomeres it is rapidly removed with the help of proteins Rat1 and RNase H2. These proteins bind preferentially to the long telomeres and ensure that TERRA is removed, but they are not present at the critically short telomeres, which means that TERRA remains for a longer time. This mechanism ensures the subsequent repair of the short telomere, which is crucial for the cell to survive and keep dividing."

Comment: Again this is a biochemical mechanism that must develop all at once, that is, as chromosomes were created, the protection mechanisms had to be present also or life would not have survived. Not chance, a inventive intelligent had to do this: God!

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11506 views

Stem cells which can become any type of cell can move genes around:

"Moving genes about could help cells to respond to change according to scientists at the Babraham Institute in Cambridge, UK and the Weizmann Institute, Israel. Changing the location of a gene within a cell alters its activity. Like mixing music, different locations can make a gene 'louder' or 'quieter', with louder genes contributing more actively to the life of a cell.

"Contrary to expectations, this latest study reveals that each gene doesn't have an ideal location in the cell nucleus. Instead, genes are always on the move. Published in the journal Nature, researchers examined the organisation of genes in stem cells from mice. They revealed that these cells continually remix their genes, changing their positions as they progress though different stages. This work, which has also inspired a musical collaboration, suggests that moving genes about in this way could help cells to fine-tune the volume of each gene to suit the cell's needs.

***

"This is the first time that gene organisation in individual cells has been studied in detail. The results provide snapshots of gene organisation, with each cell arranging genes in unique ways.

"Co-first authors, Dr Takashi Nagano in the UK and Yaniv Lubling in Israel have collected and individually analysed information one-by-one from over 4000 cells for this study. Speaking about the work, Dr Nagano said: "We've never had access to this level of information about how genes are organised before. Being able to compare between thousands of individual cells is an extremely powerful tool and adds an important dimension to our understanding of how cells position their genes."

***

"Lead author from the Babraham Institute, Professor Peter Fraser said: "We typically see that changes to gene activity have a great impact on health, disease and evolution. It's now obvious that genome organisation may have a part to play in this and our research shows that the effects of location on genes may be a constantly moving target. Understanding how the genome is controlled during this constant re-shuffling is an important step towards understanding how our genomes and genes effect our lives."

"The team now plan to examine whether changing the locations of genes actually has a significant effect on the volume of each gene and to study different types of cells to understand whether they move genes about less once they stop dividing or if all cells behave like stem cells do."

Comment: this research applies to stem cells which can turn into many different functioning cells. In view of that, I don't think the result is surprising, but it shows how much control the genome has over itself. Certainly looks designed and not by chance. The ability may go as far back as bacteria as shown in Shapiro's work demonstrating bacteria can modify their own DNA.

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11326 views

In C. elegans nematode worms histones maintain warmth experience over 14 generations:

http://www.the-scientist.com/?articles.view/articleNo/49848/title/Epigenetic-Inheritanc...

"When genomicist Ben Lehner and his colleagues at the Centre for Genomic Regulation in Barcelona engineered nematode worms to express a fluorescent reporter, they were hoping to learn about the control of gene expression. Fluorescence indicated activation of the promoter for the gene daf-21, which encodes an essential C. elegans heat-shock protein. Glowing worms meant high expression levels; dull worms, low expression. But during the project, the team stumbled across something else.

“'Working with this strain, we noticed that if you had individuals that were brighter, their progeny tended to be brighter,” says Lehner. With lab worms that are genetically identical, “this is something you don’t normally see. There seemed to be inheritance.”

"Suspecting they had an epigenetic phenomenon on their hands, and knowing that daf-21 is temperature-sensitive, the researchers decided to grow worms at different temperatures to see if it would affect gene-expression levels through the generations. Sure enough, worms grown at 25 degrees Celsius had offspring that were brighter at normal temperature (20 degrees) than the offspring of worms that had always been kept at 20 degrees.

"In worms engineered with multiple copies of the fluorescence transgene, this effect persisted for seven generations after the temperature spike, and even longer when the scientists raised multiple generations at 25 degrees. In one nematode line, the worms’ glow persisted for 14 generations after the temperature had been dialed back to normal.

***

"Looking more closely, the team found that offspring of worms grown in warmer temperatures showed reduced modification of histone proteins around the transgenes from an early stage of embryonic development. Over generations kept at normal temperature, this histone modification gradually returned to normal, suggesting epigenetic readjustment. These findings, says Rechavi, are “the most surprising and interesting part.'”

Comment: Epigenetics usually works with methylation, but in this case it is histone modulation. More than likely other mechanisms will be found. Too complex for chance development.

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11292 views

There are perhaps 200 different cell types in humans, all with the same basic DNA, but expressing the DNA differently produces the cell differences. This study shows part of that mechanism:

https://phys.org/news/2017-07-boundaries-dna.html

"Despite all these different functions and the need for different tools, all our cells contain the exact same DNA sequence. But one central question remains unanswered – how does a cell know which combination of the 20,000 genes it should activate to produce its specific toolkit?

"The answer to this question may be found in the pieces of DNA that lie between our protein-producing genes. Although our cells contain a lot of DNA, only a small part of this is actually composed of genes. We don't really understand the function of most of this other sequence, but we do know that some of it has a function in regulating the activity of genes.
An important class of such regulatory DNA sequences are the enhancers, which act as switches that can turn genes on in the cells where they are required.

"However, we still don't understand how these enhancers know which genes should be activated in which cells. It is becoming clear that the way DNA is folded inside the cell is a crucial factor, as enhancers need to be able to interact physically with genes in order to activate them. It is important to realise that our cells contain an enormous amount of DNA – approximately two meters! – which is compacted in a very complex structure to allow it to fit into our tiny cells. The long strings of DNA are folded into domains, which cluster together to form larger domains, creating an intricate hierarchical structure. This domain organisation prevents DNA from tangling together like it would if it were an unwound ball of wool, and allows specific domains to be unwound and used when they are needed.

"Researchers have identified key proteins that appear to define and help organise this domain structure. One such protein is called CTCF, which sticks to a specific sequence of DNA that is frequently found at the boundaries of these domains. To explore the function of these CTCF boundaries in more detail and to investigate what role they may play in connecting enhancers to the right genes, our team studied the domain that contains the α-globin genes, which produce the haemoglobin that our red blood cells use to circulate oxygen in our bodies.

***

"Firstly, as expected from CTCF's role in defining boundaries, we showed that CTCF boundaries help organise the α-globin genes into a specific domain structure within red blood cells. This allows the enhancers to physically interact with and switch on the α-globin genes in this specific cell type. We then used the gene editing technology of CRISPR/Cas9 to snip out the DNA sequences that normally bind CTCF, and found that the boundaries in these edited cells become blurred and the domain loses its specific shape. The α-globin enhancers now not only activate the α-globin genes, but cross the domain boundaries and switch on genes in the neighbouring domain.

"This study provides new insights into the contribution of CTCF in helping define these domain boundaries to help organise our DNA and restrict the regulation of gene activity within the cells where it is needed. "

Comment: The study is not complete but it shows part of the way DNA is modified to be used in differentiated ways to make differently functioning cells. Again this is a complexity beyond the capacity of chance development.

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11287 views

QUOTE (my bold): But one central question remains unanswered – how does a cell know which combination of the 20,000 genes it should activate to produce its specific toolkit?
"The answer to this question may be found in the pieces of DNA that lie between our protein-producing genes. Although our cells contain a lot of DNA, only a small part of this is actually composed of genes. We don't really understand the function of most of this other sequence, but we do know that some of it has a function in regulating the activity of genes.
An important class of such regulatory DNA sequences are the enhancers, which act as switches that can turn genes on in the cells where they are required.
"However, we still don't understand how these enhancers know which genes should be activated in which cells.”

How do cells know xyz? Great question. Maybe they have an intelligence of their own. Just a thought! ;-)

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11266 views

David: QUOTE (my bold): But one central question remains unanswered – how does a cell know which combination of the 20,000 genes it should activate to produce its specific toolkit?
"The answer to this question may be found in the pieces of DNA that lie between our protein-producing genes. Although our cells contain a lot of DNA, only a small part of this is actually composed of genes. We don't really understand the function of most of this other sequence, but we do know that some of it has a function in regulating the activity of genes.
An important class of such regulatory DNA sequences are the enhancers, which act as switches that can turn genes on in the cells where they are required.
"However, we still don't understand how these enhancers know which genes should be activated in which cells.”

dhw: How do cells know xyz? Great question. Maybe they have an intelligence of their own. Just a thought!

Like good little soldiers they follow instructions in their genome.

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11269 views

dhw: How do cells know xyz? Great question. Maybe they have an intelligence of their own. Just a thought! ;-)

DAVID: Like good little soldiers they follow instructions in their genome.

Yeah, but who/what issues the instructions? General God or General Genome?

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11231 views

dhw: How do cells know xyz? Great question. Maybe they have an intelligence of their own. Just a thought!

DAVID: Like good little soldiers they follow instructions in their genome.

dhw: Yeah, but who/what issues the instructions? General God or General Genome?

Of course, God, who started life, set up the instructions and marching orders.

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11303 views

dhw: How do cells know xyz? Great question. Maybe they have an intelligence of their own. Just a thought! ;-)

DAVID: Like good little soldiers they follow instructions in their genome.

dhw: Yeah, but who/what issues the instructions? General God or General Genome?

DAVID: Of course, God, who started life, set up the instructions and marching orders.

Or perhaps Genome, who perhaps is intelligent enough to do his own information-processing and take his own decisions and give his own instructions, and who perhaps was given his intelligence by your God, who perhaps exists.

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11187 views

Another study is more explicit:

https://www.quantamagazine.org/how-cells-pack-tangled-dna-into-neat-chromosomes-20180222/

"Their models determined that in the lead-up to mitosis, a ring-shaped protein molecule called condensin II, composed of two connected motors, lands on the DNA. Each of its motors move in opposite directions along the strand while remaining attached to one another, causing a loop to form; as the motors continue to move, that loop gets larger and larger. (Mirny demonstrated the process for me by clasping a piece of his computer’s power cord with both hands, held knuckles to knuckles, through which he then proceeded to push a loop of cord.) As tens of thousands of these protein molecules do their work, a series of loops emerges. The ringlike proteins, positioned at the base of each loop, create a central scaffolding from which the loops emanate, and the entire chromosome becomes shorter and stiffer.

***

"After about 10 minutes, the nuclear envelope keeping the chromosomes together broke down, giving a second ring-shaped motor protein, condensin I, access to the DNA. Those molecules performed loop extrusion on the loops that had already formed, splitting each into around five smaller loops on average. Nesting loops in this way enabled the chromosome to become narrower and prevented the initial loops from growing large enough to mix or interact.

"After approximately 15 minutes, as these loops were forming, the Hi-C data showed something that the researchers found even more unexpected. Typically, sequences located close together along the string of DNA were most likely to interact, while those farther apart were less likely to do so. But the team’s measurements showed that “things [then] kind of came back again in a circle,” Mirny said. That is, once the distance between sequences had grown even further, they again had a higher probability of interacting. “It was obvious from the first glance at this data that we’d never seen something like this before,” he said. His model suggested that condensin II molecules assembled into a helical scaffold, as in the famous Leonardo staircase found in the Chambord Castle in France. The nested loops of DNA radiated out like steps from that spiraling scaffold, packing snuggly into the cylindrical configuration that characterizes the chromosome.

“'So this single process immediately solves three problems,” Mirny said. “It creates a scaffold. It linearly orders the chromosome. And it compacts it in such a way that it becomes an elongated object.'”

Comment: The complexity of this design requires a designing mind to create it. There is no why is could have evolved by chance.

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10359 views

We have one DNA but it can make all sorts of different functioning cells:

https://phys.org/news/2018-04-discovery-cells-identical-genes-unique.html

"Scientists have made a significant discovery that explains how and why the billions of different cells in our bodies look and act so differently despite containing identical genes.

***

"The team has discovered a completely new family of proteins in animals with vertebrae—including fish, reptiles, birds and mammals—that they have named PALI1 and PALI2. Fascinatingly, these families of proteins both originated from genes that have gained new functions since vertebrate and invertebrate species evolved from one another millions of years ago. Specifically, PALI1 is vital for embryonic development and in particular for controlling cellular identity.

"The new work helps towards understanding why a blood cell and a brain cell look and act very differently yet contain exactly the same genes. This puzzling question about the so-called 'cellular identity' is central to the field of epigenetics, which strives to explain how cells in your body, with identical sets of genes, can look and behave so differently. The study of epigenetics has provided key molecular insights into how every type of cell has its own unique pattern of genes that are either switched on or off in a tightly controlled manner.

"Central to this is a group of epigenetic regulators, called Polycombs, which are vital to regulating cellular identity in multicellular organisms of both the plant and animal kingdoms. The Bracken lab studies the biology of these Polycomb epigenetic regulators, and their newly discovered PALI1 and PALI2 proteins form a new family of Polycombs that are unique in that they are only present in vertebrates—they are not found in invertebrate animals, or plants. (my bold)

"Commenting on the findings, Professor Bracken said: "This discovery of PALI1 and PALI2 is an important step forward in our understanding of how stem cells specialise in complex animals, such as fish, reptiles, birds and mammals."

"'In addition to its relevance to stem cell biology and regenerative medicine, it may also have implications for future cancer therapies. For example, we are also studying a related Polycomb protein called EZH2, whose function is deregulated in certain blood and brain cancers. Several new drugs have been developed to target EZH2 to treat these patients, but our new results suggest these patients could also potentially be treated by drugs targeting the PALI1 and PALI2 Polycomb proteins, which might provide additional benefit.'"

Comment: Note my bold. A chance evolutionary process did not find this group of proteins to direct this differentiation method. Must be designed.

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10154 views

When pollen from the same plant falls on the stamen the last thing desired is fertilization which could lead to inbreeding, a process to be avoided if a species of plant is to survive:

https://www.sciencedaily.com/releases/2018/07/180711105654.htm

"Recognition systems that prevent self-fertilization have evolved to ensure that a plant mates only with a genetically different plant and not with itself. The recognition systems underlying self-incompatibility are found all around us in nature, and can be found in at least 100 plant families and 40% of species. Until now, however, researchers have not known how the astonishing diversity in these systems evolves.

***

"In non-self recognition systems, the male (pollen) and female (stigma) genes work together as a team to determine recognition, so that a particular variation of the male- and female-genes forms a mating type. Non-self recognition systems are found all around us in nature and have an astonishing diversity of mating types, so the big question in their evolution is: how do you evolve a new mating type when doing so requires a mutation in both sides? For example, when there is a change in the female side (stigma), it produces a new toxin for which no other pollen has an antidote -- so mating can't occur. Does this means that there needs to be a change in the male side (pollen) first, so that the antidote appears and then waits for a corresponding change in the stigma (female side)? But how does this co-evolution work when evolution is a random process? (my bold)

"Through theoretical analysis and simulation, the researchers investigated how new mating types can evolve in a non-self recognition system. They found that there are different pathways by which new types can evolve. In some cases this happens through an intermediate stage of being able to self-fertilize; but in other cases it happens by staying self-incompatible. They also found that new mating types only evolved when the cost of self-fertilization (through inbreeding) was high. Being incomplete -- i.e., having missing F-box genes that produce antidotes to female toxins -- was found to be important for the evolution of new mating types: complete mating types (with a full set of F-Box genes) stayed around for the longest time, as they have the highest number of mating partners. New mating types evolved more readily when there was less mating types in the population. Also, the demographics in a population affect the evolution of non-self recognition systems: population size and mutation rates all influence how this system evolves.

"So although it seems like having a full team of F-box pollen genes (and therefore antidotes) is the best way for new mating types to evolve, this system is complex and can change via a number of different pathways. Interestingly, while the researchers found that new mating types could evolve, the diversity of genes in their theoretical simulations were fewer compared to what is seen in nature. For Melinda Pickup, this observation is intriguing: "We have provided some understanding of the system, but there are still many more questions and the mystery of the high diversity in nature still exists.'"

Comment: Note how Darwinist scientists struggle when the concept of the necessity of co-evolution appears. See my bold above. How about designed from the beginning.

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9770 views

I'll wager that their next step will be to try and modify the genes to circumvent the things, but that it will endanger the plants survivability.

--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.

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9758 views

Tony: I'll wager that their next step will be to try and modify the genes to circumvent the things, but that it will endanger the plants survivability.

I don't follow.

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9737 views

Tony: I'll wager that their next step will be to try and modify the genes to circumvent the things, but that it will endanger the plants survivability.

David:I don't follow.

They fou d a new toy, and will do what scientist do, and play with it. See what happens if they try to work around that system. I predict the results will be grossly deleterious to the plant, if it survives.

--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.

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9733 views

Another view of the poor Darwin approach:

https://evolutionnews.org/2018/07/three-ways-that-plants-defy-darwins-mechanism/

"People know better than to marry their relatives, but how can a blind flower, with no brain or eyes, recognize “self” so as to prevent fertilizing itself? It’s a trick that both gametes have to cooperate on. A mutation in the pollen that enables it to recognize self won’t help if the ovum doesn’t get a corresponding mutation. The Austrian IST researchers were curious about this and decided to take a look.

"In plants such as snapdragons and Petunia, when the pollen lands on the stigma, it germinates and starts growing. The stigma, however, contains a toxin (an SRNase) that stops pollen growth. Pollen in turn has a team of genes (F-box genes) that produce antidotes to all toxins except for the toxin produced by the “self” stigma. Therefore, pollen can fertlize [sic] when it lands on stigma that does not belong to the same plant, but not when it lands on the plant’s own stigma. It may seem like a harsh system, but plants can use this toxin-antidote system to ensure that they only mate with a genetically different plant. This is important as self-fertilization leads to inbreeding, which is detrimental for the offspring.

"Do you see a problem for neo-Darwinism? The stigma basically has a lock that the “self” pollen cannot unlock. The pollen, though, has a key that only works on other flowers’ locks. How could such lock-and-key systems arise in a single plant that will work on unrelated plants? They not only have to evolve the toxin and the antidote, but ensure that the key doesn’t work locally — only with unrelated plants. And that’s not the only conundrum. NSR systems use a different trick. The authors puzzle over how this one evolved:

"In non-self recognition systems, the male (pollen) and female (stigma) genes work together as a team to determine recognition, so that a particular variation of the male- and female-genes forms a mating type. Non-self recognition systems are found all around us in nature and have an astonishing diversity of mating types, so the big question in their evolution is: how do you evolve a new mating type when doing so requires a mutation in both sides? For example, when there is a change in the female side (stigma), it produces a new toxin for which no other pollen has an antidote – so mating can’t occur. Does this means [sic] that there needs to be a change in the male side (pollen) first, so that the antidote appears and then waits for a corresponding change in the stigma (female side)? But how does this co-evolution work when evolution is a random process? Is there a particular order of mutations that is more likely to create a new mating type?

***

"Through theoretical analysis and simulation, the researchers investigated how new mating types can evolve in a non-self recognition system. They found that there are different pathways by which new types can evolve. In some cases this happens through an intermediate stage of being able to self-fertilize; but in other cases it happens by staying self-incompatible. They also found that new mating types only evolved when the cost of self-fertilization (through inbreeding) was high. Being incomplete – i.e., having missing F-box genes that produce antidotes to female toxins — was found to be important for the evolution of new mating types: complete mating types (with a full set of F-Box genes) stayed around for the longest time, as they have the highest number of mating partners. New mating types evolved more readily when there was [sic] less mating types in the population. Also, the demographics in a population affect the evolution of non-self recognition systems: population size and mutation rates all influence how this system evolves.

"The analytical model worked in the committee, but does it work in the real world? In a model, you can assume that beneficial mutations will arise on cue. Nature, however, doesn’t work that way. Their model didn’t compare very well with real flowers:

"So although it seems like having a full team of F-box pollen genes (and therefore antidotes) is the best way for new mating types to evolve, this system is complex and can change via a number of different pathways. Interestingly, while the researchers found that new mating types could evolve, the diversity of genes in their theoretical simulations were fewer compared to what is seen in nature. For Melinda Pickup, this observation is intriguing: “We have provided some understanding of the system, but there are still many more questions and the mystery of the high diversity in nature still exists.'”

Comment: Obviously Darwinists have no idea how the diversity mechanism happened.

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9653 views

... "Through theoretical analysis and simulation, the researchers investigated how new mating types can evolve in a non-self recognition system. They found that there are different pathways by which new types can evolve. In some cases this happens through an intermediate stage of being able to self-fertilize; but in other cases it happens by staying self-incompatible. They also found that new mating types only evolved when the cost of self-fertilization (through inbreeding) was high. Being incomplete – i.e., having missing F-box genes that produce antidotes to female toxins — was found to be important for the evolution of new mating types: complete mating types (with a full set of F-Box genes) stayed around for the longest time, as they have the highest number of mating partners. New mating types evolved more readily when there was [sic] less mating types in the population. Also, the demographics in a population affect the evolution of non-self recognition systems: population size and mutation rates all influence how this system evolves.

I love this. It says they tried to figure it out, sat down, did some brain storming on the subject:
Scientist One Talking to a Reporter: "Ah! We [sic] got a few good ideas."
Scientist Two, Talking from off screen: "Pssst, but they don't work in the real world."
Reporter: What?
Scientist One: Well, it's complicated, you know? Trust us, evolution can do it.
Scientist Two: No it can't.
Reporter: What?
Scientist (To other scientist..covering camera and mic): Someone get this idiot out of here before we lose all our funding. And blacklist them from academic positions and journals.
Scientist Two: NO! Wai....
Reporter: What?
Scientist One: Well, you see, we believe these flowers survived by breeding with themselves, and then one day saying 'Well, that's enough of that rot, I want plant sex'. And of course all the other flowers thought that was a jolly good idea and went ahead and changed their genes to accommodate.
Reporter: What?
Scientist One: Exactly. Now, do run along, can't have you asking any real questions.

"The analytical model worked in the committee, but does it work in the real world? In a model, you can assume that beneficial mutations will arise on cue. Nature, however, doesn’t work that way. Their model didn’t compare very well with real flowers:

"So although it seems like having a full team of F-box pollen genes (and therefore antidotes) is the best way for new mating types to evolve, this system is complex and can change via a number of different pathways. Interestingly, while the researchers found that new mating types could evolve, the diversity of genes in their theoretical simulations were fewer compared to what is seen in nature. For Melinda Pickup, this observation is intriguing: “We have provided some understanding of the system, but there are still many more questions and the mystery of the high diversity in nature still exists.'”

Comment: Obviously Darwinists have no idea how the diversity mechanism happened.

--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.

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9638 views

It is found that cells compartmentalize genes:

https://phys.org/news/2018-11-gene.html

"Regulation of gene expression—turning genes on or off, increasing or decreasing their expression—is critical for defining cell identity during development and coordinating cellular activity throughout the cell's lifetime. The common model of gene regulation imagines the nucleus of the cell as a large space in which molecules involved in DNA transcription float around seemingly at random until they stumble across a DNA sequence or other transcriptional machinery to which they can bind, in other words, a haphazard approach.

"This paradigm is being upended, however, as over the last few years researchers have discovered that rather than being amorphous spaces dependent upon fortuitous collisions, cells actually compartmentalize their processes into discrete membraneless structures in order to congregate relevant molecules, thereby better coordinating their interactions. Research from the lab of Whitehead Institute member Richard Young and others earlier this year reported that such compartmentalization is a crucial, previously-unobserved aspect of gene regulation.

***

"One side of transcription factors, containing the DNA binding domain, binds to a region of DNA near a gene. The other end, called the activation domain, then captures molecules that impact gene expression, anchoring that transcriptional machinery near the gene.

"This most recent work reveals that activation domains do their job by meshing with other transcription proteins to form liquid droplets near the genes they regulate. The process by which the molecules form a distinct liquid compartment within the environment of the cell—like oil refusing to mix with vinegar in a salad dressing—is called phase separation.

***

"Most proteins settle into defined three-dimensional structures and can only bind with other molecules that fit them perfectly in a specific orientation, like a key in a lock. The activation domains of transcription factor proteins, however, contain what are known as intrinsically disordered regions, which behave more like strands of cooked spaghetti, tangling at random into flexible shapes. This disorder allows the molecules to bind at many points, creating a dynamic network of loose connections that appears to precipitate phase separation.

"'I have taught regulatory biology for decades using inspiration from lock-and-key structures. They are elegant, and easy to visualize and model, but they don't tell the whole story," says Young, who is also a professor of biology at MIT. "Phase separation was the missing piece."

"In experiments with a variety of transcription factors, Boija and co-first author Isaac Klein, a postdoc in Young's lab and medical oncology fellow at the Dana-Farber Cancer Institute, found that the transcription factors meshed with Mediator, a molecule that helps activate genes, and phase separated into droplets, and that this process was associated with gene activation. The transcription factors they investigated included OCT4, which is important for maintaining the state of embryonic stem cells; the estrogen receptor (ER), which plays a role in breast cancer; and GCN4, a well-studied model transcription factor in yeast.

"'We found a link between gene activation and phase separation across a broad spectrum of contexts," Klein says, suggesting that this mechanism is a common feature of transcriptional regulation."

Comment: Even more complexity in how a cell handles its gene locations for transcription. Obviously such an intricate system is designed. Chanced cannot accomplish this. A designing mind must exist.

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9266 views

A careful article on the limits to what we understand about genes:

http://nautil.us//issue/68/context/its-the-end-of-the-gene-as-we-know-it

"So the accepted “central dogma” could be conceived as the one-way flow of information from the code in the gene:

"DNA template → proteins → developing characteristics; as if production of the words alone is tantamount to writing the whole “book” of a complex being.

"Then came the brilliant technology for sequencing genes (the components or “letters” in the DNA) in the whole genome.

"Now, in low-cost, highly mechanized procedures, the search has become even easier. The DNA components—the letters in the words—that can vary from person to person are called single nucleotide polymorphisms, or SNPs. The genetic search for our human definition boiled down to looking for statistical associations between such variations and differences in IQ, education, disease, or whatever.

" Only a few extremely weak associations between SNPs and observable human characteristics could be found.

"Scientists now understand that the information in the DNA code can only serve as a template for a protein. It cannot possibly serve as instructions for the more complex task of putting the proteins together into a fully functioning being, no more than the characters on a typewriter can produce a story. (my bold)

***

"Accordingly, even single cells change their metabolic pathways, and the way they use their genes to suit those patterns. That is, they “learn,” and create instructions on the hoof. Genes are used as templates for making vital resources, of course. But directions and outcomes of the system are not controlled by genes. Like colonies of ants or bees, there are deeper dynamical laws at work in the development of forms and variations.

"Some have likened the process to an orchestra without a conductor. Physiologist Denis Noble has described it as Dancing to the Tune of Life (the title of his recent book). It is most stunningly displayed in early development. Within hours, the fertilized egg becomes a ball of identical cells—all with the same genome, of course. But the cells are already talking to each other with storms of chemical signals. Through the statistical patterns within the storms, instructions are, again, created de novo. The cells, all with the same genes, multiply into hundreds of starkly different types, moving in a glorious ballet to find just the right places at the right times. That could not have been specified in the fixed linear strings of DNA.

***

" as the British biologist Denis Noble insists in an interview with the writer Suzan Mazur,1 “The modern synthesis has got causality in biology wrong … DNA on its own does absolutely nothing until activated by the rest of the system … DNA is not a cause in an active sense. I think it is better described as a passive data base which is used by the organism to enable it to make the proteins that it requires.” (my bold)

***

"more evolved functions—and associated diseases—depend upon the vast regulatory networks mentioned above, and thousands of genes. Far from acting as single-minded executives, genes are typically flanked, on the DNA sequence, by a dozen or more “regulatory” sequences used by wider cell signals and their dynamics to control genetic transcription.

"This explains why humans seem to have only a few more genes than flies or mice (around 20,000), while a carrot has 45,000! There is no correlation between the complexity of living things and the number of genes they have. But there is a correlation with the evolving complexity of regulatory networks. Counting genes to understand the whole is like judging a body of literature by counting letters. It can’t be done.

***

"it is now well known that a group of genetically identical individuals, reared in identical environments—as in pure-bred laboratory animals—do not become identical adults. Rather, they develop to exhibit the full range of bodily and functional variations found in normal, genetically-variable, groups. In a report in Science in 2013, Julia Fruend and colleagues observed this effect in differences in developing brain structures.

" we can now understand why the same genetic resources can be used in many different ways in different organs and tissues. Genes now utilized in the development of our arms and legs, first appeared in organisms that have neither. Genes used in fruit flies for gonad development are now used in the development of human brains. And most genes are used in several different tissues for different purposes at the same time.

"In a paper in Physics of Life Reviews in 2013, James Shapiro describes how cells and organisms are capable of “natural genetic engineering.” That is, they frequently alter their own DNA sequences, rewriting their own genomes throughout life. The startling implication is that the gene as popularly conceived—a blueprint on a strand of DNA, determining development and its variations—does not really exist."

Comment: We have a long way to go to really understand how the orchestrated layers of the genome works. Note my bolds. Fascinating article in the whole.

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9052 views

DAVID: A careful article on the limits to what we understand about genes:
http://nautil.us//issue/68/context/its-the-end-of-the-gene-as-we-know-it

Once more my thanks for your integrity in presenting such articles.

This, together with the two quotes that follow, presents an interesting contrast to two of your earlier statements: “…the original DNA may have contained all the info for evolution”. Your definition of intelligent information was “a complete set of instructions for cells to respond to all stimuli they must deal with.”

QUOTES: "Accordingly, even single cells change their metabolic pathways, and the way they use their genes to suit those patterns. That is, they “learn,” and create instructions on the hoof.” (dhw’s bold)

“Through the statistical patterns within the storms, instructions are, again, created de novo. The cells, all with the same genes, multiply into hundreds of starkly different types, moving in a glorious ballet to find just the right places at the right times. That could not have been specified in the fixed linear strings of DNA.”

I really don’t see how your definitions are compatible with the statements I have bolded.

QUOTE: " as the British biologist Denis Noble insists in an interview with the writer Suzan Mazur,1 “The modern synthesis has got causality in biology wrong … DNA on its own does absolutely nothing until activated by the rest of the system … DNA is not a cause in an active sense. I think it is better described as a passive data base which is used by the organism to enable it to make the proteins that it requires.” (DAVID’s bold)

If DNA is not a cause and is not a set of instructions, the cell communities of which the organism is composed and which “talk to each other with storms of chemical signals” must be creating their own instructions.

QUOTE:: "In a paper in Physics of Life Reviews in 2013, James Shapiro describes how cells and organisms are capable of “natural genetic engineering.” That is, they frequently alter their own DNA sequences, rewriting their own genomes throughout life. The startling implication is that the gene as popularly conceived—a blueprint on a strand of DNA, determining development and its variations—does not really exist."

And let us not forget that James Shapiro believes that cells are intelligent organisms.

DAVID’s comment: We have a long way to go to really understand how the orchestrated layers of the genome works.

Yes, we do. And therefore we should at the very least remain open-minded on the subject of cellular intelligence versus automaticity.

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9029 views

DAVID: A careful article on the limits to what we understand about genes:
http://nautil.us//issue/68/context/its-the-end-of-the-gene-as-we-know-it

dhw: Once more my thanks for your integrity in presenting such articles.

QUOTE: "Scientists now understand that the information in the DNA code can only serve as a template for a protein. It cannot possibly serve as instructions for the more complex task of putting the proteins together into a fully functioning being, no more than the characters on a typewriter can produce a story.(David’s bold)

This, together with the two quotes that follow, presents an interesting contrast to two of your earlier statements: “…the original DNA may have contained all the info for evolution”. Your definition of intelligent information was “a complete set of instructions for cells to respond to all stimuli they must deal with.”

QUOTES: "Accordingly, even single cells change their metabolic pathways, and the way they use their genes to suit those patterns. That is, they “learn,” and create instructions on the hoof.” (dhw’s bold)

“Through the statistical patterns within the storms, instructions are, again, created de novo. The cells, all with the same genes, multiply into hundreds of starkly different types, moving in a glorious ballet to find just the right places at the right times. That could not have been specified in the fixed linear strings of DNA.”

dhw: I really don’t see how your definitions are compatible with the statements I have bolded.

Sloppy thinking and writing. My boldings above and below are my thoughts exactly.

QUOTE: " as the British biologist Denis Noble insists in an interview with the writer Suzan Mazur,1 “The modern synthesis has got causality in biology wrong … DNA on its own does absolutely nothing until activated by the rest of the system … DNA is not a cause in an active sense. I think it is better described as a passive data base which is used by the organism to enable it to make the proteins that it requires.” (DAVID’s bold)

dhw: If DNA is not a cause and is not a set of instructions, the cell communities of which the organism is composed and which “talk to each other with storms of chemical signals” must be creating their own instructions.

QUOTE:: "In a paper in Physics of Life Reviews in 2013, James Shapiro describes how cells and organisms are capable of “natural genetic engineering.” That is, they frequently alter their own DNA sequences, rewriting their own genomes throughout life. The startling implication is that the gene as popularly conceived—a blueprint on a strand of DNA, determining development and its variations—does not really exist."

dhw: And let us not forget that James Shapiro believes that cells are intelligent organisms.

DAVID’s comment: We have a long way to go to really understand how the orchestrated layers of the genome works.

dhw: Yes, we do. And therefore we should at the very least remain open-minded on the subject of cellular intelligence versus automaticity.

DNA codes for protein but most of the so-called junk DNA provides the modifiers for gene expression. We still don 't know how it all works. It is far more complex than we demonstrate at this point. There must be integrated levels of control. Looking at a code as simply a code doesn't see the whole picture.

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9040 views

dhw: I really don’t see how your definitions are compatible with the statements I have bolded.

DAVID: Sloppy thinking and writing. My boldings above and below are my thoughts exactly.

Just to recap: your statements were: “…the original DNA may have contained all the info for evolution”, and your definition of intelligent information was “a complete set of instructions for cells to respond to all stimuli they must deal with.”

You are now agreeing that:
QUOTE: Scientists now understand that the information in the DNA code can only serve as a template for a protein. It cannot possibly serve as instructions for the more complex task of putting the proteins together into a fully functioning being, no more than the characters on a typewriter can produce a story.

And:

DNA is not a cause in an active sense. I think it is better described as a passive data base which is used by the organism to enable it to make the proteins that it requires.

I added the following quotes:
QUOTES: "Accordingly, even single cells change their metabolic pathways, and the way they use their genes to suit those patterns. That is, they “learn,” and create instructions on the hoof.[/b]”
“Through the statistical patterns within the storms, instructions are, again, created de novo. The cells, all with the same genes, multiply into hundreds of starkly different types, moving in a glorious ballet to find just the right places at the right times. That could not have been specified in the fixed linear strings of DNA.”

I would just like to be sure that I have understood you correctly. Are you now saying that the original DNA could not have contained complete instructions for the whole of evolution, apart from when your God dabbled?

DAVID’s comment: We have a long way to go to really understand how the orchestrated layers of the genome works.

dhw: Yes, we do. And therefore we should at the very least remain open-minded on the subject of cellular intelligence versus automaticity.

DAVID: DNA codes for protein but most of the so-called junk DNA provides the modifiers for gene expression. We still don 't know how it all works. It is far more complex than we demonstrate at this point. There must be integrated levels of control. Looking at a code as simply a code doesn't see the whole picture.

Of course it doesn’t. But since you now agree that the organism (= a collection of cell communities) uses the passive data base - and perhaps you also agree that instructions are created de novo? - wouldn’t you say that one should at the very least remain open-minded on the subject of cellular intelligence versus automaticity?

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8965 views

I posted this last Tuesday, and since it has a vital bearing on your pet theory that your God preprogrammed all undabbled innovations, lifestyles and natural wonders, I was a little surprised that you didn't respond. However, you accidentally repeated the same response to another piece on "Big brain evolution", so I'm wondering if in fact you did answer my post but pressed the wrong button and are now waiting for my reply! Anyway, here it is again, just in case...

dhw: I really don’t see how your definitions are compatible with the statements I have bolded.

DAVID: Sloppy thinking and writing. My boldings above and below are my thoughts exactly.

You are now agreeing that:

QUOTE: Scientists now understand that the information in the DNA code can only serve as a template for a protein. It cannot possibly serve as instructions for the more complex task of putting the proteins together into a fully functioning being, no more than the characters on a typewriter can produce a story.

And:

DNA is not a cause in an active sense. I think it is better described as a passive data base which is used by the organism to enable it to make the proteins that it requires.

I added the following quotes:

QUOTES: "Accordingly, even single cells change their metabolic pathways, and the way they use their genes to suit those patterns. That is, they “learn,” and create instructions on the hoof.”
“Through the statistical patterns within the storms, instructions are, again, created de novo. The cells, all with the same genes, multiply into hundreds of starkly different types, moving in a glorious ballet to find just the right places at the right times. That could not have been specified in the fixed linear strings of DNA.”

I would just like to be sure that I have understood you. Are you now saying that the original DNA could not have contained complete instructions for the whole of evolution, apart from when your God dabbled?

DAVID’s comment: We have a long way to go to really understand how the orchestrated layers of the genome works.

dhw: Yes, we do. And therefore we should at the very least remain open-minded on the subject of cellular intelligence versus automaticity.

Of course it doesn’t. But since you now agree that the organism (= a collection of cell communities) uses the passive data base -and perhaps you also agree that instructions are created de novo - wouldn’t you say that one should at the very least remain open-minded on the subject of cellular intelligence versus automaticity?

Post reply

9028 views

dhw: I posted this last Tuesday, and since it has a vital bearing on your pet theory that your God preprogrammed all undabbled innovations, lifestyles and natural wonders, I was a little surprised that you didn't respond. However, you accidentally repeated the same response to another piece on "Big brain evolution", so I'm wondering if in fact you did answer my post but pressed the wrong button and are now waiting for my reply! Anyway, here it is again, just in case...

I thought we had done responses in this subject, but we shall continue

dhw: I really don’t see how your definitions are compatible with the statements I have bolded.

DAVID: Sloppy thinking and writing. My boldings above and below are my thoughts exactly.

dhw: Just to recap: your statements were: “…the original DNA may have contained all the info for evolution”, and your definition of intelligent information was “a complete set of instructions for cells to respond to all stimuli they must deal with.”

You are now agreeing that:

QUOTE: Scientists now understand that the information in the DNA code can only serve as a template for a protein. It cannot possibly serve as instructions for the more complex task of putting the proteins together into a fully functioning being, no more than the characters on a typewriter can produce a story.

And:

DNA is not a cause in an active sense. I think it is better described as a passive data base which is used by the organism to enable it to make the proteins that it requires.

I added the following quotes:

QUOTES: "Accordingly, even single cells change their metabolic pathways, and the way they use their genes to suit those patterns. That is, they “learn,” and create instructions on the hoof.”
“Through the statistical patterns within the storms, instructions are, again, created de novo. The cells, all with the same genes, multiply into hundreds of starkly different types, moving in a glorious ballet to find just the right places at the right times. That could not have been specified in the fixed linear strings of DNA.”

dhw: I would just like to be sure that I have understood you. Are you now saying that the original DNA could not have contained complete instructions for the whole of evolution, apart from when your God dabbled?

See below.

DAVID’s comment: We have a long way to go to really understand how the orchestrated layers of the genome works.

dhw: Yes, we do. And therefore we should at the very least remain open-minded on the subject of cellular intelligence versus automaticity.

DAVID: DNA codes for protein but most of the so-called junk DNA provides the modifiers for gene expression. We still don 't know how it all works. It is far more complex than we demonstrate at this point. There must be integrated levels of control. Looking at a code as simply a code doesn't see the whole picture.

dhw: Of course it doesn’t. But since you now agree that the organism (= a collection of cell communities) uses the passive data base -and perhaps you also agree that instructions are created de novo - wouldn’t you say that one should at the very least remain open-minded on the subject of cellular intelligence versus automaticity?

I'll stick to my approach that everything needed was there from the beginning, except for minor coursed-direction dabbles. All I will accept that cells do is some editing of DNA and the other somewhat unknown genome layers for minor adaptations and primarily all automatic.

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9040 views

dhw: I really don’t see how your definitions are compatible with the statements I have bolded.

DAVID: Sloppy thinking and writing. My boldings above and below are my thoughts exactly.

Here are the two bolded quotes you regard as your exact thoughts:
QUOTE: Scientists now understand that the information in the DNA code can only serve as a template for a protein. It cannot possibly serve as instructions for the more complex task of putting the proteins together into a fully functioning being, no more than the characters on a typewriter can produce a story.

And:

DNA is not a cause in an active sense. I think it is better described as a passive data base which is used by the organism to enable it to make the proteins that it requires.

I added the following quotes:
QUOTES: "Accordingly, even single cells change their metabolic pathways, and the way they use their genes to suit those patterns. That is, they “learn,” and create instructions on the hoof.”
“Through the statistical patterns within the storms, instructions are, again, created de novo. The cells, all with the same genes, multiply into hundreds of starkly different types, moving in a glorious ballet to find just the right places at the right times. That could not have been specified in the fixed linear strings of DNA.”

dhw: I would just like to be sure that I have understood you. Are you now saying that the original DNA could not have contained complete instructions for the whole of evolution, apart from when your God dabbled?

DAVID: I'll stick to my approach that everything needed was there from the beginning, except for minor coursed-direction dabbles. All I will accept that cells do is some editing of DNA and the other somewhat unknown genome layers for minor adaptations and primarily all automatic.

I’m sorry, but this is all very confusing. Firstly, your latest comment means your God dabbles the minor changes, and yet the cells edit their DNA for minor changes. Which is it? Secondly, you say “everything” - except minor changes – was there from the beginning, but apparently your exact thoughts are 1) that the DNA code cannot possibly serve as instructions to create a fully functioning being, whereas earlier you claimed that “the original DNA may have contained all the info for evolution” which meant “a complete set of instructions for cells to respond to all stimuli…”. And you have agreed 2) that DNA is a "PASSIVE data base which is used by the organism to enable it to make the proteins that it requires.” A passive data base used by the organism is absolutely not a complete set of instructions, so how can “everything needed” have been there from the beginning? At the start of this post I’ve quoted your self-deprecating comment on your own “sloppy thinking and writing”, but I’m afraid this latest post hasn’t made your thoughts any clearer.

Post reply

8979 views

dhw: I would just like to be sure that I have understood you. Are you now saying that the original DNA could not have contained complete instructions for the whole of evolution, apart from when your God dabbled?

DAVID: I'll stick to my approach that everything needed was there from the beginning, except for minor coursed-direction dabbles. All I will accept that cells do is some editing of DNA and the other somewhat unknown genome layers for minor adaptations and primarily all automatic.

dhw: I’m sorry, but this is all very confusing. Firstly, your latest comment means your God dabbles the minor changes, and yet the cells edit their DNA for minor changes. Which is it? Secondly, you say “everything” - except minor changes – was there from the beginning, but apparently your exact thoughts are 1) that the DNA code cannot possibly serve as instructions to create a fully functioning being, whereas earlier you claimed that “the original DNA may have contained all the info for evolution” which meant “a complete set of instructions for cells to respond to all stimuli…”. And you have agreed 2) that DNA is a "PASSIVE data base which is used by the organism to enable it to make the proteins that it requires.” A passive data base used by the organism is absolutely not a complete set of instructions, so how can “everything needed” have been there from the beginning? At the start of this post I’ve quoted your self-deprecating comment on your own “sloppy thinking and writing”, but I’m afraid this latest post hasn’t made your thoughts any clearer.

I'm sorry if I am confusing you, but you want theoretical exactitudes in an area of research in which we have a partial glimpse into the complexity. DNA is simply a passive code used by the entirety of the various layers of the controls in the genome. I believe many of those layers existed in first life or life would mot have happened. The stupidity is in looking at RNA as having appeared somehow and then life popped up. A code is passive!

Possibilities: 1)That first life contained everything needed then and perhaps for all
of evolution to happen either automatically or as next:
2) God used the initial genome's layers to create each big step/gap in
evolution
3) God only had to step in and make an occasional minor course correction
4) God deleted from the beginning genome and new forms appeared.

Since I believe God ran the process of evolution, it is therefore logical to create the above possibilities, from which I cannot see a defining discovery to tell us which are most possible. I think I have answered your questions.

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8966 views

dhw: I’m sorry, but this is all very confusing. Firstly, your latest comment means your God dabbles the minor changes, and yet the cells edit their DNA for minor changes. Which is it? Secondly, you say “everything” - except minor changes – was there from the beginning, but apparently your exact thoughts are 1) that the DNA code cannot possibly serve as instructions to create a fully functioning being, whereas earlier you claimed that “the original DNA may have contained all the info for evolution” which meant “a complete set of instructions for cells to respond to all stimuli…”. And you have agreed 2) that DNA is a "PASSIVE data base which is used by the organism to enable it to make the proteins that it requires.” A passive data base used by the organism is absolutely not a complete set of instructions, so how can “everything needed” have been there from the beginning? At the start of this post I’ve quoted your self-deprecating comment on your own “sloppy thinking and writing”, but I’m afraid this latest post hasn’t made your thoughts any clearer.

DAVID: I'm sorry if I am confusing you, but you want theoretical exactitudes in an area of research in which we have a partial glimpse into the complexity.

No I don’t. I want a coherent account of your beliefs, as explained above.

DAVID: DNA is simply a passive code used by the entirety of the various layers of the controls in the genome. I believe many of those layers existed in first life or life would not have happened….

So DNA never did contain a “complete set of instructions for cells to respond to.” Thank you. What do you mean by “layers of controls in the genome”? How does this differ from the cell communities having the ability to reconstruct their DNA?

DAVID: Possibilities: 1)That first life contained everything needed then and perhaps for all of evolution to happen either automatically…

Why automatically? Your “perhaps” means the first cells would have contained a complete set of instructions for every single innovation in the history of evolution (not to mention the lifestyles and natural wonders which you insist could only have been programmed or dabbled). But those instructions were not in the DNA, which is merely a passive code. So what uses the passive code in this first possibility?

DAVID …or as next:
2) God used the initial genome's layers to create each big step/gap in
evolution

Which means every big step required an individual dabble. There was never any preprogramming for evolution, but your God separately designed each innovation.

DAVID: 3) God only had to step in and make an occasional minor course correction

If your God only had to dabble minor changes, every big step was the result of instructions contained in the original cells – but not in the DNA. In that case, somewhere within the cell is a controller, but it’s not God, because God-control = dabbling, not automatic preprogramming. Implications to be seen below.

DAVID: 4) God deleted from the beginning genome and new forms appeared.

Which means the original genome contained complete instructions for all innovations – but not in the DNA – and God dabbled to remove them. One wonders why he bothered to put them all there in the first place, if he had to remove a million or so programmes every time he wanted to dabble just one. A nightmare for Ockham!

DAVID: Since I believe God ran the process of evolution, it is therefore logical to create the above possibilities, from which I cannot see a defining discovery to tell us which are most possible. I think I have answered your questions.

You have glossed over the most important question of all, as above. What do you mean by “layers of control”? In your first and third possibilities, the major innovations are preprogrammed, but God plays no part in the implementation (it’s automatic) and yet something controls the use of the passive code. In the passage you bolded as representing your exact thoughts, that “something” was the organism itself, which means the cell communities of which every organism (bar single-celled) is made. And yet, although your exact thoughts are that DNA is a passive data base which is used by the organism, nowhere in your list of alternatives do we find the possibility that your God might have designed a control system that enabled the organism (cell community) itself to use the passive code!

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9048 views

Is increasing organismal complexity associated with increasing genome complexity? This article says perhaps not:

http://nautil.us//blog/jellyfish-genome-hints-that-complexity-isnt-genetically-complex

"An overarching theme in the story of evolution, at least over the past half billion years or so, is rising complexity. There are other themes, of course, but life has undoubtedly become more complicated since its origin. Early cells globbed together to form multicellular coalitions. Those developed more complex bodies and lifestyles as the millennia passed, finding ever more varied ways to make a living. You might expect that as bodies became more complex, genomes did as well.

"But a recent study appearing in Nature Ecology & Evolution shows that not to be the case—at least for jellyfish, humble organisms that evolved at a crucial juncture in animal history. They did not need more genes—or even notably different ones—to power their giant leap in complexity. This new study adds to a growing body of work that casts doubt on finding straightforward genomic signatures of the evolution of complexity.

***

"Srivastava and Gold agree that if you tie complexity to life history, jellyfish are more complex than their cnidarian kin. But how they made this jump was unclear. “We just had no idea of what sort of genetic changes were needed to go from this more simple lifestyle to this more complex lifestyle,” said Gold. To find out, the researchers decided to sequence the genome of Aurelia, the moon jellyfish, and then compare it to those of cnidarians without medusas.

"If a radical shift in life history requires a big boost in gene content, the Aurelia genome should be riddled with novel genes unique to jellyfish. Instead, Gold found that, broadly speaking, “there really isn’t a whole lot of difference between Aurelia and their relatives with simpler lifestyles.” There were some new genes, but no more than you might expect from any distinct group.

***

"Gold thought that genes unique to jellyfish would be active during the transformation from polyp to medusa.

"But to his surprise, that’s not what he found. New genes unique to jellyfish were no more likely to be expressed in the medusa stage, or any stage of development, than other, older genes were. “At the broad genetic level, it doesn’t seem like you need major changes in the genome to make these big changes in your life history,” Gold said.

***

“'It’s not that surprising that the jellyfish didn’t just invent a whole bunch of new genes to make a medusa stage,” said Srivastava, “but we don’t know until we look.” She was intrigued by the finding that novel genes weren’t overrepresented in the medusa stage because it suggests that “very different body plans can arise by connecting the same genes in different ways.”

"In any case, for now, the genetic changes that orchestrate this metamorphosis in jellyfish remain unknown. The transformation may depend on regions of the genome that don’t encode proteins, but instead regulate when genes are turned on and off. Perhaps it’s easier for life to innovate by rearranging its existing gene networks instead of evolving scores of new genes. Or perhaps the broad first pass at the genomes simply missed a handful of coding genes that play an outsized role in the process.

"The Aurelia genome joins a growing number of studies that complicate our view of complexity. When scientists began comparing the genes and genomes of different branches of the tree of life, they expected to find vast differences, but instead discovered remarkable similarity. For example, humans and cats share about 90 percent of our genes; we share nearly two-thirds of our genome with fruit flies, despite being separated for approximately 800 million years.

"Even the earliest animal lineages harbor unexpected complexities. When Srivastava and colleagues sequenced the first sponge genome in 2010, they were stunned to find genes that built the brains and muscles of other animals already present in this brainless, muscleless sponge. “The genes are the same, but clearly they aren’t working together to do the same things,” she said.

***

“'I can give you a list of genes that seem to be associated with an increase in complexity,” Srivastava said, “but at some level that’s not very powerful information. It can’t explain why a human looks like a human and a sponge looks like a sponge.'”

Comment: Any metamorphosing species fits this idea that it mimics speciation. Studies like this one support my contention that the first DNA might have contained all the information needed for all stages of evolution to occur, but rearranging genes and by alternate expression of genes, known processes. What we don't know is that there has to be a layer of control to make these decisions and we don't see that natural layer at this point. Could this be God making the decisions which is my theory?

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DAVID: I'm sorry if I am confusing you, but you want theoretical exactitudes in an area of research in which we have a partial glimpse into the complexity.

No I don’t. I want a coherent account of your beliefs, as explained above.

DAVID: DNA is simply a passive code used by the entirety of the various layers of the controls in the genome. I believe many of those layers existed in first life or life would not have happened….

dhw: So DNA never did contain a “complete set of instructions for cells to respond to.” Thank you. What do you mean by “layers of controls in the genome”? How does this differ from the cell communities having the ability to reconstruct their DNA?

See my entry today in this string about metamorphosis and speciation. DNA is a basic code but obviously does not contain the way life evolves. Other layers cause slicing and dicing to make genes do differing things, or transform gene expression in other ways to create different outcomes. We see it happening but still have not uncovered a primary control mechanism, just as we don't know how genes exert their outcomes.

DAVID: Possibilities: 1)That first life contained everything needed then and perhaps for all of evolution to happen either automatically…

dhw: Why automatically? Your “perhaps” means the first cells would have contained a complete set of instructions for every single innovation in the history of evolution (not to mention the lifestyles and natural wonders which you insist could only have been programmed or dabbled). But those instructions were not in the DNA, which is merely a passive code. So what uses the passive code in this first possibility?

I have said in the new entry and at other times we don't really know those layers, which could simply be God acting, or are acting in ways we will find following information God implanted. There have to be other ways of control, and I've used the term 'layers' to describe them. Like a corporate diagram of a business.

DAVID …or as next:
2) God used the initial genome's layers to create each big step/gap in
evolution

dhw: Which means every big step required an individual dabble. There was never any preprogramming for evolution, but your God separately designed each innovation.

DAVID: 3) God only had to step in and make an occasional minor course correction

dhw: If your God only had to dabble minor changes, every big step was the result of instructions contained in the original cells – but not in the DNA. In that case, somewhere within the cell is a controller, but it’s not God, because God-control = dabbling, not automatic preprogramming. Implications to be seen below.

DAVID: 4) God deleted from the beginning genome and new forms appeared.

dhw: Which means the original genome contained complete instructions for all innovations – but not in the DNA – and God dabbled to remove them. One wonders why he bothered to put them all there in the first place, if he had to remove a million or so programmes every time he wanted to dabble just one. A nightmare for Ockham!

Back to Behe and elimination.

DAVID: Since I believe God ran the process of evolution, it is therefore logical to create the above possibilities, from which I cannot see a defining discovery to tell us which are most possible. I think I have answered your questions.

dhw: You have glossed over the most important question of all, as above. What do you mean by “layers of control”? In your first and third possibilities, the major innovations are preprogrammed, but God plays no part in the implementation (it’s automatic) and yet something controls the use of the passive code. In the passage you bolded as representing your exact thoughts, that “something” was the organism itself, which means the cell communities of which every organism (bar single-celled) is made. And yet, although your exact thoughts are that DNA is a passive data base which is used by the organism, nowhere in your list of alternatives do we find the possibility that your God might have designed a control system that enabled the organism (cell community) itself to use the passive code!

I've always admitted that an 'inventive mechanism' is possible. but you won't accept it as under God's developmental guidelines. Without those guiding principals evolution could proceed helter-skelter.

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DAVID: Is increasing organismal complexity associated with increasing genome complexity? This article says perhaps not:
http://nautil.us//blog/jellyfish-genome-hints-that-complexity-isnt-genetically-complex

QUOTE: “Early cells globbed together to form multicellular coalitions. Those developed more complex bodies and lifestyles as the millennia passed, finding ever more varied ways to make a living.”

Please note in passing that “to make a living” means to survive.

QUOTES: “At the broad genetic level, it doesn’t seem like you need major changes in the genome to make these big changes in your life history...”

“Perhaps it’s easier for life to innovate by rearranging its existing gene networks instead of evolving scores of new genes.”

Life doesn’t innovate. Living organisms innovate, and living organisms are composed of cells. The implication here seems to be that innovation is not the giant step we have imagined it to be, but is more simply a matter of cell communities rearranging themselves.

DAVID’s comment: Any metamorphosing species fits this idea that it mimics speciation. Studies like this one support my contention that the first DNA might have contained all the information needed for all stages of evolution to occur, but rearranging genes and by alternate expression of genes, known processes. What we don't know is that there has to be a layer of control to make these decisions and we don't see that natural layer at this point. Could this be God making the decisions which is my theory?

When I asked you to define what you called the “intelligent information” in the DNA, you said it was "a complete set of instructions for cells to respond to all stimuli.” You have now agreed that DNA is a passive code, and so cannot be a complete list of instructions. Now you slide back to your woolly use of “information”, so perhaps you’d better give us a new definition. Meanwhile, you also revert to your nebulous “layer of control” to make the decisions. So now what is your theory? That your God is sitting inside every cell? If not, you are back to your preprogramming, which means your complete list of instructions. Or God constantly popping in to dabble with all the individual cell communities. Why can’t you at least countenance the possibility that the layer of control is cellular, decision-making intelligence, possibly designed by your God? Most of your remaining comments deal with this same point, so I’ll only cover those that are different.

DAVID: 4) God deleted from the beginning genome and new forms appeared.

dhw: Which means the original genome contained complete instructions for all innovations – but not in the DNA – and God dabbled to remove them. One wonders why he bothered to put them all there in the first place, if he had to remove a million or so programmes every time he wanted to dabble just one. A nightmare for Ockham!

DAVID: Back to Behe and elimination.

You've included this in your list of possibilities, so please explain why you think your God might have used a method that would entail removing millions of his specially designed programmes each time he wanted to implement one.

Dhw: And yet, although your exact thoughts are that DNA is a passive data base which is used by the organism, nowhere in your list of alternatives do we find the possibility that your God might have designed a control system that enabled the organism (cell community) itself to use the passive code!

DAVID: I've always admitted that an 'inventive mechanism' is possible. but you won't accept it as under God's developmental guidelines. Without those guiding principals evolution could proceed helter-skelter.

Your developmental guidelines have always turned out to be instructions, and that is not what I mean by an AUTONOMOUS inventive mechanism. “Helter-skelter” is precisely what I see (though that does not in any way preclude the possibility that there is a God who deliberately designed the helter-skelter), with millions and millions of life forms, lifestyles and natural wonders coming and going as the bush diversifies. But you see all these millions of life forms etc. as having been specially designed to eat one another so that life could survive for 3.5+ billion years (although apparently survival played no role in evolution) until your fully-in-control God could specially design the only thing he wanted to design.

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dhw: Please note in passing that “to make a living” means to survive.

Organisms are designed to survive or evolution can't continue.

DAVID’s comment: Any metamorphosing species fits this idea that it mimics speciation. Studies like this one support my contention that the first DNA might have contained all the information needed for all stages of evolution to occur, but rearranging genes and by alternate expression of genes, known processes. What we don't know is that there has to be a layer of control to make these decisions and we don't see that natural layer at this point. Could this be God making the decisions which is my theory?

dhw: When I asked you to define what you called the “intelligent information” in the DNA, you said it was "a complete set of instructions for cells to respond to all stimuli.” You have now agreed that DNA is a passive code, and so cannot be a complete list of instructions. Now you slide back to your woolly use of “information”, so perhaps you’d better give us a new definition.

I might ask whether you think DNA is a code which contains information for protein formation? DNA has also has areas of differing modifying factors, which is information of a different kind. My changing views come from new research as it appears.

dhw: Meanwhile, you also revert to your nebulous “layer of control” to make the decisions. So now what is your theory? That your God is sitting inside every cell? If not, you are back to your preprogramming, which means your complete list of instructions. Or God constantly popping in to dabble with all the individual cell communities. Why can’t you at least countenance the possibility that the layer of control is cellular, decision-making intelligence, possibly designed by your God?

If it is accepted that God is in control of evolution, as I do, the cells make adaptations within His limits.

DAVID: 4) God deleted from the beginning genome and new forms appeared.

dhw: Which means the original genome contained complete instructions for all innovations – but not in the DNA – and God dabbled to remove them. One wonders why he bothered to put them all there in the first place, if he had to remove a million or so programmes every time he wanted to dabble just one. A nightmare for Ockham!

DAVID: Back to Behe and elimination.

dhw: You've included this in your list of possibilities, so please explain why you think your God might have used a method that would entail removing millions of his specially designed programmes each time he wanted to implement one.

Behe explains that small alterations in DNA can make evolutionary advances. You assume large.

Dhw: And yet, although your exact thoughts are that DNA is a passive data base which is used by the organism, nowhere in your list of alternatives do we find the possibility that your God might have designed a control system that enabled the organism (cell community) itself to use the passive code!

DAVID: I've always admitted that an 'inventive mechanism' is possible. but you won't accept it as under God's developmental guidelines. Without those guiding principals evolution could proceed helter-skelter.

dhw: Your developmental guidelines have always turned out to be instructions, and that is not what I mean by an AUTONOMOUS inventive mechanism. “Helter-skelter” is precisely what I see (though that does not in any way preclude the possibility that there is a God who deliberately designed the helter-skelter), with millions and millions of life forms, lifestyles and natural wonders coming and going as the bush diversifies. But you see all these millions of life forms etc. as having been specially designed to eat one another so that life could survive for 3.5+ billion years (although apparently survival played no role in evolution) until your fully-in-control God could specially design the only thing he wanted to design.

Distortion of the survival issue as usual. Survival is built in to each advanced form or evolution would grind to a halt.

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DAVID’s comment: Studies like this one support my contention that the first DNA might have contained all the information needed for all stages of evolution to occur, but rearranging genes and by alternate expression of genes, known processes. What we don't know is that there has to be a layer of control to make these decisions and we don't see that natural layer at this point. Could this be God making the decisions which is my theory?

dhw: When I asked you to define what you called the “intelligent information” in the DNA, you said it was "a complete set of instructions for cells to respond to all stimuli.” You have now agreed that DNA is a passive code, and so cannot be a complete list of instructions. Now you slide back to your woolly use of “information”, so perhaps you’d better give us a new definition.

DAVID: I might ask whether you think DNA is a code which contains information for protein formation? DNA has also has areas of differing modifying factors, which is information of a different kind. My changing views come from new research as it appears.

I trust your judgement when you say the article expresses your thoughts exactly: i.e. DNA is a passive data base which has to be used by the organism to make new proteins. You appear to have withdrawn your definition of information as instructions, but you still haven’t redefined it. I understand it as meaning facts or details about a particular subject. It cannot do anything, but has to be used. In this post you claim again that the first DNA might have contained all the information needed for all stages of evolution. I don’t understand how 3.8 billion years ago the first DNA could have contained all the facts and details about every future innovation, lifestyle and natural wonder in the history of evolution. The article states that cells learn “on the hoof”, and create instructions de novo. Sounds convincing to me.

dhw: Meanwhile, you also revert to your nebulous “layer of control” to make the decisions. […] Why can’t you at least countenance the possibility that the layer of control is cellular, decision-making intelligence, possibly designed by your God?
DAVID: If it is accepted that God is in control of evolution, as I do, the cells make adaptations within His limits.

We have discussed the “limits”, and you could only come up with restrictions imposed by the environment and by the capabilities of the cells themselves. Now please explain what you mean by a “layer of control” if it does not mean your God sitting in every cell, or preprogramming every development with a 3.8 byo list of instructions, or dabbling every individual innovation, lifestyle and natural wonder.

DAVID: 4) God deleted from the beginning genome and new forms appeared.

dhw: You've included this in your list of possibilities, so please explain why you think your God might have used a method that would entail removing millions of his specially designed programmes each time he wanted to implement one.

DAVID: Behe explains that small alterations in DNA can make evolutionary advances. You assume large.

Small alterations do not mean God removing 99% of his 3.8 byo programmes in order to produce one new species (= “new form”). Speciation implies large changes, but the second article suggested that these can result from small adjustments to the genome – which implies that innovation might not be the large-scale operation you like to emphasize in your argument concerning the gaps in the fossil record.

Dhw: […] nowhere in your list of alternatives do we find the possibility that your God might have designed a control system that enabled the organism (cell community) itself to use the passive code!

DAVID: I've always admitted that an 'inventive mechanism' is possible. but you won't accept it as under God's developmental guidelines. Without those guiding principals evolution could proceed helter-skelter.

dhw: Your developmental guidelines have always turned out to be instructions, and that is not what I mean by an AUTONOMOUS inventive mechanism. “Helter-skelter” is precisely what I see (though that does not in any way preclude the possibility that there is a God who deliberately designed the helter-skelter), with millions and millions of life forms, lifestyles and natural wonders coming and going as the bush diversifies. But you see all these millions of life forms etc. as having been specially designed to eat one another so that life could survive for 3.5+ billion years (although apparently survival played no role in evolution) until your fully-in-control God could specially design the only thing he wanted to design.

DAVID: Distortion of the survival issue as usual. Survival is built in to each advanced form or evolution would grind to a halt.

Sorry you choose only to pick on the parenthesis concerning survival, which is dealt with under “Little Foot”.

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DAVID: I might ask whether you think DNA is a code which contains information for protein formation? DNA has also has areas of differing modifying factors, which is information of a different kind. My changing views come from new research as it appears.

dhw: I trust your judgement when you say the article expresses your thoughts exactly: i.e. DNA is a passive data base which has to be used by the organism to make new proteins. You appear to have withdrawn your definition of information as instructions, but you still haven’t redefined it. I understand it as meaning facts or details about a particular subject. It cannot do anything, but has to be used.

You have followed instructions in learning how to use a new machine, your computer for
instance. Life emerges from a very complex set of biochemical reactions. Shapiro tells us that the cells in all of this massive activity can modify their genome to alter their function. This implies that the instructions for life are used and malleable. You appear to approach information as descriptive, but in life it is a central active component which makes life emerge.

DAVID: If it is accepted that God is in control of evolution, as I do, the cells make adaptations within His limits.[/i]

dhw: We have discussed the “limits”, and you could only come up with restrictions imposed by the environment and by the capabilities of the cells themselves. Now please explain what you mean by a “layer of control”

It is a concept. Just as you have an idea that cells contain their own inventive mechanism (IM) I can see it existing with God-imposed limits to the degree of modification,

DAVID: Behe explains that small alterations in DNA can make evolutionary advances. You assume large.

dhw: Small alterations do not mean God removing 99% of his 3.8 byo programmes in order to produce one new species (= “new form”).

Strange response. Loss of 99% of species in no way implies 99% of the original DNA is lost. For example genes are only 2-4% of human DNA with the rest containing modifiers. Advances do require deletions per Behe, but also rearrangements. Our DNA with 3.3 billion bases has lots of room to do this.

dhw: Your developmental guidelines have always turned out to be instructions, and that is not what I mean by an AUTONOMOUS inventive mechanism. “Helter-skelter” is precisely what I see (though that does not in any way preclude the possibility that there is a God who deliberately designed the helter-skelter), with millions and millions of life forms, lifestyles and natural wonders coming and going as the bush diversifies. But you see all these millions of life forms etc. as having been specially designed to eat one another so that life could survive for 3.5+ billion years (although apparently survival played no role in evolution) until your fully-in-control God could specially design the only thing he wanted to design.

DAVID: Distortion of the survival issue as usual. Survival is built in to each advanced form or evolution would grind to a halt.

dhw: Sorry you choose only to pick on the parenthesis concerning survival, which is dealt with under “Little Foot”.

I saw nothing to respond to besides survival. You made your usual attempt to interpret the bush of life as something God produced but offered none of your humanizing reasons for God doing it. My idea that it is for food fits the facts of natures balance each ecosystem with its top predator.

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dhw: You appear to have withdrawn your definition of information as instructions, but you still haven’t redefined it. I understand it as meaning facts or details about a particular subject. It cannot do anything, but has to be used.

DAVID: You have followed instructions in learning how to use a new machine, your computer for instance.

I can’t follow your analogy. We’re dealing with the invention of the machine (the "fully functioning being" or species) not how the invention is to be used! You have told us the article is an exact expression of your thoughts, and the article quite specifically states that the DNA code is a passive data base (= passive information) “cannot possibly serve as instructions”, cells “learn” and “create instructions on the hoof” and create instructions “de novo”. Now you’ve reverted to your belief that information means instructions, and lower down (bolded) you will tell us it is active.

DAVID: Life emerges from a very complex set of biochemical reactions.

Of course. That does not mean that the first DNA contained “a complete list of instructions for cells to respond to all stimuli”.

DAVID: Shapiro tells us that the cells in all of this massive activity can modify their genome to alter their function. This implies that the instructions for life are used and malleable. You appear to approach information as descriptive, but in life it is a central active component which makes life emerge.

And Shapiro tells us that cells are sentient, intelligent, decision-making beings, and anyone who thinks otherwise is guilty of “large organisms chauvinism”. Intelligent modification of the genome does not imply using existing instructions, and according to the article which expressed your thoughts exactly, the information in the code is a passive data base which “cannot possibly serve as instructions” etc. – as quoted above. Also we are talking about evolution. Life emerging = the first cells, which one day apparently contain all the instructions for every innovation, lifestyle and natural wonder in the history of life, the next day they don’t, and now they do again.

DAVID: If it is accepted that God is in control of evolution, as I do, the cells make adaptations within His limits.

dhw: We have discussed the “limits”, and you could only come up with restrictions imposed by the environment and by the capabilities of the cells themselves. Now please explain what you mean by a “layer of control”

DAVID: It is a concept. Just as you have an idea that cells contain their own inventive mechanism (IM) I can see it existing with God-imposed limits to the degree of modification.

And apart from limits imposed by the environment and by their own capabilities, what “limits” do you see?

DAVID: Behe explains that small alterations in DNA can make evolutionary advances. You assume large.

dhw: Small alterations do not mean God removing 99% of his 3.8 byo programmes in order to produce one new species (= “new form”).

DAVID: Strange response. Loss of 99% of species in no way implies 99% of the original DNA is lost. For example genes are only 2-4% of human DNA with the rest containing modifiers. Advances do require deletions per Behe, but also rearrangements. Our DNA with 3.3 billion bases has lots of room to do this.

I didn’t say 99% of the DNA was lost! According to this theory, your God implanted instructions (programmes) in the DNA for every future species. And so for each new species, all the other instructions/programmes had to be deleted. It’s you and Behe who are promoting the idea of deletion, so what exactly do you think is deleted if not your instructions/programmes? In passing, I don’t like the word “advances” on its own. I don’t regard whale fins as an advance on pre-whale legs, or toothlessness/baleens as an advance on teeth, but I do accept your own contention that evolution is a bush and not a tree. The higgledy-piggledy bush of evolution sprawls outwards (not an advance) as well as upwards. And yes, our DNA has lots of room for rearrangements, and the articles suggest that only small rearrangements are necessary for large changes, but if DNA is a passive data base, it is the active organisms (comprising cell communities) that use the passive information.

dhw: Sorry you choose only to pick on the parenthesis concerning survival, which is dealt with under “Little Foot”.

DAVID: I saw nothing to respond to besides survival. You made your usual attempt to interpret the bush of life as something God produced but offered none of your humanizing reasons for God doing it. My idea that it is for food fits the facts of natures balance each ecosystem with its top predator.

On the subject of survival, see “Little Foot” again. Your idea is that your always-in-control God specially designed a bush of food to fill in 3.5+ billion years of life until he could specially design the only thing he wanted to design. I suggest that the helter-skelter bush is the result of him wishing to create a helter-skelter bush. We needn’t go into the “humanizing” reasons we both hypothesize.

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dhw: I can’t follow your analogy. We’re dealing with the invention of the machine (the "fully functioning being" or species) not how the invention is to be used! You have told us the article is an exact expression of your thoughts, and the article quite specifically states that the DNA code is a passive data base (= passive information) “cannot possibly serve as instructions”, cells “learn” and “create instructions on the hoof” and create instructions “de novo”. Now you’ve reverted to your belief that information means instructions, and lower down (bolded) you will tell us it is active.

Very simply information can do both, supply instruction for new speciation and how it should react to challenges. DNA is just the code level of protein production. There must be other levels of the genome to contain that function, and some may be hidden in the vast size of DNA inthe non-coding regions (96-98%).

DAVID: Shapiro tells us that the cells in all of this massive activity can modify their genome to alter their function. This implies that the instructions for life are used and malleable. You appear to approach information as descriptive, but in life it is a central active component which makes life emerge.

dhw: And Shapiro tells us that cells are sentient, intelligent, decision-making beings, and anyone who thinks otherwise is guilty of “large organisms chauvinism”.

Shapiro studied bacteria which he interpreted as having a read/write control over their DNA. There is no way he could tell if this was independent activity or acting under response instructions.

DAVID: It is a concept. Just as you have an idea that cells contain their own inventive mechanism (IM) I can see it existing with God-imposed limits to the degree of modification.

dhw: And apart from limits imposed by the environment and by their own capabilities, what “limits” do you see?

They cannot speciate themselves into a new form

dhw: In passing, I don’t like the word “advances” on its own. I don’t regard whale fins as an advance on pre-whale legs, or toothlessness/baleens as an advance on teeth, but I do accept your own contention that evolution is a bush and not a tree. The higgledy-piggledy bush of evolution sprawls outwards (not an advance) as well as upwards. And yes, our DNA has lots of room for rearrangements, and the articles suggest that only small rearrangements are necessary for large changes, but if DNA is a passive data base, it is the active organisms (comprising cell communities) that use the passive information.

Your invention of cell communities does not prove there is any evidence of cells having any ability to communicate new design plans for advancing modification or speciation. Your entire idea is based on the tenuous conclusion Shapiro made after studies of single cell bacteria which can do specific gene transfer for specific purposes like antibacterial resistance..

dhw: Sorry you choose only to pick on the parenthesis concerning survival, which is dealt with under “Little Foot”.

DAVID: I saw nothing to respond to besides survival. You made your usual attempt to interpret the bush of life as something God produced but offered none of your humanizing reasons for God doing it. My idea that it is for food fits the facts of natures balance each ecosystem with its top predator.

dhw: On the subject of survival, see “Little Foot” again. Your idea is that your always-in-control God specially designed a bush of food to fill in 3.5+ billion years of life until he could specially design the only thing he wanted to design. I suggest that the helter-skelter bush is the result of him wishing to create a helter-skelter bush. We needn’t go into the “humanizing” reasons we both hypothesize.

But all you have done is look for humanizing reasons. There is no reason for humans with consciousness to appear unless God desired that result of evolution.

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dhw: I can’t follow your analogy. We’re dealing with the invention of the machine (the "fully functioning being" or species) not how the invention is to be used! You have told us the article is an exact expression of your thoughts, and the article quite specifically states that the DNA code is a passive data base (= passive information) “cannot possibly serve as instructions”, cells “learn” and “create instructions on the hoof” and create instructions “de novo”. Now you’ve reverted to your belief that information means instructions, and lower down (bolded) you will tell us it is active.

DAVID: Very simply information can do both, supply instruction for new speciation and how it should react to challenges. DNA is just the code level of protein production. There must be other levels of the genome to contain that function, and some may be hidden in the vast size of DNA inthe non-coding regions (96-98%).

So you agree with the article that DNA is a passive data base which cannot possibly serve as instructions for “putting proteins together into a fully functioning being”, but all the same DNA might contain the instructions. If it doesn’t, the instructions are hidden somewhere in the genome. And “very simply”, information (active – see below) can use information (passive), although the article with which you agree specifies that cells use their genes, the organism uses the information, and cells “learn” and “create instructions on the hoof”. I can’t find any reference to information using information.

dhw: And Shapiro tells us that cells are sentient, intelligent, decision-making beings, and anyone who thinks otherwise is guilty of “large organisms chauvinism”.

DAVID: Shapiro studied bacteria which he interpreted as having a read/write control over their DNA. There is no way he could tell if this was independent activity or acting under response instructions.

And there is no way you can tell either, but you insist that Shapiro (not to mention Margulis, McClintock, Buehler et al) doesn’t know what he’s talking about. Why not keep an open mind if neither of you can possibly know the truth?

DAVID: It is a concept. Just as you have an idea that cells contain their own inventive mechanism (IM) I can see it existing with God-imposed limits to the degree of modification.

dhw: And apart from limits imposed by the environment and by their own capabilities, what “limits” do you see?

DAVID: They cannot speciate themselves into a new form.

That is the subject of the debate, and is your fixed belief to which I am offering an alternative!

dhw: In passing, I don’t like the word “advances” on its own. I don’t regard whale fins as an advance on pre-whale legs, or toothlessness/baleens as an advance on teeth, but I do accept your own contention that evolution is a bush and not a tree. The higgledy-piggledy bush of evolution sprawls outwards (not an advance) as well as upwards. And yes, our DNA has lots of room for rearrangements, and the articles suggest that only small rearrangements are necessary for large changes, but if DNA is a passive data base, it is the active organisms (comprising cell communities) that use the passive information.

DAVID: Your invention of cell communities does not prove there is any evidence of cells having any ability to communicate new design plans for advancing modification or speciation. Your entire idea is based on the tenuous conclusion Shapiro made after studies of single cell bacteria which can do specific gene transfer for specific purposes like antibacterial resistance.

"Invention of cell communities? What do you think your organs consist of, if not cells cooperating with one another? What does your body consist of, if not organs (cell communities) communicating with one another? Come on, Dr David, cell communities are not my “invention”. But I don’t know how often you want me to repeat that we don’t know whether their intelligence can extend to innovation, which is why my idea remains an unproven hypothesis, just as your divine 3.8 byo computer programme for all innovations and your divine dabbling remain unproven hypotheses.

On the subject of “humanizing”, see the post under “Little Foot”.

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DAVID: Very simply information can do both, supply instruction for new speciation and how it should react to challenges. DNA is just the code level of protein production. There must be other levels of the genome to contain that function, and some may be hidden in the vast size of DNA in the non-coding regions (96-98%).

dhw: So you agree with the article that DNA is a passive data base which cannot possibly serve as instructions for “putting proteins together into a fully functioning being”, but all the same DNA might contain the instructions. If it doesn’t, the instructions are hidden somewhere in the genome. And “very simply”, information (active – see below) can use information (passive), although the article with which you agree specifies that cells use their genes, the organism uses the information, and cells “learn” and “create instructions on the hoof”. I can’t find any reference to information using information.

Information is instructions as to how to respond. Information is not active in and of itself, but is reference material which can be used to create actions.

DAVID: Shapiro studied bacteria which he interpreted as having a read/write control over their DNA. There is no way he could tell if this was independent activity or acting under response instructions.

dhw: And there is no way you can tell either, but you insist that Shapiro (not to mention Margulis, McClintock, Buehler et al) doesn’t know what he’s talking about. Why not keep an open mind if neither of you can possibly know the truth?

All reactions in the cell are always shown to be molecules acting on molecules automatically. Anything else is presumption as to underlying controls, which may well be automatic as all our organs show.>

dhw: In passing, I don’t like the word “advances” on its own. I don’t regard whale fins as an advance on pre-whale legs, or toothlessness/baleens as an advance on teeth, but I do accept your own contention that evolution is a bush and not a tree. The higgledy-piggledy bush of evolution sprawls outwards (not an advance) as well as upwards. And yes, our DNA has lots of room for rearrangements, and the articles suggest that only small rearrangements are necessary for large changes, but if DNA is a passive data base, it is the active organisms (comprising cell communities) that use the passive information.

Agreed, but I view the advance of evolution from simple to complex as advancing. Whatever jumped into the water and started the whale series advanced their form into an aquatic mammalian form. 'Advance' means forward in time and form. I view evolution as containing the arrow of time in one direction.

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dhw: So you agree with the article that DNA is a passive data base which cannot possibly serve as instructions for “putting proteins together into a fully functioning being”, but all the same DNA might contain the instructions. If it doesn’t, the instructions are hidden somewhere in the genome. And “very simply”, information (active – see below) can use information (passive), although the article with which you agree specifies that cells use their genes, the organism uses the information, and cells “learn” and “create instructions on the hoof”. I can’t find any reference to information using information.

DAVID: Information is instructions as to how to respond. Information is not active in and of itself, but is reference material which can be used to create actions.

Your second sentence is precisely what I keep saying, so we can now dismiss your earlier statement that information is a “central active component”. The article you agreed with states that “the information in the DNA code “cannot possibly serve as instructions” for creating a “fully functioning being”, and that “cells “learn” and “create instructions on the hoof” and create them “de novo”. It also tells us that information (= passive “reference material”) is used by the organism, and organisms are communities of cells. We are left, then, with the hypothesis that cells use passive information to create actions. This doesn’t sound to me like the first DNA containing “a complete list of instructions for cells to respond to all stimuli”.

DAVID: Shapiro studied bacteria which he interpreted as having a read/write control over their DNA. There is no way he could tell if this was independent activity or acting under response instructions.

dhw: And there is no way you can tell either, but you insist that Shapiro (not to mention Margulis, McClintock, Buehler et al) doesn’t know what he’s talking about. Why not keep an open mind if neither of you can possibly know the truth?

DAVID: All reactions in the cell are always shown to be molecules acting on molecules automatically. Anything else is presumption as to underlying controls, which may well be automatic as all our organs show.

“May well be automatic” = your 50%, and may well be intelligent = Shapiro’s 50%, so why not keep an open mind?

DAVID: Agreed, but I view the advance of evolution from simple to complex as advancing. Whatever jumped into the water and started the whale series advanced their form into an aquatic mammalian form. 'Advance' means forward in time and form. I view evolution as containing the arrow of time in one direction.

All change involves the arrow of time, since what changes follows on from what went before. This is a complete cop-out. Things can change from bad to worse, and do you then call them an “advance”? Of course you don’t. Do you believe that aquatic life is an advance on terrestrial life, or vice versa? Of course you don’t. They're simply different.

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DAVID: Information is instructions as to how to respond. Information is not active in and of itself, but is reference material which can be used to create actions.

dhw: Your second sentence is precisely what I keep saying, so we can now dismiss your earlier statement that information is a “central active component”. The article you agreed with states that “the information in the DNA code “cannot possibly serve as instructions” for creating a “fully functioning being”, and that “cells “learn” and “create instructions on the hoof” and create them “de novo”. It also tells us that information (= passive “reference material”) is used by the organism, and organisms are communities of cells. We are left, then, with the hypothesis that cells use passive information to create actions.

See my entry today about Davies' news book on information and life. "Comment: Information is either descriptive or provide instructions for functions. ID has always pointed to the latter as very important. Davies is joining in." The information just lying there is inactive, of course, but he cells are totally aware of it and use it in various required actions.

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DAVID: Information is instructions as to how to respond. Information is not active in and of itself, but is reference material which can be used to create actions.

dhw: Your second sentence is precisely what I keep saying, so we can now dismiss your earlier statement that information is a “central active component”. The article you agreed with states that “the information in the DNA code “cannot possibly serve as instructions” for creating a “fully functioning being”, and that “cells “learn” and “create instructions on the hoof” and create them “de novo”. It also tells us that information (= passive “reference material”) is used by the organism, and organisms are communities of cells. We are left, then, with the hypothesis that cells use passive information to create actions.

DAVID: See my entry today about Davies' news book on information and life. "Comment: Information is either descriptive or provide instructions for functions. ID has always pointed to the latter as very important. Davies is joining in." The information just lying there is inactive, of course, but the cells are totally aware of it and use it in various required actions.

There is no mention of instructions in Davies’s article, and you have already agreed with the previous article that passive information cannot serve as instructions, and cells create instructions “on the hoof”. Your last sentence sums up the hypothesis I have been trying to put to you for the last few years. Cells are aware and they actively use passive information to decide what actions to perform. Thank you for putting it so succinctly.

QUOTE from Davies: The resolution to this paradox seems to lie in the fact that the demon must gather information about the properties of each molecule, and for this it requires a recording device, such as a brain or a miniature notebook.

In our context, the “demon” would therefore be that part of the cell which is the equivalent of a brain.

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DAVID: Information is instructions as to how to respond. Information is not active in and of itself, but is reference material which can be used to create actions.

dhw: Your second sentence is precisely what I keep saying, so we can now dismiss your earlier statement that information is a “central active component”. The article you agreed with states that “the information in the DNA code “cannot possibly serve as instructions” for creating a “fully functioning being”, and that “cells “learn” and “create instructions on the hoof” and create them “de novo”. It also tells us that information (= passive “reference material”) is used by the organism, and organisms are communities of cells. We are left, then, with the hypothesis that cells use passive information to create actions.

DAVID: See my entry today about Davies' news book on information and life. "Comment: Information is either descriptive or provide instructions for functions. ID has always pointed to the latter as very important. Davies is joining in." The information just lying there is inactive, of course, but the cells are totally aware of it and use it in various required actions.

dhw: There is no mention of instructions in Davies’s article, and you have already agreed with the previous article that passive information cannot serve as instructions, and cells create instructions “on the hoof”. Your last sentence sums up the hypothesis I have been trying to put to you for the last few years. Cells are aware and they actively use passive information to decide what actions to perform. Thank you for putting it so succinctly.

QUOTE from Davies: The resolution to this paradox seems to lie in the fact that the demon must gather information about the properties of each molecule, and for this it requires a recording device, such as a brain or a miniature notebook.

In our context, the “demon” would therefore be that part of the cell which is the equivalent of a brain.

It is all in the interpretation. If the cells are programmed to review instructional information and follow algorithms of necessary choices, it can all be automatic. Taht is still my position.

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DAVID: Information is instructions as to how to respond. Information is not active in and of itself, but is reference material which can be used to create actions.

dhw: Your second sentence is precisely what I keep saying, so we can now dismiss your earlier statement that information is a “central active component”. The article you agreed with states that “the information in the DNA code “cannot possibly serve as instructions” for creating a “fully functioning being”, and that “cells “learn” and “create instructions on the hoof” and create them “de novo”. It also tells us that information (= passive “reference material”) is used by the organism, and organisms are communities of cells. We are left, then, with the hypothesis that cells use passive information to create actions.

DAVID: The information just lying there is inactive, of course, but the cells are totally aware of it and use it in various required actions.

dhw: Your last sentence sums up the hypothesis I have been trying to put to you for the last few years. Cells are aware and they actively use passive information to decide what actions to perform. Thank you for putting it so succinctly.

dhw: In our context, the “demon” would therefore be that part of the cell which is the equivalent of a brain.

DAVID: It is all in the interpretation. If the cells are programmed to review instructional information and follow algorithms of necessary choices, it can all be automatic. That is still my position.

So your interpretation, just to sum up all the bolded statements above, is that information is passive reference material and cannot serve as instructions, and the cells are totally aware of it and use it in performing their actions. However, (latest statement) the information does contain instructions and cells are not aware of them but are programmed to follow them in performing their actions. I suspect I am not alone in finding these two sets of statements confusing.

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DAVID: Information is instructions as to how to respond. Information is not active in and of itself, but is reference material which can be used to create actions.

dhw: Your second sentence is precisely what I keep saying, so we can now dismiss your earlier statement that information is a “central active component”. The article you agreed with states that “the information in the DNA code “cannot possibly serve as instructions” for creating a “fully functioning being”, and that “cells “learn” and “create instructions on the hoof” and create them “de novo”. It also tells us that information (= passive “reference material”) is used by the organism, and organisms are communities of cells. We are left, then, with the hypothesis that cells use passive information to create actions.

DAVID: The information just lying there is inactive, of course, but the cells are totally aware of it and use it in various required actions.

dhw: Your last sentence sums up the hypothesis I have been trying to put to you for the last few years. Cells are aware and they actively use passive information to decide what actions to perform. Thank you for putting it so succinctly.

QUOTE from Davies: The resolution to this paradox seems to lie in the fact that the demon must gather information about the properties of each molecule, and for this it requires a recording device, such as a brain or a miniature notebook.

dhw: In our context, the “demon” would therefore be that part of the cell which is the equivalent of a brain.

DAVID: It is all in the interpretation. If the cells are programmed to review instructional information and follow algorithms of necessary choices, it can all be automatic. That is still my position.

dhw: So your interpretation, just to sum up all the bolded statements above, is that information is passive reference material and cannot serve as instructions, and the cells are totally aware of it and use it in performing their actions. However, (latest statement) the information does contain instructions and cells are not aware of them but are programmed to follow them in performing their actions. I suspect I am not alone in finding these two sets of statements confusing.

Davies is coming to agree with my ID folks who believe life runs on information. In my mind I break this up into procedural information which runs most of life's activities automatically and reaction information which instructs appropriate reactions to new stimuli. I believe the cells are instructed to use the information and instructions appropriately.

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dhw: So your interpretation, just to sum up all the bolded statements above, is that information is passive reference material and cannot serve as instructions, and the cells are totally aware of it and use it in performing their actions. However, (latest statement) the information does contain instructions and cells are not aware of them but are programmed to follow them in performing their actions. I suspect I am not alone in finding these two sets of statements confusing.

DAVID: Davies is coming to agree with my ID folks who believe life runs on information. In my mind I break this up into procedural information which runs most of life's activities automatically and reaction information which instructs appropriate reactions to new stimuli. I believe the cells are instructed to use the information and instructions appropriately.

You have agreed that information (a passive data base) cannot possibly serve as instructions, and you cannot passively "be instructed" without instructions. You have said unequivocally that “the information just lying there is inactive, of course, but the cells are totally aware of it and use it in various required actions.” I would say, then, that life "runs on" cells being aware of and actively using the passive information that is lying there inactive. All your own words.

I don’t know what this has to do with ID. An atheist can believe in exactly the same process.

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dhw: So your interpretation, just to sum up all the bolded statements above, is that information is passive reference material and cannot serve as instructions, and the cells are totally aware of it and use it in performing their actions. However, (latest statement) the information does contain instructions and cells are not aware of them but are programmed to follow them in performing their actions. I suspect I am not alone in finding these two sets of statements confusing.

DAVID: Davies is coming to agree with my ID folks who believe life runs on information. In my mind I break this up into procedural information which runs most of life's activities automatically and reaction information which instructs appropriate reactions to new stimuli. I believe the cells are instructed to use the information and instructions appropriately.

dhw: You have agreed that information (a passive data base) cannot possibly serve as instructions, and you cannot passively "be instructed" without instructions. You have said unequivocally that “the information just lying there is inactive, of course, but the cells are totally aware of it and use it in various required actions.” I would say, then, that life "runs on" cells being aware of and actively using the passive information that is lying there inactive. All your own words.

I don’t know what this has to do with ID. An atheist can believe in exactly the same process.

All of my thoughts come from an acceptance that life is the result of design. Life emerges from all of the biochemical processes that are running in unison and in complete cooperation. The genome is coded information and instructions. Of course the atheist can accept this only he would say it all appeard naturally . What are your thoughts about this issue of information in this context of what makes life operate?

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dhw: You have agreed that information (a passive data base) cannot possibly serve as instructions, and you cannot passively "be instructed" without instructions. You have said unequivocally that “the information just lying there is inactive, of course, but the cells are totally aware of it and use it in various required actions.” I would say, then, that life "runs on" cells being aware of and actively using the passive information that is lying there inactive. All your own words.

[To this I would add that I do not accept the term "reaction information". Information is passive, and new stimuli provide new information. Cells, as you say, become aware of it and use it. I don't believe passive information can actively instruct passive information to become active. But see later for my "caveat".]

I don’t know what this has to do with ID. An atheist can believe in exactly the same process.

DAVID: All of my thoughts come from an acceptance that life is the result of design.

It is not an acceptance, it is a belief.

DAVID: Life emerges from all of the biochemical processes that are running in unison and in complete cooperation.

Yes.

DAVID: The genome is coded information and instructions.

And yet you have agreed that DNA cannot possibly serve as instructions.

DAVID: Of course the atheist can accept this only he would say it all appeared naturally.

So Davies is apparently coming to terms with your ID folks and all those atheists and agnostics who believe life “runs on information”.

DAVID: What are your thoughts about this issue of information in this context of what makes life operate?

My thoughts favour the hypothesis described above, using your very own words: “life "runs on" cells being aware of and actively using the passive information that is lying there inactive.” To complete the picture, I must add that for me there is a 50/50 chance that the active awareness and ability (or intelligence) of cells to use the information may have been designed by your God.

Under “Magic embryology”:

QUOTE: "After the fertilisation of an egg cell, two become one; two sets of genetic information combine to form a genome. We can think of the egg and sperm as information capsules with stored instructions for starting a new life, but post fertilisation, what kick starts the interpretation of these instructions? (David’s bold)

We are getting into special territory here. See below for my “caveat”.

QUOTE: “The model proposed by the research connects genome activation with epigenetic reprogramming of the cells that eventually form the sperm and eggs, forming a connected chain of events that secures Dppa2 and 4 expression in egg cells ready to initiate genome activation when the time is right.” (David’s bold)

Of course it’s a connected chain of events. That doesn’t mean that cells obey instructions issued 3.8 billion years ago; the article you agreed with said that cells “learn” and “create instructions on the hoof” and create them “de novo”. (But again, see below for my “caveat”.)

DAVID: It is all set to start making a fetus as these proteins act automatically as noted by the bolds above. Information and instructions ready to go.

Information yes, but according to the article you agreed with, the instructions are issued by the cells, which actively use the passive information. However, in the context of heredity and evolution, I need to repeat the caveat I have always offered in response to your posts highlighting automaticity and ignoring origins and problems. Every innovation does require “de novo” instructions from the cells, but once any process has proved successful, I agree that the cells will then follow “stored instructions”, as the successful process has to be passed on. And the cells will go on performing that process automatically unless problems or new conditions arise. It is the solution of new problems that provides us with the evidence that cells (including bacteria) are aware of passive information and, in your own words, “use it in various required actions”. That is when they create instructions on the hoof/de novo. And that is the basis of my hypothesis: we know cells can solve new problems and can restructure themselves in response to environmental change, and although we don’t know the extent to which they can do this, I suggest that by the same process they can also invent the new structures that constitute evolution.

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dhw: You have agreed that information (a passive data base) cannot possibly serve as instructions, and you cannot passively "be instructed" without instructions. You have said unequivocally that “the information just lying there is inactive, of course, but the cells are totally aware of it and use it in various required actions.” I would say, then, that life "runs on" cells being aware of and actively using the passive information that is lying there inactive. All your own words.[/b]

I agree

dhw: [To this I would add that I do not accept the term "reaction information". Information is passive, and new stimuli provide new information. Cells, as you say, become aware of it and use it. I don't believe passive information can actively instruct passive information to become active.

'Reaction information' is my term for instructions as to how to respond to various stimuli.

DAVID: What are your thoughts about this issue of information in this context of what makes life operate?

dhw: My thoughts favour the hypothesis described above, using your very own words: “life "runs on" cells being aware of and actively using the passive information that is lying there inactive.” To complete the picture, I must add that for me there is a 50/50 chance that the active awareness and ability (or intelligence) of cells to use the information may have been designed by your God.

Agreed

Under “Magic embryology”:

QUOTE: "After the fertilisation of an egg cell, two become one; two sets of genetic information combine to form a genome. We can think of the egg and sperm as information capsules with stored instructions for starting a new life, but post fertilisation, what kick starts the interpretation of these instructions? (David’s bold)

We are getting into special territory here. See below for my “caveat”.

QUOTE: “The model proposed by the research connects genome activation with epigenetic reprogramming of the cells that eventually form the sperm and eggs, forming a connected chain of events that secures Dppa2 and 4 expression in egg cells ready to initiate genome activation when the time is right.” (David’s bold)

Of course it’s a connected chain of events. That doesn’t mean that cells obey instructions issued 3.8 billion years ago; the article you agreed with said that cells “learn” and “create instructions on the hoof” and create them “de novo”. (But again, see below for my “caveat”.)

DAVID: It is all set to start making a fetus as these proteins act automatically as noted by the bolds above. Information and instructions ready to go.

dhw: Information yes, but according to the article you agreed with, the instructions are issued by the cells, which actively use the passive information. However, in the context of heredity and evolution, I need to repeat the caveat I have always offered in response to your posts highlighting automaticity and ignoring origins and problems. Every innovation does require “de novo” instructions from the cells, but once any process has proved successful, I agree that the cells will then follow “stored instructions”, as the successful process has to be passed on. And the cells will go on performing that process automatically unless problems or new conditions arise. It is the solution of new problems that provides us with the evidence that cells (including bacteria) are aware of passive information and, in your own words, “use it in various required actions”. That is when they create instructions on the hoof/de novo. And that is the basis of my hypothesis: we know cells can solve new problems and can restructure themselves in response to environmental change, and although we don’t know the extent to which they can do this, I suggest that by the same process they can also invent the new structures that constitute evolution.

We disagree about automaticity, since I think almost all of what cells do or respond to is automatic in multicellular organisms. Shapiro's work is on bacteria which is a whole different ballgame. They have to have some way to alter themselves. That doesn't really translate to what happens in multicellular. I also disagree with cells cannot create new species. That requires design beyond their capacities.

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DAVID: I agree.

I would regard your agreement as another red letter day in the history of the AgnosticWeb, but experience teaches me that agreements are not always what they seem.

dhw: [...] To this I would add that I do not accept the term "reaction information". Information is passive, and new stimuli provide new information. Cells, as you say, become aware of it and use it. I don't believe passive information can actively instruct passive information to become active.

DAVID: 'Reaction information' is my term for instructions as to how to respond to various stimuli.

Why mess about with language? Information means passive facts or details about a subject. Instructions are not facts or details, they are commands. And the article you initially agreed with said specifically that the passive data base could NOT serve as instructions.

DAVID: What are your thoughts about this issue of information in this context of what makes life operate?

dhw: My thoughts favour the hypothesis described above, using your very own words: “life "runs on" cells being aware of and actively using the passive information that is lying there inactive.” To complete the picture, I must add that for me there is a 50/50 chance that the active awareness and ability (or intelligence) of cells to use the information may have been designed by your God.

DAVID: Agreed.

Still hope for a red letter day!

dhw: […] in the context of heredity and evolution, I need to repeat the caveat I have always offered in response to your posts highlighting automaticity and ignoring origins and problems. Every innovation does require “de novo” instructions from the cells, but once any process has proved successful, I agree that the cells will then follow “stored instructions”, as the successful process has to be passed on. And the cells will go on performing that process automatically unless problems or new conditions arise. It is the solution of new problems that provides us with the evidence that cells (including bacteria) are aware of passive information and, in your own words, “use it in various required actions”. That is when they create instructions on the hoof/de novo. And that is the basis of my hypothesis: we know cells can solve new problems and can restructure themselves in response to environmental change, and although we don’t know the extent to which they can do this, I suggest that by the same process they can also invent the new structures that constitute evolution.

DAVID: We disagree about automaticity, since I think almost all of what cells do or respond to is automatic in multicellular organisms.

That may well be so, but the crucial word in your statement is “almost”. Once the process has been successful, it has to be repeated “automatically”, as described above. Only when there are problems/new conditions do the cells have to – in your own words – become aware of them and actively use the new information to perform the required actions. Your "almost" is the area in which cellular intelligence comes into play.

DAVID: Shapiro's work is on bacteria which is a whole different ballgame. They have to have some way to alter themselves. That doesn't really translate to what happens in multicellular. I also disagree with cells cannot create new species. That requires design beyond their capacities.

Correction: you disagree with the hypothesis that cells can create new species. I know you do. We also know that bacteria, like all cells and cell communities, “have some way to alter themselves”. That’s what the discussion is all about! Shapiro thinks it’s cellular intelligence, and I keep emphasizing that since we have never witnessed any innovations leading to new species, cellular intelligence as the means of innovation is a hypothesis. So too is your fixed belief that your God designed every species so that they could all eat one another until he designed the only thing he wanted to design.

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dhw: [...] To this I would add that I do not accept the term "reaction information". Information is passive, and new stimuli provide new information. Cells, as you say, become aware of it and use it. I don't believe passive information can actively instruct passive information to become active.

DAVID: 'Reaction information' is my term for instructions as to how to respond to various stimuli.

dhw: Why mess about with language? Information means passive facts or details about a subject. Instructions are not facts or details, they are commands. And the article you initially agreed with said specifically that the passive data base could NOT serve as instructions.

Of course there are instructions in the information. The cell must activate those instructions and follow them as the cells react to a stimulus.

DAVID: What are your thoughts about this issue of information in this context of what makes life operate?

dhw: My thoughts favour the hypothesis described above, using your very own words: “life "runs on" cells being aware of and actively using the passive information that is lying there inactive.” To complete the picture, I must add that for me there is a 50/50 chance that the active awareness and ability (or intelligence) of cells to use the information may have been designed by your God.

DAVID: Agreed.

Still hope for a red letter day!

dhw: […] in the context of heredity and evolution, I need to repeat the caveat I have always offered in response to your posts highlighting automaticity and ignoring origins and problems. Every innovation does require “de novo” instructions from the cells, but once any process has proved successful, I agree that the cells will then follow “stored instructions”, as the successful process has to be passed on. And the cells will go on performing that process automatically unless problems or new conditions arise. It is the solution of new problems that provides us with the evidence that cells (including bacteria) are aware of passive information and, in your own words, “use it in various required actions”. That is when they create instructions on the hoof/de novo. And that is the basis of my hypothesis: we know cells can solve new problems and can restructure themselves in response to environmental change, and although we don’t know the extent to which they can do this, I suggest that by the same process they can also invent the new structures that constitute evolution.

DAVID: We disagree about automaticity, since I think almost all of what cells do or respond to is automatic in multicellular organisms.

dhw: That may well be so, but the crucial word in your statement is “almost”. Once the process has been successful, it has to be repeated “automatically”, as described above. Only when there are problems/new conditions do the cells have to – in your own words – become aware of them and actively use the new information to perform the required actions. Your "almost" is the area in which cellular intelligence comes into play.

The 'almost' is carefully included as I discuss multicellular life. A kidney cell has no ability to do anything different than its assigned tasks. But we know the brain has plasticity and perhaps some neurons may follow your concept of cell intelligence. Remember your concept is based on Shapiro who studied all-in-one bacteria who carry a different set of responsibilities. I do not think Shapiro generally carries over to multicellular organisms.

DAVID: Shapiro's work is on bacteria which is a whole different ballgame. They have to have some way to alter themselves. That doesn't really translate to what happens in multicellular. I also disagree with cells cannot create new species. That requires design beyond their capacities.

dhw: Correction: you disagree with the hypothesis that cells can create new species. I know you do. We also know that bacteria, like all cells and cell communities, “have some way to alter themselves”. That’s what the discussion is all about! Shapiro thinks it’s cellular intelligence, and I keep emphasizing that since we have never witnessed any innovations leading to new species, cellular intelligence as the means of innovation is a hypothesis. So too is your fixed belief that your God designed every species so that they could all eat one another until he designed the only thing he wanted to design.

I think you are not discussing my points as presented above. To change a leg into a flipper you will first find the bones have a very similar pattern with altered joint shapes. The blood vessels and nerves will be the same. The muscles will have changed to allows the wave motion of flippers instead of the walking motion. The brain's controls will be changed to use this different way of locomotion, Nothing like Shapiro's bacteria and how they adapt. Your concept is a huge extrapolation to accomplish this design change.

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dhw: Information means passive facts or details about a subject. Instructions are not facts or details, they are commands. And the article you initially agreed with said specifically that the passive data base could NOT serve as instructions.

DAVID: Of course there are instructions in the information. The cell must activate those instructions and follow them as the cells react to a stimulus.

Why “of course”, when you have already agreed that the information cannot possibly serve as instructions (= what genes DON'T do), and have stated explicitly that “the information just lying there is inactive, of course, but the cells are totally aware of it and use it in various required actions”?

DAVID: We disagree about automaticity, since I think almost all of what cells do or respond to is automatic in multicellular organisms.

dhw: That may well be so, but the crucial word in your statement is “almost”. Once the process has been successful, it has to be repeated “automatically”, as described above. Only when there are problems/new conditions do the cells have to – in your own words – become aware of them and actively use the new information to perform the required actions. Your "almost" is the area in which cellular intelligence comes into play.

DAVID: The 'almost' is carefully included as I discuss multicellular life. A kidney cell has no ability to do anything different than its assigned tasks. But we know the brain has plasticity and perhaps some neurons may follow your concept of cell intelligence.

When organisms (= cell communities) are exposed to new conditions, we know for a fact that some of them are able to adapt, i.e. organs like kidneys remain the same, but nevertheless the cells make adjustments. However, the great mystery is INNOVATION. Nobody knows how it happens. But if the cell communities are aware of new information and are capable of using it for adaptation, perhaps they are capable of using it for innovation too, which requires cooperation between all the communities. My “perhaps” echoes your “perhaps”. It is a hypothesis. I’m glad you are now accepting it as a possibility.

DAVID: Remember your concept is based on Shapiro who studied all-in-one bacteria who carry a different set of responsibilities. I do not think Shapiro generally carries over to multicellular organisms.

His concept of “natural genetic engineering” refers to all organisms, and since he believes in cellular intelligence, I really can’t imagine that he believes single cells are intelligent but cell communities aren’t.

DAVID: To change a leg into a flipper you will first find the bones have a very similar pattern with altered joint shapes [etc.] Nothing like Shapiro's bacteria and how they adapt. Your concept is a huge extrapolation to accomplish this design change.

You don’t need to tell me that whales are different from bacteria, and I don’t know often you want me to acknowledge that adaptation is different from innovation, and that is why my concept - just like your own - is an unproven hypothesis. See above re Shapiro.

Under "STICKLEBACKS":
QUOTE: Genetic analysis of the marine ancestor also showed that the genetic variants that are beneficial for adapting to acidic or alkaline water are all present in the ancestor. Similar life forms, therefore, didn't occur randomly, but independently of each other through the predictable sorting of advantageous genetic variants that were already present in the genome. " (David’s bold)

DAVID: It certainly looks as if the existing genome can guide future adaptations, but in case within related species. Note the bold statement.

Of course the potential for variation must already be present, and we know that this extends as far as adaptation. The stickleback cells, in your words, are “totally aware of it and use it” to perform the “various required actions”.

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dhw: Information means passive facts or details about a subject. Instructions are not facts or details, they are commands. And the article you initially agreed with said specifically that the passive data base could NOT serve as instructions.

DAVID: Of course there are instructions in the information. The cell must activate those instructions and follow them as the cells react to a stimulus.

dhw: Why “of course”, when you have already agreed that the information cannot possibly serve as instructions (= what genes DON'T do), and have stated explicitly that “the information just lying there is inactive, of course, but the cells are totally aware of it and use it in various required actions”?

You still seem totally confused about the issue of information in the genome. I see the cells as actively entering their genome for instructions to be activated. The information is always available, just as you enter a library to review a subject from inactive books. As Davies points out life runs on information.

DAVID: Remember your concept is based on Shapiro who studied all-in-one bacteria who carry a different set of responsibilities. I do not think Shapiro generally carries over to multicellular organisms.

dhw: His concept of “natural genetic engineering” refers to all organisms, and since he believes in cellular intelligence, I really can’t imagine that he believes single cells are intelligent but cell communities aren’t.

We really need to ask Shapiro. I can't see the jump since I know all human organs act automatically. See my entry on skin color for adaptation.

Under "STICKLEBACKS":
QUOTE: Genetic analysis of the marine ancestor also showed that the genetic variants that are beneficial for adapting to acidic or alkaline water are all present in the ancestor. Similar life forms, therefore, didn't occur randomly, but independently of each other through the predictable sorting of advantageous genetic variants that were already present in the genome. " (David’s bold)

DAVID: It certainly looks as if the existing genome can guide future adaptations, but in case within related species. Note the bold statement.

dhw: Of course the potential for variation must already be present, and we know that this extends as far as adaptation. The stickleback cells, in your words, are “totally aware of it and use it” to perform the “various required actions”.

Exactly as in the information discussion above. The cells can look into their library of information to guide adaptations.

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DAVID: Of course there are instructions in the information. The cell must activate those instructions and follow them as the cells react to a stimulus.

dhw: Why “of course”, when you have already agreed that the information cannot possibly serve as instructions (= what genes DON'T do), and have stated explicitly that “the information just lying there is inactive, of course, but the cells are totally aware of it and use it in various required actions”?

DAVID: You still seem totally confused about the issue of information in the genome. I see the cells as actively entering their genome for instructions to be activated. The information is always available, just as you enter a library to review a subject from inactive books. As Davies points out life runs on information.

The genome is part of the cell, so you now have the cell consciously entering part of itself to look for instructions to tell it how to use the part of itself which it has entered. You also have a fixed belief that 3.8 billion years ago, your God provided the original cells with instructions for every undabbled innovation, lifestyle and natural wonder. I wonder how your researching cell knows which of the billions of instructions it’s supposed to use. And you have now gone back on your original agreement that information (a passive data base) “cannot possibly serve as instructions”. You also agreed when I wrote: “I would say, then, that life “runs on” cells being aware of and actively using the passive information that is lying there inactive.” Life does not run on information, it runs on the active use of passive information. But you think I’m confused.

DAVID: Remember your concept is based on Shapiro who studied all-in-one bacteria who carry a different set of responsibilities. I do not think Shapiro generally carries over to multicellular organisms.

dhw: His concept of “natural genetic engineering” refers to all organisms, and since he believes in cellular intelligence, I really can’t imagine that he believes single cells are intelligent but cell communities aren’t.

DAVID: We really need to ask Shapiro. I can't see the jump since I know all human organs act automatically. See my entry on skin color for adaptation.

You needn’t ask Shapiro. I propose that since several prominent scientists believe that cells are intelligent, it is possible that cellular intelligence is responsible for the innovations that result in speciation. You do not “know” that cells are not intelligent, and neither of us “knows” whether this proposal is true. Ditto your own library proposal above. Re skin colour, see “Little foot”.

From the thread on Paul Davies:
dhw: I would like to know what Davies believes actually does the information processing, i.e. what it is that chunters away inside living cells and “manipulates” or “exploits” information. (“Life” doesn’t exploit anything – that is done by living organisms.)

DAVID: This is all concepts about the use of information in the genome. Obviously the information in the genome is available for the cells to use. We still don't have a laid-bare description of how it works.

No, we haven’t. But you think your cells enter their genome to look for one set of instructions out of billions passed down through 3.8 billion years. I suggest that cells actively use passive information to work out the best way to deal with new conditions.***

DAVID: When I first introduced the concept of information running life to you, you were startled and resisted the idea. I won't bother looking for quotes.

I am still startled, and I still resist it. Once more: information is passive, and it is the use of information that runs life, but we don't know how cells are able to use the information. You agreed when I said so, but now you disagree.

DAVID: ...this is not descriptive information. it is instructional information both as to structure and appropriate reactions to stimuli. Without this onboard information life would cease to exist. And what created this information? My answer is God. Information without a source is impossible.

dhw: Where have you found “instructional information”, and why can’t you just call it “instructions”? In this article we are simply not told what processes or manipulates or exploits information (but maybe he makes it clear elsewhere). It’s as if you and he both think the word itself has magic explanatory properties. Of course all information has a source: you can’t have facts and details about a subject without having a subject. We humans extract the passive information from everything we can set our eyes and minds on, then we actively use it. And in certain contexts we even create information that isn’t there!

DAVID: Yes, exactly. The genome creates the structure of organisms and offers ways for appropriate responses to stimuli.

I did not say the genome offers ways to respond! The genome, as you agreed earlier, offers nothing but passive information which “cannot possibly serve as instructions”. The genome can be restructured, but we do not know what organizes the restructuring. See above*** for two unproven hypotheses.

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DAVID: You still seem totally confused about the issue of information in the genome. I see the cells as actively entering their genome for instructions to be activated. The information is always available, just as you enter a library to review a subject from inactive books. As Davies points out life runs on information.

dhw: The genome is part of the cell, so you now have the cell consciously entering part of itself to look for instructions to tell it how to use the part of itself which it has entered....And you have now gone back on your original agreement that information (a passive data base) “cannot possibly serve as instructions”. You also agreed when I wrote: “I would say, then, that life “runs on” cells being aware of and actively using the passive information that is lying there inactive.” Life does not run on information, it runs on the active use of passive information. But you think I’m confused.

This is just semantics. What I bolded in your comment is correct. My library analogy is correct. A library is passive, but one can actively use it. Cells use their library of information in the genome. There are instructions telling cells how to act. Note the entry on stickleback fish evolution. ( 2019-01-31, 01:22 )

From the thread on Paul Davies:
dhw: I would like to know what Davies believes actually does the information processing, i.e. what it is that chunters away inside living cells and “manipulates” or “exploits” information. (“Life” doesn’t exploit anything – that is done by living organisms.)

DAVID: This is all concepts about the use of information in the genome. Obviously the information in the genome is available for the cells to use. We still don't have a laid-bare description of how it works.

No, we haven’t. But you think your cells enter their genome to look for one set of instructions out of billions passed down through 3.8 billion years. I suggest that cells actively use passive information to work out the best way to deal with new conditions.***

DAVID: When I first introduced the concept of information running life to you, you were startled and resisted the idea. I won't bother looking for quotes.

dhw: I am still startled, and I still resist it. Once more: information is passive, and it is the use of information that runs life, but we don't know how cells are able to use the information. You agreed when I said so, but now you disagree.

Above I haven't disagreed.

DAVID: Yes, exactly. The genome creates the structure of organisms and offers ways for appropriate responses to stimuli.

dhw: I did not say the genome offers ways to respond! The genome, as you agreed earlier, offers nothing but passive information which “cannot possibly serve as instructions”. The genome can be restructured, but we do not know what organizes the restructuring. See above*** for two unproven hypotheses.

There must be a misunderstanding. I don't understand the bolded quote. It does not represent any of my thinking. I have always viewed the genome as creating structure, but also instructions for biochemical reactions and also responses to stimuli. I'd like to see the entire context of the quote.

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dhw: The genome is part of the cell, so you now have the cell consciously entering part of itself to look for instructions to tell it how to use the part of itself which it has entered....And you have now gone back on your original agreement that information (a passive data base) “cannot possibly serve as instructions”. You also agreed when I wrote: “I would say, then, that life “runs on” cells being aware of and actively using the passive information that is lying there inactive.” Life does not run on information, it runs on the active use of passive information. But you think I’m confused.

DAVID: This is just semantics.

There is a world of difference between passive information and active use of information. Our whole discussion revolves around what it is that uses the passive information.

DAVID: What I bolded in your comment is correct. My library analogy is correct. A library is passive, but one can actively use it. Cells use their library of information in the genome. There are instructions telling cells how to act. [dhw: The whole article clearly distinguishes between information and instructions, but you refuse to do so.] Note the entry on stickleback fish evolution. ( 2019-01-31, 01:22 ) [dhw: I answered it on this thread, 31 January at 12.15]

So (a) the “reviewer” cells know how to pick out one set of instructions from the billions stored in the 3.8 billion-year-old library, or (b) there are no instructions, and they work out for themselves how to use the passive information in the genome, as you agreed earlier: [DNA] offers nothing but passive information which “cannot possibly serve as instructions”. The genome can be restructured, but we do not know what organizes the restructuring.

DAVID: There must be a misunderstanding. I don't understand the bolded quote. It does not represent any of my thinking. I have always viewed the genome as creating structure, but also instructions for biochemical reactions and also responses to stimuli. I'd like to see the entire context of the quote.

See our exchanges on this thread, 14/15 January: You wrote initially: “The original DNA may have contained all the info for evolution”, and when I asked you for a definition of info, you wrote: “a complete set of instructions for cells to respond to all the stimuli they must deal with.”

However, I pointed out that this contradicted the article you were agreeing with, and you responded: “Sloppy thinking and writing. My boldings above and below are my thoughts exactly.” Now you have reverted to exactly the same “sloppy thinking and writing”. Here are the two quotes:

QUOTE: "as the British biologist Denis Noble insists in an interview with the writer Suzan Mazur,1 “The modern synthesis has got causality in biology wrong … DNA on its own does absolutely nothing until activated by the rest of the system … DNA is not a cause in an active sense. I think it is better described as a passive data base which is used by the organism to enable it to make the proteins that it requires.”(David’s bold)

If DNA is a passive data base which cannot possibly serve as instructions, does nothing and is incapable of forming a fully functioning being but is used by the organism, how can you argue that it is a library of instructions telling the organism how to form a fully functioning being (I don't think you can have evolution without fully functioning beings)? The article itself tells us that cells “learn” and “create instructions on the hoof”, and “instructions are, again, created de novo”, and the “glorious ballet of different cells finding just the right places at the right times “could not have been specified in the fixed linear strings of DNA.”

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dhw: There is a world of difference between passive information and active use of information. Our whole discussion revolves around what it is that uses the passive information.

DAVID: What I bolded in your comment is correct. My library analogy is correct. A library is passive, but one can actively use it. Cells use their library of information in the genome. There are instructions telling cells how to act. [dhw: The whole article clearly distinguishes between information and instructions, but you refuse to do so.] Note the entry on stickleback fish evolution. ( 2019-01-31, 01:22 ) [dhw: I answered it on this thread, 31 January at 12.15]

dhw: So (a) the “reviewer” cells know how to pick out one set of instructions from the billions stored in the 3.8 billion-year-old library, or (b) there are no instructions, and they work out for themselves how to use the passive information in the genome, as you agreed earlier: [DNA] offers nothing but passive information which “cannot possibly serve as instructions”. The genome can be restructured, but we do not know what organizes the restructuring.

I'm convinced there are instructions, but nothing as simple as DNA coding for protein. There are many other layers of the genome which modify coded instructions. HOX genes run a committee of lesser genes, but we have idea how. We identify genes that control a function, but have no idea how that really works,

dhw: However, I pointed out that this contradicted the article you were agreeing with, and you responded: “Sloppy thinking and writing. My boldings above and below are my thoughts exactly.” Now you have reverted to exactly the same “sloppy thinking and writing”. Here are the two quotes:

QUOTE: "Scientists now understand that the information in the DNA code can only serve as a template for a protein. It cannot possibly serve as instructions for the more complex task of putting the proteins together into a fully functioning being, no more than the characters on a typewriter can produce a story.(David’s bold)

QUOTE: "as the British biologist Denis Noble insists in an interview with the writer Suzan Mazur,1 “The modern synthesis has got causality in biology wrong … DNA on its own does absolutely nothing until activated by the rest of the system … DNA is not a cause in an active sense. I think it is better described as a passive data base which is used by the organism to enable it to make the proteins that it requires.”(David’s bold)

If DNA is a passive data base which cannot possibly serve as instructions, does nothing and is incapable of forming a fully functioning being but is used by the organism, how can you argue that it is a library of instructions telling the organism how to form a fully functioning being (I don't think you can have evolution without fully functioning beings)? The article itself tells us that cells “learn” and “create instructions on the hoof”, and “instructions are, again, created de novo”, and the “glorious ballet of different cells finding just the right places at the right times “could not have been specified in the fixed linear strings of DNA.”

Note my above comment. We know what a gene controls, but not how it is actually done. That is exactly what the quotes are saying. I've pointed out the 3-D relationships in the coils of DNA. What the article says to use your words differently is that the cells appear to 'learn' and 'construct information on the hoof', but it is my word 'appear' that applies. We are still looking in from the outside and making assumptions. Yes, DNA is a passive code but we see the system creating life running intelligently, and I propose there are layers of the genome where Davies 'ghost in the system' exists. That is what activates. It is all still a
black box. As usual I am interpreting the bolded statements in my way.

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dhw: There is a world of difference between passive information and active use of information. Our whole discussion revolves around what it is that uses the passive information.

DAVID: What I bolded in your comment is correct. My library analogy is correct. A library is passive, but one can actively use it. Cells use their library of information in the genome. There are instructions telling cells how to act.[dhw: The whole article clearly distinguishes between information and instructions, but you refuse to do so.]

dhw: So (a) the “reviewer” cells know how to pick out one set of instructions from the billions stored in the 3.8 billion-year-old library, or (b) there are no instructions, and they work out for themselves how to use the passive information in the genome, as you agreed earlier: [DNA] offers nothing but passive information which “cannot possibly serve as instructions”. The genome can be restructured, but we do not know what organizes the restructuring.

DAVID: I'm convinced there are instructions, but nothing as simple as DNA coding for protein. There are many other layers of the genome which modify coded instructions. HOX genes run a committee of lesser genes, but we have idea how. We identify genes that control a function, but have no idea how that really works.

You are echoing my last sentence (now bolded), and have ignored the rest. I know you are convinced that the genome stores billions of instructions planted 3.8 billion years ago, and the cell enters the genome and picks out the relevant one. I find it less than convincing.

dhw: However, I pointed out that this contradicted the article you were agreeing with, and you responded: “Sloppy thinking and writing. My boldings above and below are my thoughts exactly.” Now you have reverted to exactly the same “sloppy thinking and writing”. Here are the two quotes:

QUOTE: "Scientists now understand that the information in the DNA code can only serve as a template for a protein. It cannot possibly serve as instructions for the more complex task of putting the proteins together into a fully functioning being, no more than the characters on a typewriter can produce a story."(David’s bold)
QUOTE: "as the British biologist Denis Noble insists in an interview with the writer Suzan Mazur,1 “The modern synthesis has got causality in biology wrong … DNA on its own does absolutely nothing until activated by the rest of the system … DNA is not a cause in an active sense. I think it is better described as a passive data base which is used by the organism to enable it to make the proteins that it requires.”(David’s bold)

dhw: If DNA is a passive data base which cannot possibly serve as instructions, does nothing and is incapable of forming a fully functioning being but is used by the organism, how can you argue that it is a library of instructions telling the organism how to form a fully functioning being (I don't think you can have evolution without fully functioning beings)? The article itself tells us that cells “learn” and “create instructions on the hoof”, and “instructions are, again, created de novo”, and the “glorious ballet of different cells finding just the right places at the right times “could not have been specified in the fixed linear strings of DNA.”

DAVID: Note my above comment. We know what a gene controls, but not how it is actually done. That is exactly what the quotes are saying. I've pointed out the 3-D relationships in the coils of DNA. What the article says to use your words differently is that the cells appear to 'learn' and 'construct information on the hoof', but it is my word 'appear' that applies.

The article does not use the word “appear”, unless you have misquoted it. The quotes with which you agreed are unequivocal.

DAVID: We are still looking in from the outside and making assumptions. Yes, DNA is a passive code but we see the system creating life running intelligently, and I propose there are layers of the genome where Davies 'ghost in the system' exists. That is what activates. It is all still a black box. As usual I am interpreting the bolded statements in my way.

Yes, the system runs intelligently. I also propose a “ghost in the system”, which is cellular intelligence. Your “ghost” is a 3.8-billion-year old library of instructions, and presumably another set of instructions instructing the ghost to pick out volume 3,000,000,007, under “fin”, or “camouflage”, or “flight path”, or “nest”. You described as “sloppy thinking and writing” your earlier proposal – that DNA may have contained all the info for evolution, and “info” meant a complete set of instructions. The only change appears to be that you have substituted “genome” for DNA.

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DAVID: I'm convinced there are instructions, but nothing as simple as DNA coding for protein. There are many other layers of the genome which modify coded instructions. HOX genes run a committee of lesser genes, but we have idea how. We identify genes that control a function, but have no idea how that really works.

dhw: You are echoing my last sentence (now bolded), and have ignored the rest. I know you are convinced that the genome stores billions of instructions planted 3.8 billion years ago, and the cell enters the genome and picks out the relevant one. I find it less than convincing.

dhw: However, I pointed out that this contradicted the article you were agreeing with, and you responded: “Sloppy thinking and writing. My boldings above and below are my thoughts exactly.” Now you have reverted to exactly the same “sloppy thinking and writing”. Here are the two quotes:

QUOTE: "Scientists now understand that the information in the DNA code can only serve as a template for a protein. It cannot possibly serve as instructions for the more complex task of putting the proteins together into a fully functioning being, no more than the characters on a typewriter can produce a story."(David’s bold)
QUOTE: "as the British biologist Denis Noble insists in an interview with the writer Suzan Mazur,1 “The modern synthesis has got causality in biology wrong … DNA on its own does absolutely nothing until activated by the rest of the system … [/i[/color]]

DNA is not a cause in an active sense. I think it is better described as a passive data base which is used by the organism to enable it to make the proteins that it requires.”[/b](David’s bold)

We disagree about the source of the colored portion of the second quote as you note below.

dhw: If DNA is a passive data base which cannot possibly serve as instructions, does nothing and is incapable of forming a fully functioning being but is used by the organism, how can you argue that it is a library of instructions telling the organism how to form a fully functioning being (I don't think you can have evolution without fully functioning beings)? The article itself tells us that cells “learn” and “create instructions on the hoof”, and “instructions are, again, created de novo”, and the “glorious ballet of different cells finding just the right places at the right times “could not have been specified in the fixed linear strings of DNA.”

DAVID: Note my above comment. We know what a gene controls, but not how it is actually done. That is exactly what the quotes are saying. I've pointed out the 3-D relationships in the coils of DNA. What the article says to use your words differently is that the cells appear to 'learn' and 'construct information on the hoof', but it is my word 'appear' that applies.

dhw: The article does not use the word “appear”, unless you have misquoted it. The quotes with which you agreed are unequivocal.

I said it was my word, 'appear'.

DAVID: We are still looking in from the outside and making assumptions. Yes, DNA is a passive code but we see the system creating life running intelligently, and I propose there are layers of the genome where Davies 'ghost in the system' exists. That is what activates. It is all still a black box. As usual I am interpreting the bolded statements in my way.

dhw: Yes, the system runs intelligently. I also propose a “ghost in the system”, which is cellular intelligence. Your “ghost” is a 3.8-billion-year old library of instructions, and presumably another set of instructions instructing the ghost to pick out volume 3,000,000,007, under “fin”, or “camouflage”, or “flight path”, or “nest”. You described as “sloppy thinking and writing” your earlier proposal – that DNA may have contained all the info for evolution, and “info” meant a complete set of instructions. The only change appears to be that you have substituted “genome” for DNA.

You have summarized our differences. As for following instructions from 3 billion+7 , a bacteria, following instructions, splits in two every 20 minutes. The biochemical reactions are in nanoseconds. This goes on constantly throughout a multicellular organism. They don't have to search the library, the one weakness in a library analogy, they know the whole library constantly, a requirement for the emergence of a living system.

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The two quotes that David said were exact expressions of his thoughts:

QUOTE: "as the British biologist Denis Noble insists in an interview with the writer Suzan Mazur,1 “The modern synthesis has got causality in biology wrong … DNA on its own does absolutely nothing until activated by the rest of the system … [/i[/color]] “DNA is not a cause in an active sense. I think it is better described as a passive data base which is used by the organism to enable it to make the proteins that it requires.”[/b](David’s bold)

DAVID: We disagree about the source of the colored portion of the second quote as you note below.

So you agree that the cell communities (organism) use the passive information, but you disagree. (See below re the “library”).

DAVID: What the article says to use your words differently is that the cells appear to 'learn' and 'construct information on the hoof', but it is my word 'appear' that applies.

dhw: The article does not use the word “appear”, unless you have misquoted it. The quotes with which you agreed are unequivocal.

DAVID: I said it was my word, 'appear'.
Even if cells “appear” to learn etc., this should at least allow you to say that maybe they do learn etc., as the article states unequivocally - in keeping with the findings of Shapiro & Co.

dhw: Yes, the system runs intelligently. I also propose a “ghost in the system”, which is cellular intelligence. Your “ghost” is a 3.8-billion-year old library of instructions, and presumably another set of instructions instructing the ghost to pick out volume 3,000,000,007, under “fin”, or “camouflage”, or “flight path”, or “nest”. You described as “sloppy thinking and writing” your earlier proposal – that DNA may have contained all the info for evolution, and “info” meant a complete set of instructions. The only change appears to be that you have substituted “genome” for DNA.

DAVID: You have summarized our differences. As for following instructions from 3 billion+7 , a bacteria, following instructions, splits in two every 20 minutes. The biochemical reactions are in nanoseconds. This goes on constantly throughout a multicellular organism. They don't have to search the library, the one weakness in a library analogy, they know the whole library constantly, a requirement for the emergence of a living system.

So cells already know all the information necessary for every single innovation, lifestyle and natural wonder in the history of evolution, and along with that, your God has provided them with all the instructions necessary for picking out the one instruction (out of the billions) required for their particular situation. And this is your fixed belief?

QUOTES from “How cells use genetic information”, with dhw’s bold:

"[The scientists] found that during embryo formation fruit fly cells use “all information available from the genetic code” to position themselves within a single cell’s width of where they are supposed to be.

“'The theoretical idea is very simple, which is that every cell is using all the information that it can squeeze out of the relevant genes," says physicist William Bialek.

“One can imagine cells as GPS devices which, instead of satellite signals, collect molecular ones to figure out their locations.”

“'This gives us an amazing tool for understanding how decision-making in biology actually works,

DAVID’s comment: Note the automaticity of the cells response to changed directions. The scientists could not have gotten these results if the cells did not automatically follow the substituted gene patterns.

Where do you find automaticity in these quotes? GPS devices are a form of artificial intelligence. If you changed the information from the satellite, no doubt you would be able to predict which way the GPS would send you. Fruit flies are not man-made: their intelligence is natural. The article says they “figure” things out, and if the information is changed, they change their response. So would you.

DAVID: This still does [not] tell us how genes act to create the final physical results they control. We do see they order the production of certain proteins at certain places b ut we do not know exactly how they exert their controls. we just beginning and end but not much of the middle molecular activity.

Precisely. We do not know how cells exert their controls. And yet you insist that, in spite of Shapiro & Co and the article you quoted and initially agreed with, the control cannot possibly be cellular intelligence but must be a 3.8-billion-year-old library of information together with a 3.8 billion-year-old set of instructions for every single situation in life's history bar those that your God dabbles in directly.

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DAVID: We disagree about the source of the colored portion of the second quote as you note below.

dhw: so you agree that the cell communities (organism) use the passive information, but you disagree. (See below re the “library”).

You constantly stick to your interpretations of cell intelligence when below the quotes indicate they use available info.

dhw: So cells already know all the information necessary for every single innovation, lifestyle and natural wonder in the history of evolution, and along with that, your God has provided them with all the instructions necessary for picking out the one instruction (out of the billions) required for their particular situation. And this is your fixed belief?

Unless I see research to convince me otherwise

QUOTES from “How cells use genetic information”, with dhw’s bold:

"[The scientists] found that during embryo formation fruit fly cells use “all information available from the genetic code” to position themselves within a single cell’s width of where they are supposed to be.

“'The theoretical idea is very simple, which is that every cell is using all the information that it can squeeze out of the relevant genes," says physicist William Bialek.

“One can imagine cells as GPS devices which, instead of satellite signals, collect molecular ones to figure out their locations.”

“'This gives us an amazing tool for understanding how decision-making in biology actually works,

DAVID’s comment: Note the automaticity of the cells response to changed directions. The scientists could not have gotten these results if the cells did not automatically follow the substituted gene patterns.

dhw: Where do you find automaticity in these quotes? GPS devices are a form of artificial intelligence. If you changed the information from the satellite, no doubt you would be able to predict which way the GPS would send you. Fruit flies are not man-made: their intelligence is natural. The article says they “figure” things out, and if the information is changed, they change their response. So would you.

My bolds are all analogies that are imagined by the authors. The scientists re-directed cell activity by changing genes and the cells changed. The genes told them to change! All we know is the cells know how to interpret gene instructions. "An amazing tool' bold is the scientists praising heir new technique! All comment hyperbole. Remember these guys live by grant money, which they have to justify by touting their results. Please keep that in mind when you swallow the propaganda hook line and sinker. An interesting point: do you fully understand how the grant game is conducted?? I've had grants.

DAVID: This still does [not] tell us how genes act to create the final physical results they control. We do see they order the production of certain proteins at certain places b ut we do not know exactly how they exert their controls. We just see beginning and end but not much of the middle molecular activity.

dhw: Precisely. We do not know how cells exert their controls.

Misinterpreted. Note I said the genes control cell reactions. We don't know how that is done. Cells access the gene and respond. All we know is from outside the actual process. The gene may precisely tell the cell what to do, which is to make a precise set of protein molecules, and in this case placed at a precise position. An automatic response to direct instructions.

dhw: And yet you insist that, in spite of Shapiro & Co and the article you quoted and initially agreed with, the control cannot possibly be cellular intelligence but must be a 3.8-billion-year-old library of information together with a 3.8 billion-year-old set of instructions for every single situation in life's history bar those that your God dabbles in directly.

I still have a totally different interpretation as seen in my current comments.

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An axon carries electrical signals from the body of the neuron. The neuron is the only cell that has an enormous extension,think from your lower back to a toe:

https://medicalxpress.com/news/2019-02-neural-heaven-neuron-axon.html

"In a new paper, a researcher at the University of California, Riverside, and his colleagues describe the genetic switches that ignite axon formation. Their work focuses on two molecular components—polypyrimidine tract binding protein 2 (PTBP2) and the shootin gene (SHTN1).

"'Neurons are so distinct from other cells in the body," said Sika Zheng, assistant professor of biomedical sciences in the School of Medicine at the University of California, Riverside. "They are the only cells that can grow a protrusion (the axon) that can become hundreds and thousands of times longer than the cell body itself."

***

"Previous studies have identified more than 150 genes that play some roles in axon function. Zheng and his team were surprised to find the overall expression levels of these genes stay relatively flat as the axon grows. If these genes do not change their abundance, how then do they dictate neurons to produce axons?

"These genes do change their "character" through a gene regulatory process called alternative splicing. Alternative splicing allows a single gene to produce multiple similar protein isoforms with different functions or identities. According to Zheng, it is as if these genes are transformed to shoulder a new task—in this case generating an axon.

"PTBP2, a specialized RNA binding protein, was about to take center stage in the study. Zheng and his team found PTBP2 spiked in immature neuron cells. This protein orchestrates the precise choreography behind those splicing events by acting like a switchboard controlling every step of the process that produces the one, essential axon.

"At the early stage of axon formation, PTBP2 turns on the long isoform of the SHTN1 gene, which promotes growth of the axon. As the neuron matures, PTBP2 is gradually down regulated and the SHTN1 gene switches from the long isoform to the short isoform. Axon growth stops as the neuron and its axon connect to the neural circuit.

"'PTBP2 and SHTN1 give us an entry point to understand how splicing changes occur to promote axon growth," Zheng said. "We can use this information to tease out what is happening at the cellular level, and we are only at the tip of the iceberg."

"While this study focused on PTBP2 and the SHTN1 gene, Zheng notes that other proteins or genes and their isoforms could also play a role in axon formation. This study was also conducted using mouse neural cells. Zheng and his team do not know if the same mechanisms will be active in human neural cells. While the study offers a new perspective to this fundamental question, Zheng cautions that it may be years before these findings could be translated into future therapies."

Comment: Once again we see the complex controls and the resulting axon formation, but we have no information about how it all works, or how the cell and the cells genes manipulate each other. The inner workings are all a black box. We do not know whether all of this is automatic, or alternatively there must be some independent initiation activity

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DAVID: You constantly stick to your interpretations of cell intelligence when below the quotes indicate they use available info.

Of course they use available info. And that is the opposite of your hypothesis that the info uses them by giving them “reaction information” (= instructions). The scientists themselves believe cells create instructions on the hoof, de novo, and since you yourself agree that cells “appear” to show intelligence, there is no reason categorically to say they don’t have it.

dhw: So cells already know all the information necessary for every single innovation, lifestyle and natural wonder in the history of evolution, and along with that, your God has provided them with all the instructions necessary for picking out the one instruction (out of the billions) required for their particular situation. And this is your fixed belief?

DAVID: Unless I see research to convince me otherwise.

So whereabouts in the cell have you found the evidence for a 3.8-billion-year-old library of information and instructions for every single undabbled innovation, lifestyle and natural wonder in the history of life?

QUOTES from “How cells use genetic information”, with dhw’s bold:

“'The theoretical idea is very simple, which is that every cell is using all the information that it can squeeze out of the relevant genes," says physicist William Bialek.

“One can imagine cells as GPS devices which, instead of satellite signals, collect molecular ones to figure out their locations.”

“'This gives us an amazing tool for understanding how decision-making in biology actually works,

dhw: Where do you find automaticity in these quotes? GPS devices are a form of artificial intelligence. If you changed the information from the satellite, no doubt you would be able to predict which way the GPS would send you. Fruit flies are not man-made: their intelligence is natural. The article says they “figure” things out, and if the information is changed, they change their response. So would you.

DAVID: My bolds are all analogies that are imagined by the authors. The scientists re-directed cell activity by changing genes and the cells changed. The genes told them to change! All we know is the cells know how to interpret gene instructions. "An amazing tool' bold is the scientists praising heir new technique! All comment hyperbole. Remember these guys live by grant money, which they have to justify by touting their results. Please keep that in mind when you swallow the propaganda hook line and sinker. An interesting point: do you fully understand how the grant game is conducted?? I've had grants.

So now we should ignore the findings of Margulis, McClintock, Shapiro, Buehler, and the authors of the different articles you have quoted, because they are/were all only touting these views in order to gain grant money. I hope Shapiro never sees your comments.

DAVID: This still does [not] tell us how genes act to create the final physical results they control. We do see they order the production of certain proteins at certain places b ut we do not know exactly how they exert their controls. We just see beginning and end but not much of the middle molecular activity.

dhw: Precisely. We do not know how cells exert their controls.

DAVID: Misinterpreted. Note I said the genes control cell reactions. We don't know how that is done. Cells access the gene and respond. All we know is from outside the actual process. The gene may precisely tell the cell what to do, which is to make a precise set of protein molecules, and in this case placed at a precise position. An automatic response to direct instructions.

We do not know how the process works, but according to the articles, it is the cells that actively use passive genetic information and create or “figure out” their own instructions. I am not questioning that when the cell issues an instruction, the rest of the system automatically obeys.

DAVID: I still have a totally different interpretation as seen in my current comments.

And of course you have every right to your interpretation. But that does not mean no other interpretation is possible.

Under “How neurons grow their axons”

DAVID: Once again we see the complex controls and the resulting axon formation, but we have no information about how it all works, or how the cell and the cells genes manipulate each other. The inner workings are all a black box. We do not know whether all of this is automatic, or alternatively there must be some independent initiation activity.

After all the above, we now have a glimmer of recognition. Yes indeed, the alternative to your fixed belief is an INDEPENDENT - I call it “autonomous” - activity, whereby the cells independently create their own instructions by using their perhaps God-given intelligence.

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9005 views

dhw: So cells already know all the information necessary for every single innovation, lifestyle and natural wonder in the history of evolution, and along with that, your God has provided them with all the instructions necessary for picking out the one instruction (out of the billions) required for their particular situation. And this is your fixed belief?

DAVID: Unless I see research to convince me otherwise.

dhw: So whereabouts in the cell have you found the evidence for a 3.8-billion-year-old library of information and instructions for every single undabbled innovation, lifestyle and natural wonder in the history of life?

It is theoretical just like your cell committees.

DAVID: My bolds are all analogies that are imagined by the authors. The scientists re-directed cell activity by changing genes and the cells changed. The genes told them to change! All we know is the cells know how to interpret gene instructions. "An amazing tool' bold is the scientists praising heir new technique! All comment hyperbole. Remember these guys live by grant money, which they have to justify by touting their results. Please keep that in mind when you swallow the propaganda hook line and sinker. An interesting point: do you fully understand how the grant game is conducted?? I've had grants.

dhw: So now we should ignore the findings of Margulis, McClintock, Shapiro, Buehler, and the authors of the different articles you have quoted, because they are/were all only touting these views in order to gain grant money. I hope Shapiro never sees your comments.

I did not bring up MMSB. They existed before the current mess of ecstatic fake reviews of science overstating what the results mean, fraudulent peer reviews ,and actually proven fake results. I see what you don't. Chasing grant money for the sake of income. You sidestepped my question to you.

DAVID: This still does [not] tell us how genes act to create the final physical results they control. We do see they order the production of certain proteins at certain places b ut we do not know exactly how they exert their controls. We just see beginning and end but not much of the middle molecular activity.

dhw: Precisely. We do not know how cells exert their controls.

DAVID: Misinterpreted. Note I said the genes control cell reactions. We don't know how that is done. Cells access the gene and respond. All we know is from outside the actual process. The gene may precisely tell the cell what to do, which is to make a precise set of protein molecules, and in this case placed at a precise position. An automatic response to direct instructions.

dhw: We do not know how the process works, but according to the articles, it is the cells that actively use passive genetic information and create or “figure out” their own instructions. I am not questioning that when the cell issues an instruction, the rest of the system automatically obeys.

Of course cells use the information they have. Each cell follows what it is told to do by the genome.

DAVID: I still have a totally different interpretation as seen in my current comments.

And of course you have every right to your interpretation. But that does not mean no other interpretation is possible.

Under “How neurons grow their axons”

DAVID: Once again we see the complex controls and the resulting axon formation, but we have no information about how it all works, or how the cell and the cells genes manipulate each other. The inner workings are all a black box. We do not know whether all of this is automatic, or alternatively there must be some independent initiation activity.

dhw: After all the above, we now have a glimmer of recognition. Yes indeed, the alternative to your fixed belief is an INDEPENDENT - I call it “autonomous” - activity, whereby the cells independently create their own instructions by using their perhaps God-given intelligence.

And I am sure it is all following instructions from each cell genome.

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8940 views

DAVID: Unless I see research to convince me otherwise.

dhw: So whereabouts in the cell have you found the evidence for a 3.8-billion-year-old library of information and instructions for every single undabbled innovation, lifestyle and natural wonder in the history of life?

DAVID: It is theoretical just like your cell committees.

Of course it is. But despite the lack of evidence you are convinced that this astonishingly convoluted hypothesis is true, and you see no reason even to consider the possibility that one single mechanism might explain all the developments that have led to the vast higgledy-piggledy bush of life, allowing – theistic version – for dabbles.

DAVID: Remember these guys live by grant money, which they have to justify by touting their results. Please keep that in mind when you swallow the propaganda hook line and sinker. An interesting point: do you fully understand how the grant game is conducted?? I've had grants.

dhw: So now we should ignore the findings of Margulis, McClintock, Shapiro, Buehler, and the authors of the different articles you have quoted, because they are/were all only touting these views in order to gain grant money. I hope Shapiro never sees your comments.

DAVID: I did not bring up MMSB. They existed before the current mess of ecstatic fake reviews of science overstating what the results mean, fraudulent peer reviews ,and actually proven fake results. I see what you don't. Chasing grant money for the sake of income. You sidestepped my question to you.

Of course I sidestepped the question. Our subject is cellular intelligence, not the shenanigans of grant-hunting! Suddenly, an article which you quoted and said was an exact expression of your thoughts has become the product of fake results because you realize that its conclusions contradict your own beliefs. You could end up in court over such allegations!

DAVID: Note I said the genes control cell reactions. We don't know how that is done. Cells access the gene and respond. All we know is from outside the actual process. The gene may precisely tell the cell what to do, which is to make a precise set of protein molecules, and in this case placed at a precise position. An automatic response to direct instructions.

dhw: We do not know how the process works, but according to the articles, it is the cells that actively use passive genetic information and create or “figure out” their own instructions. I am not questioning that when the cell issues an instruction, the rest of the system automatically obeys.

DAVID: Of course cells use the information they have. Each cell follows what it is told to do by the genome.

Even if you were right, it could simply mean that the cell’s intelligence is located in the genome. But according to you, there is no intelligence. As above, your fixed belief is that the genome is a library containing not only all the passive information but also all the instructions necessary for the whole of evolution, and furthermore instructions on how to pick out the one and only instruction applicable to each individual situation.

DAVID: […] we have no information about how it all works, or how the cell and the cells genes manipulate each other. The inner workings are all a black box. We do not know whether all of this is automatic, or alternatively there must be some independent initiation activity.

dhw: After all the above, we now have a glimmer of recognition. Yes indeed, the alternative to your fixed belief is an INDEPENDENT - I call it “autonomous” - activity, whereby the cells independently create their own instructions by using their perhaps God-given intelligence.

DAVID: And I am sure it is all following instructions from each cell genome.

Despite your fixed belief, at least for once you have allowed for an autonomous alternative.

DAVID (under “Magic embryology”): The stem cells (blastocyst cells) must follow exact directions in their genomes to make perfectly functioning kidneys. This is the expectation of the authors of this study. True automaticity of cells following instructions to make perfectly functional kidneys. […]
All the processes of life must follow instructions or result in an aberration that is not viable. This is the theory behind my position on automaticity.

Of course all the processes must follow instructions. The great question is where those instructions come from in the first place. You have no evidence for your “library” hypothesis, as described above, but you don’t need any for it to be your fixed belief. Only alternative hypotheses require evidence.

I would love to know more about stem cells, as it seems to me that their versatility could provide a vital clue as to how evolutionary innovation works.

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8978 views

dhw: So whereabouts in the cell have you found the evidence for a 3.8-billion-year-old library of information and instructions for every single undabbled innovation, lifestyle and natural wonder in the history of life?

DAVID: It is theoretical just like your cell committees.

dhw: Of course it is. But despite the lack of evidence you are convinced that this astonishingly convoluted hypothesis is true, and you see no reason even to consider the possibility that one single mechanism might explain all the developments that have led to the vast higgledy-piggledy bush of life, allowing – theistic version – for dabbles.

But my opinion is based the fact that life continues through automatic activity,with no evidence of inventive activity except in Shapiro's bacterial studies..

dhw: So now we should ignore the findings of Margulis, McClintock, Shapiro, Buehler, and the authors of the different articles you have quoted, because they are/were all only touting these views in order to gain grant money. I hope Shapiro never sees your comments.

DAVID: I did not bring up MMSB. They existed before the current mess of ecstatic fake reviews of science overstating what the results mean, fraudulent peer reviews ,and actually proven fake results. I see what you don't. Chasing grant money for the sake of income. You sidestepped my question to you.

dhw: Of course I sidestepped the question. Our subject is cellular intelligence, not the shenanigans of grant-hunting! Suddenly, an article which you quoted and said was an exact expression of your thoughts has become the product of fake results because you realize that its conclusions contradict your own beliefs. You could end up in court over such allegations!

I think you know I use current science news reports and some actual papers to present here. We can only conclude a view or views based on the information presented, not the hyperbole that always seems to accompany their description. Note my entries about origin of life and how each new piece of lab work provides a way for life to easily appear, until you note the 'maybes' or 'possiblies' interspersed in some of the verbiage. My caution above is right on point. You love to look into the articles and quote, which I think you should, but I see you swallowing the hyperbole.

DAVID: Of course cells use the information they have. Each cell follows what it is told to do by the genome.

dhw: Even if you were right, it could simply mean that the cell’s intelligence is located in the genome. But according to you, there is no intelligence. As above, your fixed belief is that the genome is a library containing not only all the passive information but also all the instructions necessary for the whole of evolution, and furthermore instructions on how to pick out the one and only instruction applicable to each individual situation.

How do stem cells become a whole organism? Follow instructions to make an identical copy.

DAVID (under “Magic embryology”): The stem cells (blastocyst cells) must follow exact directions in their genomes to make perfectly functioning kidneys. This is the expectation of the authors of this study. True automaticity of cells following instructions to make perfectly functional kidneys. […]

All the processes of life must follow instructions or result in an aberration that is not viable. This is the theory behind my position on automaticity.[/i]

dhw: Of course all the processes must follow instructions. The great question is where those instructions come from in the first place. You have no evidence for your “library” hypothesis, as described above, but you don’t need any for it to be your fixed belief. Only alternative hypotheses require evidence.

I have my view of God the designer and instructor.

dhw: I would love to know more about stem cells, as it seems to me that their versatility could provide a vital clue as to how evolutionary innovation works.

The zygote (sperm and egg joined) become a hollow sphere of blastocyst cells, each one determined to direct construction of different parts of the embryo. A head/tail axis is established, and both genetic instructions for protein production and mechanical-biological forces play a role, as cells grow and push push other cells around. Most of it is still poorly understood.

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8920 views

DAVID: It is theoretical just like your cell committees.

dhw: Of course it is. But despite the lack of evidence you are convinced that this astonishingly convoluted hypothesis is true, and you see no reason even to consider the possibility that one single mechanism might explain all the developments that have led to the vast higgledy-piggledy bush of life, allowing – theistic version – for dabbles.

DAVID: But my opinion is based the fact that life continues through automatic activity, with no evidence of inventive activity except in Shapiro's bacterial studies.

The whole of evolution depends on inventive activity! Once the innovation has been invented, then it will be automatically repeated until conditions change, in which case there may be adaptation, extinction, and/or innovation. You have no evidence that all undabbled innovations (new inventions) derive from a 3.8-billion-year old library of information and instructions, plus instructions on how to choose the right instruction, but you are convinced that it is true because new inventions are automatically repeated and you reject the concept of cellular intelligence, although it has a 50/50 chance of being right. How does this count as evidence for your "library"?

dhw: Our subject is cellular intelligence, not the shenanigans of grant-hunting! Suddenly, an article which you quoted and said was an exact expression of your thoughts has become the product of fake results because you realize that its conclusions contradict your own beliefs. You could end up in court over such allegations!

DAVID: I think you know I use current science news reports and some actual papers to present here. We can only conclude a view or views based on the information presented, not the hyperbole that always seems to accompany their description. Note my entries about origin of life and how each new piece of lab work provides a way for life to easily appear, until you note the 'maybes' or 'possiblies' interspersed in some of the verbiage. My caution above is right on point. You love to look into the articles and quote, which I think you should, but I see you swallowing the hyperbole.

You quoted the article, and said it was an exact expression of your thoughts. You quote article after article that dwells on the automaticity of cellular behaviour, and never complain about the grant system (but in such cases frequently ignore the fact that nobody knows where the original instructions came from). Why don’t you stick to the subject and acknowledge that some highly reputable scientists believe/believed in cellular intelligence, and in your fairer moments you acknowledge that cellular behaviour appears to be intelligent, and there is a 50/50 chance that it is, but you yourself simply don’t believe in it?

DAVID: Of course cells use the information they have. Each cell follows what it is told to do by the genome.

dhw: Even if you were right, it could simply mean that the cell’s intelligence is located in the genome.

DAVID: How do stem cells become a whole organism? Follow instructions to make an identical copy.

The issue is where the instructions came from in the first place: your 3.8 billion-year-old library etc. as bolded above, or the cells themselves, with an inbuilt and perhaps God-given ability to process information and take their own decisions.

dhw: I would love to know more about stem cells, as it seems to me that their versatility could provide a vital clue as to how evolutionary innovation works.

DAVID: The zygote (sperm and egg joined) become a hollow sphere of blastocyst cells, each one determined to direct construction of different parts of the embryo. A head/tail axis is established, and both genetic instructions for protein production and mechanical-biological forces play a role, as cells grow and push push other cells around. Most of it is still poorly understood.

Yet again, the issue is where the original instructions came from, but what interests me here is the versatility of stem cells. When conditions change, cells/cell communities must also change if they are to survive (adaptation), but perhaps innovation takes place when certain cells are given totally new functions. It seems that stem cells can do precisely this.

DAVID: (under “How macrophages repair nerves”): Note how precise this mechanism is. The cells obviously don't stop and think about a plan of action. My usual question. How did chance evolution find this exact set of proteins?

Since these discussions have become confined to you and me, your usual question has become irrelevant. Both of us reject chance. The usual question has now become: did the process originate 1) through a 3.8-billion-year-old library of information and instructions to cover the whole of evolution, plus instructions on which instructions to follow; 2) divine dabbling; 3) the intelligence of cells working out ways to repair damage, precisely as bacteria work out ways to cope with new threats?

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8952 views

DAVID: But my opinion is based the fact that life continues through automatic activity, with no evidence of inventive activity except in Shapiro's bacterial studies.

dhw: The whole of evolution depends on inventive activity! Once the innovation has been invented, then it will be automatically repeated until conditions change, in which case there may be adaptation, extinction, and/or innovation. You have no evidence that all undabbled innovations (new inventions) derive from a 3.8-billion-year old library of information and instructions, plus instructions on how to choose the right instruction, but you are convinced that it is true because new inventions are automatically repeated and you reject the concept of cellular intelligence, although it has a 50/50 chance of being right. How does this count as evidence for your "library"?

I theorize and so do you. What has a 50/50 chance is only that cells have some ability to intelligently respond to stimuli with simple adaptations. The rest of your statement is conflation.

dhw: You quoted the article, and said it was an exact expression of your thoughts. You quote article after article that dwells on the automaticity of cellular behaviour, and never complain about the grant system (but in such cases frequently ignore the fact that nobody knows where the original instructions came from). Why don’t you stick to the subject and acknowledge that some highly reputable scientists believe/believed in cellular intelligence, and in your fairer moments you acknowledge that cellular behaviour appears to be intelligent, and there is a 50/50 chance that it is, but you yourself simply don’t believe in it?

Conflation again. I'm talking about current scientists, not the older ones you quote.

dhw: I would love to know more about stem cells, as it seems to me that their versatility could provide a vital clue as to how evolutionary innovation works.

DAVID: The zygote (sperm and egg joined) become a hollow sphere of blastocyst cells, each one determined to direct construction of different parts of the embryo. A head/tail axis is established, and both genetic instructions for protein production and mechanical-biological forces play a role, as cells grow and push push other cells around. Most of it is still poorly understood.

dhw:Yet again, the issue is where the original instructions came from, but what interests me here is the versatility of stem cells. When conditions change, cells/cell communities must also change if they are to survive (adaptation), but perhaps innovation takes place when certain cells are given totally new functions. It seems that stem cells can do precisely this.

Yes.

DAVID: (under “How macrophages repair nerves”): Note how precise this mechanism is. The cells obviously don't stop and think about a plan of action. My usual question. How did chance evolution find this exact set of proteins?

dhw: Since these discussions have become confined to you and me, your usual question has become irrelevant. Both of us reject chance. The usual question has now become: did the process originate 1) through a 3.8-billion-year-old library of information and instructions to cover the whole of evolution, plus instructions on which instructions to follow; 2) divine dabbling; 3) the intelligence of cells working out ways to repair damage, precisely as bacteria work out ways to cope with new threats?

Multicellular organisms are not bacteria. I don't think Shapiro's point carries over.

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8928 views

DAVID: But my opinion is based the fact that life continues through automatic activity, with no evidence of inventive activity except in Shapiro's bacterial studies.

dhw: The whole of evolution depends on inventive activity! Once the innovation has been invented, then it will be automatically repeated until conditions change, in which case there may be adaptation, extinction, and/or innovation. You have no evidence that all undabbled innovations (new inventions) derive from a 3.8-billion-year old library of information and instructions, plus instructions on how to choose the right instruction, but you are convinced that it is true because new inventions are automatically repeated and you reject the concept of cellular intelligence, although it has a 50/50 chance of being right. How does this count as evidence for your "library"?

DAVID: I theorize and so do you. What has a 50/50 chance is only that cells have some ability to intelligently respond to stimuli with simple adaptations. The rest of your statement is conflation.

The rest of my statement concerns your own hypothesis, so I don’t know what you think I’m conflating. Nobody knows how innovation takes place, although it is sometimes difficult to draw a borderline between invention and adaptation (e.g. legs becoming fins and vice versa), but at least we know that adaptation does happen, and you have not (yet) included instructions for that in your vast library. And so you have a fixed belief in an extraordinarily convoluted hypothesis, as bolded, for which there is no evidence, but you reject a far more straightforward hypothesis because there is no evidence.

dhw:[…] Why don’t you stick to the subject and acknowledge that some highly reputable scientists believe/believed in cellular intelligence, and in your fairer moments you acknowledge that cellular behaviour appears to be intelligent, and there is a 50/50 chance that it is, but you yourself simply don’t believe in it?

DAVID: Conflation again. I'm talking about current scientists, not the older ones you quote.

Shapiro is not an “older one”, and it is absurd and probably libellous to dismiss the findings of current scientists as fake simply because they confirm the findings of older scientists with whom you disagree. You never complain about the grant system if an article seems to support your own fixed belief in "automaticity", and in any case you didn’t disagree with the article you quoted: you said it expressed your own thoughts.

dhw:[…]. Both of us reject chance. The usual question has now become: did the process originate 1) through a 3.8-billion-year-old library of information and instructions to cover the whole of evolution, plus instructions on which instructions to follow; 2) divine dabbling; 3) the intelligence of cells working out ways to repair damage, precisely as bacteria work out ways to cope with new threats?

DAVID: Multicellular organisms are not bacteria. I don't think Shapiro's point carries over.

At least you now seem to be accepting Shapiro’s view that bacteria work out their own ways to cope with new threats. Do you honestly think that if single cells can do this, communities of cells can’t?

dhw:[…] what interests me here is the versatility of stem cells. When conditions change, cells/cell communities must also change if they are to survive (adaptation), but perhaps innovation takes place when certain cells are given totally new functions. It seems that stem cells can do precisely this.
DAVID: Yes.

DAVID: (under “stem cells”) I can't find my recent entry which indicated not much is known, but here is an entry about a coming conference:
https://www.the-scientist.com/sponsored-webinars/stem-cells--opportunities--hurdles--an...

"Since Sir. Martin Evans’ 1981 identification of embryonic stem cells in mice, stem cells have been at the center of the drive to revolutionize medicine and the drug discovery process. In 1998, human embryonic stem cells were grown in a lab, and the field was further boosted in 2006 with the pivotal discovery of induced pluripotent stem (iPS) cell techniques, which removed the need to destroy embryos. […] The Scientist is bringing together a panel of experts who will share their research, explore cellular reprogramming, and discuss the next steps.
"Topics to be covered:
Molecular mechanism of induced pluripotency
Roadblocks to iPSC reprogramming, and erasing transcriptional memory in cellular reprogramming"

DAVID: all that is known is from very recent work

Maybe the conference will yield more details, though the experts don't seem to be concerned with possible implications for how evolution works. What they call “pluripotency” (= my “versatility”) could be the key to the whole process. Many thanks for searching.

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DAVID: I theorize and so do you. What has a 50/50 chance is only that cells have some ability to intelligently respond to stimuli with simple adaptations. The rest of your statement is conflation.

dhw: The rest of my statement concerns your own hypothesis, so I don’t know what you think I’m conflating. Nobody knows how innovation takes place, although it is sometimes difficult to draw a borderline between invention and adaptation (e.g. legs becoming fins and vice versa), but at least we know that adaptation does happen, and you have not (yet) included instructions for that in your vast library.

The bold in your comment above is conflation. Changing leg to fin is full blown evolution of a new species, never to be compared to minor adaptation which is all bacteria do. They adapt but do not change into a new species. Lenski's E. coli are a clear example with some alterations in metabolic use of substrates. What most cells do in all organs is their job without variations.

dhw: And so you have a fixed belief in an extraordinarily convoluted hypothesis, as bolded, for which there is no evidence, but you reject a far more straightforward hypothesis because there is no evidence.

As Paul Davies notes, "we don't know how the hardware produces the software', to which
I answer, the genome has many functional layers we still do not understand. My theory lies in those areas as an expectation Davies answer will be found there. I'll change my view based on factual research. Convolution is in the eye of the beholder. Living biochemistry is extremely complicated which includes convolutions of many processes operating in concert and at times antagonistically in feedback loops.

DAVID: Conflation again. I'm talking about current scientists, not the older ones you quote.

dhw: Shapiro is not an “older one”, and it is absurd and probably libellous to dismiss the findings of current scientists as fake simply because they confirm the findings of older scientists with whom you disagree. You never complain about the grant system if an article seems to support your own fixed belief in "automaticity", and in any case you didn’t disagree with the article you quoted: you said it expressed your own thoughts.

You are off point. I'm discussing the very current overstatements of the research results as to proof. Again look at the series of theoretical origin of life for examples. The hyperbole
is a recent event in the past ten years or so. Faux articles are constantly being accepted by borderline journals. I still have the right to present and re-interpret the findings, in order to counter to the overblown conclusions. Findings are fixed fact. Interpretations are another breed of cat.

DAVID: Multicellular organisms are not bacteria. I don't think Shapiro's point carries over.

dhw: At least you now seem to be accepting Shapiro’s view that bacteria work out their own ways to cope with new threats. Do you honestly think that if single cells can do this, communities of cells can’t?

In multicellular organisms things are much more complex and cells in organs have very specific fixed jobs. Single cells must do everything and must be able to make simple altered responses to a variety of stimuli that present themselves, a wholly different set of circumstances that does not transfer over to the much more complex organisms. You are trying to compare cows to clams.

dhw:[…] what interests me here is the versatility of stem cells. When conditions change, cells/cell communities must also change if they are to survive (adaptation), but perhaps innovation takes place when certain cells are given totally new functions. It seems that stem cells can do precisely this.
DAVID: Yes.

DAVID: (under “stem cells”) I can't find my recent entry which indicated not much is known, but here is an entry about a coming conference:
https://www.the-scientist.com/sponsored-webinars/stem-cells--opportunities--hurdles--an...

"Since Sir. Martin Evans’ 1981 identification of embryonic stem cells in mice, stem cells have been at the center of the drive to revolutionize medicine and the drug discovery process. In 1998, human embryonic stem cells were grown in a lab, and the field was further boosted in 2006 with the pivotal discovery of induced pluripotent stem (iPS) cell techniques, which removed the need to destroy embryos. […] The Scientist is bringing together a panel of experts who will share their research, explore cellular reprogramming, and discuss the next steps.
"Topics to be covered:
Molecular mechanism of induced pluripotency
Roadblocks to iPSC reprogramming, and erasing transcriptional memory in cellular reprogramming"

DAVID: all that is known is from very recent work

dhw: Maybe the conference will yield more details, though the experts don't seem to be concerned with possible implications for how evolution works. What they call “pluripotency” (= my “versatility”) could be the key to the whole process. Many thanks for searching.

Speciation must be done through stem cells. We know of some processes that alter their eventual output, both chemical and mechanical.

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dhw: Nobody knows how innovation takes place, although it is sometimes difficult to draw a borderline between invention and adaptation (e.g. legs becoming fins and vice versa), but at least we know that adaptation does happen, and you have not (yet) included instructions for that in your vast library.

DAVID: [...] Changing leg to fin is full blown evolution of a new species, never to be compared to minor adaptation which is all bacteria do. They adapt but do not change into a new species. […]

In your hypothesis, apparently your God either fitted the first living cells with a programme for pre-whale leg replacement (in addition to programmes for every other change in the history of evolution), or popped in personally to amputate the legs of pre-whales and insert flippers/fins in their place. My proposal is that pre-whales entered the water, and their cell communities adapted existing structures to make the body more suited to life at sea. Three unproven hypotheses to explain speciation.

dhw: And so you have a fixed belief in an extraordinarily convoluted hypothesis, as bolded, for which there is no evidence, but you reject a far more straightforward hypothesis because there is no evidence.

DAVID: As Paul Davies notes, "we don't know how the hardware produces the software', to which I answer, the genome has many functional layers we still do not understand. My theory lies in those areas as an expectation Davies answer will be found there.

Nobody knows how speciation happened. If your 3.8 billion-year-old library of information and instructions for the whole of evolution might be found in the genome, then so might an autonomous brain equivalent which allows cells to work out their own innovations.

DAVID: I'll change my view based on factual research. […] Living biochemistry is extremely complicated which includes convolutions of many processes operating in concert and at times antagonistically in feedback loops.

You will change your “library” view, for which there is not one jot of factual evidence, only if factual evidence is found for a different view. This might be seen as the epitome of dogmatism. Nobody is denying the complexity of living biochemistry. That does not mean your “library” is more likely than a brain equivalent.

DAVID [on the subject of grants and fake research): You are off point. I'm discussing the very current overstatements of the research results as to proof. Again look at the series of theoretical origin of life for examples. The hyperbole is a recent event in the past ten years or so. Faux articles are constantly being accepted by borderline journals. I still have the right to present and re-interpret the findings, in order to counter to the overblown conclusions. Findings are fixed fact. Interpretations are another breed of cat.

All agreed, but the subject we are discussing is what genes do and don’t do. You quoted (and initially agreed with) an article which explicitly supported the view that cells issue their own instructions (as opposed to your belief that their behaviour has been preprogrammed by a divinely compiled, 3.8 billion-year-old library of information and instructions), thus supporting the views of Shapiro and older scientists who firmly believe that cells are intelligent. Sorry, but changing the subject to fake research and the grant system does not support your case for cellular “library” versus cellular intelligence.

DAVID: Multicellular organisms are not bacteria. I don't think Shapiro's point carries over.

dhw: At least you now seem to be accepting Shapiro’s view that bacteria work out their own ways to cope with new threats. Do you honestly think that if single cells can do this, communities of cells can’t?

DAVID: In multicellular organisms things are much more complex and cells in organs have very specific fixed jobs. Single cells must do everything and must be able to make simple altered responses to a variety of stimuli that present themselves, a wholly different set of circumstances that does not transfer over to the much more complex organisms. You are trying to compare cows to clams.

The greater the complexity, the more intelligence needed to run the show. If single cells can work out their own solutions to their problems, why do you think cell communities can’t do the same? Ever heard of cooperation?

DAVID: Speciation must be done through stem cells. We know of some processes that alter their eventual output, both chemical and mechanical.

Thank you. This is indeed what interests me. Once a stem cell is given a new function, it retains that function and so, following the principle of common descent, theoretically perhaps we should begin with stem cells: i.e. the original cells had the potential to develop into every form we now know. The variations and innovations brought about by multicellularity (= evolution) would then – in my hypothesis - be the result of stem cells being given new roles by existing cell communities as they respond to ever changing conditions.

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dhw: In your hypothesis, apparently your God either fitted the first living cells with a programme for pre-whale leg replacement (in addition to programmes for every other change in the history of evolution), or popped in personally to amputate the legs of pre-whales and insert flippers/fins in their place. My proposal is that pre-whales entered the water, and their cell communities adapted existing structures to make the body more suited to life at sea. Three unproven hypotheses to explain speciation.

I accept only my either/or God control.

dhw: And so you have a fixed belief in an extraordinarily convoluted hypothesis, as bolded, for which there is no evidence, but you reject a far more straightforward hypothesis because there is no evidence.

DAVID: As Paul Davies notes, "we don't know how the hardware produces the software', to which I answer, the genome has many functional layers we still do not understand. My theory lies in those areas as an expectation Davies answer will be found there.

dhw: Nobody knows how speciation happened. If your 3.8 billion-year-old library of information and instructions for the whole of evolution might be found in the genome, then so might an autonomous brain equivalent which allows cells to work out their own innovations.

The only evidence of such a cellular brain is the genome which carries instruction information.

DAVID: I'll change my view based on factual research. […] Living biochemistry is extremely complicated which includes convolutions of many processes operating in concert and at times antagonistically in feedback loops.

dhw: You will change your “library” view, for which there is not one jot of factual evidence, only if factual evidence is found for a different view. This might be seen as the epitome of dogmatism. Nobody is denying the complexity of living biochemistry. That does not mean your “library” is more likely than a brain equivalent.

How life works is still a black box. I'l wait patiently for more research.

DAVID I still have the right to present and re-interpret the findings, in order to counter to the overblown conclusions. Findings are fixed fact. Interpretations are another breed of cat.[/i]

dhw: All agreed, but the subject we are discussing is what genes do and don’t do. You quoted (and initially agreed with) an article which explicitly supported the view that cells issue their own instructions (as opposed to your belief that their behaviour has been preprogrammed by a divinely compiled, 3.8 billion-year-old library of information and instructions), thus supporting the views of Shapiro and older scientists who firmly believe that cells are intelligent. Sorry, but changing the subject to fake research and the grant system does not support your case for cellular “library” versus cellular intelligence.

DAVID: Multicellular organisms are not bacteria. I don't think Shapiro's point carries over.

dhw: At least you now seem to be accepting Shapiro’s view that bacteria work out their own ways to cope with new threats. Do you honestly think that if single cells can do this, communities of cells can’t?

DAVID: In multicellular organisms things are much more complex and cells in organs have very specific fixed jobs. Single cells must do everything and must be able to make simple altered responses to a variety of stimuli that present themselves, a wholly different set of circumstances that does not transfer over to the much more complex organisms. You are trying to compare cows to clams.

dhw: The greater the complexity, the more intelligence needed to run the show. If single cells can work out their own solutions to their problems, why do you think cell communities can’t do the same? Ever heard of cooperation?

Again your nebulous committee of cells illusion. In multicellular organs c ells have strictly bound fixed roles. Legs do not know how to become flippers. Taht change requires design from an outside designer.

dhw:[…] what interests me here is the versatility of stem cells. When conditions change, cells/cell communities must also change if they are to survive (adaptation), but perhaps innovation takes place when certain cells are given totally new functions. It seems that stem cells can do precisely this.

DAVID: Speciation must be done through stem cells. We know of some processes that alter their eventual output, both chemical and mechanical.

dhw: Thank you. This is indeed what interests me. Once a stem cell is given a new function, it retains that function and so, following the principle of common descent, theoretically perhaps we should begin with stem cells: i.e. the original cells had the potential to develop into every form we now know. The variations and innovations brought about by multicellularity (= evolution) would then – in my hypothesis - be the result of stem cells being given new roles by existing cell communities as they respond to ever changing conditions.

Stem cells were discovered about ten years ago and are known to respond to chemical and mechanical pressures as they form an organ. The rest is still a blank. Tell me how cell committees instruct new roles when cells have plenty to do constantly producing new protein product? Shapiro re-editing DNA applies only to bacteria.

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dhw: In your hypothesis, apparently your God either fitted the first living cells with a programme for pre-whale leg replacement (in addition to programmes for every other change in the history of evolution), or popped in personally to amputate the legs of pre-whales and insert flippers/fins in their place. My proposal is that pre-whales entered the water, and their cell communities adapted existing structures to make the body more suited to life at sea. Three unproven hypotheses to explain speciation.

DAVID: I accept only my either/or God control.

I am aware of your dogmatic faith in two of the three hypotheses. I am merely pointing out that there is no evidence for them, and so you can hardly reject the third on the grounds you offer below:

dhw: Nobody knows how speciation happened. If your 3.8 billion-year-old library of information and instructions for the whole of evolution might be found in the genome, then so might an autonomous brain equivalent which allows cells to work out their own innovations.

DAVID: The only evidence of such a cellular brain is the genome which carries instruction information.

dhw: You will change your “library” view, for which there is not one jot of factual evidence, only if factual evidence is found for a different view. This might be seen as the epitome of dogmatism. Nobody is denying the complexity of living biochemistry. That does not mean your “library” is more likely than a brain equivalent.

DAVID: How life works is still a black box. I'll wait patiently for more research.

But you are not waiting patiently. You have a fixed belief in your library and/or dabbling, and you reject the third hypothesis.

dhw: The greater the complexity, the more intelligence needed to run the show. If single cells can work out their own solutions to their problems, why do you think cell communities can’t do the same? Ever heard of cooperation?

DAVID: Again your nebulous committee of cells illusion. In multicellular organs cells have strictly bound fixed roles. Legs do not know how to become flippers. That change requires design from an outside designer.

Of course cells have fixed roles once speciation has taken place. Otherwise the new species would not survive! The question (your “black box”) is how legs became flippers in the first place. There is nothing nebulous about cell cooperation. We KNOW cells cooperate. What we don’t know is whether their cooperation can produce the innovations which result in speciation. Nor do we know that your 3.8-billion-year-old library exists, or that your God popped in to perform leg amputations and flipper grafts.

Thank you for the three articles (especially the James Tour one). Your comments are as applicable to speciation as to the origin of life.

Constructor theory sophistry
DAVID: Note the bolds. It is never stated where the knowledge or information comes from or how it is created. It is simply assumed to appear.

Just as it is not stated what mechanism is available to interpret and process the information, and decide on the appropriate way to use it.

Information as the source of life
DAVID: As in my entry just a few minutes ago, where does the information come from? Life must have its own operating system to interpreting the code and acting on the information contained in it.

Absolutely, but I would slightly change your wording: living organisms (= cell communities) must have their own (i.e. autonomous) operating system. I find it hard to believe that they are all mere automatons, obeying instructions issued 3.8 billion years ago, and without a clue as to what they are interpreting and what actions they should take.

James Tour: " We synthetic chemists should state the obvious. The appearance of life on earth is a mystery. We are nowhere near solving this problem. The proposals offered thus far to explain life’s origin make no scientific sense.”

Ditto the mysteries of consciousness and speciation. Great article, which should be compulsory reading for all theists and atheists!

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8976 views

dhw: You will change your “library” view, for which there is not one jot of factual evidence, only if factual evidence is found for a different view. This might be seen as the epitome of dogmatism. Nobody is denying the complexity of living biochemistry. That does not mean your “library” is more likely than a brain equivalent.

DAVID: How life works is still a black box. I'll wait patiently for more research.

dhw: But you are not waiting patiently. You have a fixed belief in your library and/or dabbling, and you reject the third hypothesis.

All hypotheses are possibilities but I am not a picket fence sitter, and based on all the evidence available pick one which is my current preference for belief. Starting with if there is overwhelming evidence of design, there must be designer

dhw: The greater the complexity, the more intelligence needed to run the show. If single cells can work out their own solutions to their problems, why do you think cell communities can’t do the same? Ever heard of cooperation?

DAVID: Again your nebulous committee of cells illusion. In multicellular organs cells have strictly bound fixed roles. Legs do not know how to become flippers. That change requires design from an outside designer.

dhw: Of course cells have fixed roles once speciation has taken place. Otherwise the new species would not survive! The question (your “black box”) is how legs became flippers in the first place. There is nothing nebulous about cell cooperation. We KNOW cells cooperate. What we don’t know is whether their cooperation can produce the innovations which result in speciation. Nor do we know that your 3.8-billion-year-old library exists, or that your God popped in to perform leg amputations and flipper grafts.

Cell cooperation is REQUIRED in organs. You just noted the fixed roles. The cells have a fixed set of requirements, which tells us they cannot change! You want them to think. That is the designer's role.

Thank you for the three articles (especially the James Tour one). Your comments are as applicable to speciation as to the origin of life.

Constructor theory sophistry
DAVID: Note the bolds. It is never stated where the knowledge or information comes from or how it is created. It is simply assumed to appear.

dhw: Just as it is not stated what mechanism is available to interpret and process the information, and decide on the appropriate way to use it.

Information as the source of life
DAVID: As in my entry just a few minutes ago, where does the information come from? Life must have its own operating system to interpreting the code and acting on the information contained in it.

dhw: Absolutely, but I would slightly change your wording: living organisms (= cell communities) must have their own (i.e. autonomous) operating system. I find it hard to believe that they are all mere automatons, obeying instructions issued 3.8 billion years ago, and without a clue as to what they are interpreting and what actions they should take.

I know that is your view, just as I view all the enormous number of automatic biochemical processes of living forms coordinate their resulting outputs to have life emerge. All designed.

James Tour: " We synthetic chemists should state the obvious. The appearance of life on earth is a mystery. We are nowhere near solving this problem. The proposals offered thus far to explain life’s origin make no scientific sense.”

dhw: Ditto the mysteries of consciousness and speciation. Great article, which should be compulsory reading for all theists and atheists!

Dr. Tour is in Houston at Rice University. He is a Jewish believer

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DAVID: How life works is still a black box. I'll wait patiently for more research.

dhw: But you are not waiting patiently. You have a fixed belief in your library and/or dabbling, and you reject the third hypothesis.

DAVID: All hypotheses are possibilities but I am not a picket fence sitter, and based on all the evidence available pick one which is my current preference for belief. Starting with if there is overwhelming evidence of design, there must be designer.

In our discussions I have always expressly allowed for the existence of a designer. And although my own credulity is stretched beyond its limits when you claim that the very first cells contained a library of information and instructions to cover the whole of evolution, you are of course entitled to believe whatever you want to believe. My objection is to your outright rejection of the alternative hypothesis I have proposed. But I quite like the moderate tone of “current preference for belief”!

dhw: Of course cells have fixed roles once speciation has taken place. Otherwise the new species would not survive! The question (your “black box”) is how legs became flippers in the first place. There is nothing nebulous about cell cooperation. We KNOW cells cooperate. What we don’t know is whether their cooperation can produce the innovations which result in speciation. Nor do we know that your 3.8-billion-year-old library exists, or that your God popped in to perform leg amputations and flipper grafts.

DAVID: Cell cooperation is REQUIRED in organs. You just noted the fixed roles. The cells have a fixed set of requirements, which tells us they cannot change! You want them to think. That is the designer's role.

Of course it’s required, so why do you keep pooh-poohing it as “cell committees”? I have answered this in the passage you have quoted, but I’d better repeat it: once an innovation has proved successful (and we have a new species), the cells MUST continue to play their fixed roles. Otherwise, the species won’t survive. “Thinking” comes into play when there are new problems or conditions to cope with. But you prefer to believe in your library and/or direct divine surgery.

dhw: Absolutely, but I would slightly change your wording: living organisms (= cell communities) must have their own (i.e. autonomous) operating system. I find it hard to believe that they are all mere automatons, obeying instructions issued 3.8 billion years ago, and without a clue as to what they are interpreting and what actions they should take.

DAVID: I know that is your view, just as I view all the enormous number of automatic biochemical processes of living forms coordinate their resulting outputs to have life emerge. All designed.

I changed your wording because “life” doesn’t interpret or act. Organisms do that. You had switched from the source of life to what living organisms do, and your wording – “own operating system” to interpret and act – sounds more convincing to me than your belief that your God preprogrammed or dabbled every innovation etc. in the history of life.

James Tour: " We synthetic chemists should state the obvious. The appearance of life on earth is a mystery. We are nowhere near solving this problem. The proposals offered thus far to explain life’s origin make no scientific sense.”

dhw: Ditto the mysteries of consciousness and speciation. Great article, which should be compulsory reading for all theists and atheists!

DAVID: Dr. Tour is in Houston at Rice University. He is a Jewish believer.

No problem, so long as he acknowledges that his own explanation of life’s origin makes no scientific sense either. I don’t object to faith. I object to people who have faith in God or in chance denigrating one another’s faith and pretending they know better.

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8980 views

dhw: Of course cells have fixed roles once speciation has taken place. Otherwise the new species would not survive! The question (your “black box”) is how legs became flippers in the first place. There is nothing nebulous about cell cooperation. We KNOW cells cooperate. What we don’t know is whether their cooperation can produce the innovations which result in speciation. Nor do we know that your 3.8-billion-year-old library exists, or that your God popped in to perform leg amputations and flipper grafts.

DAVID: Cell cooperation is REQUIRED in organs. You just noted the fixed roles. The cells have a fixed set of requirements, which tells us they cannot change! You want them to think. That is the designer's role.

dhw: Of course it’s required, so why do you keep pooh-poohing it as “cell committees”? I have answered this in the passage you have quoted, but I’d better repeat it: once an innovation has proved successful (and we have a new species), the cells MUST continue to play their fixed roles. Otherwise, the species won’t survive. “Thinking” comes into play when there are new problems or conditions to cope with. But you prefer to believe in your library and/or direct divine surgery.

Again, I don't believe the large steps required in rearranging a species into a new one is simply cell adaptation. It requires a new design only a designer can create.

Information as the source of life
DAVID: As in my entry just a few minutes ago, where does the information come from? Life must have its own operating system to interpreting the code and acting on the information contained in it.

dhw: Absolutely, but I would slightly change your wording: living organisms (= cell communities) must have their own (i.e. autonomous) operating system. I find it hard to believe that they are all mere automatons, obeying instructions issued 3.8 billion years ago, and without a clue as to what they are interpreting and what actions they should take.

DAVID: I know that is your view, just as I view all the enormous number of automatic biochemical processes of living forms coordinate their resulting outputs to have life emerge. All designed.

dhw: I changed your wording because “life” doesn’t interpret or act. Organisms do that. You had switched from the source of life to what living organisms do, and your wording – “own operating system” to interpret and act – sounds more convincing to me than your belief that your God preprogrammed or dabbled every innovation etc. in the history of life.

The use of 'life' or 'living organisms' is all the same to me, although your quibble is technically correct. My point is living organisms run on information stored in the genome, much of which had to be pre-programmed for life to have formed at all. Inorganic matter does not have functional information, which means as life started from the inorganic, information had to be GIVEN from someone.

James Tour: " We synthetic chemists should state the obvious. The appearance of life on earth is a mystery. We are nowhere near solving this problem. The proposals offered thus far to explain life’s origin make no scientific sense.”

dhw: Ditto the mysteries of consciousness and speciation. Great article, which should be compulsory reading for all theists and atheists!

DAVID: Dr. Tour is in Houston at Rice University. He is a Jewish believer.

dhw: No problem, so long as he acknowledges that his own explanation of life’s origin makes no scientific sense either. I don’t object to faith. I object to people who have faith in God or in chance denigrating one another’s faith and pretending they know better.

The difficulty in making organic molecules by human effort compared to living processes ease in doing it is his main point.

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dhw: Of course it’s required, so why do you keep pooh-poohing it as “cell committees”? […] once an innovation has proved successful (and we have a new species), the cells MUST continue to play their fixed roles. Otherwise, the species won’t survive. “Thinking” comes into play when there are new problems or conditions to cope with. But you prefer to believe in your library and/or direct divine surgery.

DAVID: Again, I don't believe the large steps required in rearranging a species into a new one is simply cell adaptation. It requires a new design only a designer can create.

I have never said speciation was “simply cell adaptation”. But it is sometimes difficult to draw a borderline between adaptation and innovation, as in legs becoming flippers. And I have repeated ad nauseam that we do not know if cell communities can innovate (= take the necessary large steps), which is why my hypothesis is an unproven hypothesis, as is your own.

DAVID: Life must have its own operating system to interpreting the code and acting on the information contained in it.
[…]
dhw: I changed your wording because “life” doesn’t interpret or act. Organisms do that. You had switched from the source of life to what living organisms do, and your wording – “own operating system” to interpret and act – sounds more convincing to me than your belief that your God preprogrammed or dabbled every innovation etc. in the history of life.

DAVID: The use of 'life' or 'living organisms' is all the same to me, although your quibble is technically correct. My point is living organisms run on information stored in the genome, much of which had to be pre-programmed for life to have formed at all. Inorganic matter does not have functional information, which means as life started from the inorganic, information had to be GIVEN from someone.

Once again you scurry back to the origin of life, whereas my point is that living organisms do NOT run on information stored in the genome but – in your own words – they run on their “own operating system” for interpreting that information and acting on it. Information without the means to interpret and act on it would be no use to any organism. But having told us that organisms must have their own operating system, you still insist that they don’t – all their actions are apparently the result of your God’s dabbles or their automatic, non-interpreting, non-decision-making obedience to instructions passed down by the first living cells through 3.8 billion years’ worth of innovations, lifestyles and natural wonders.

Under “Bacterial antibiotic resistance”

QUOTES: “No research to date has explained the underlying mechanisms of heteroresistance. “

“A range of genetic investigations also enabled the researchers to show that the underlying mechanism of heteroresistance was often spontaneous occurrence of gene amplifications of various antibiotic resistance genes.”

“These gene amplifications are unstable, and as a result, antibiotic-resistant bacteria can rapidly revert to susceptibility again. This instability makes heteroresistance difficult to detect and study[…]. Accordingly, bacteria can be classified as susceptible although they are actually resistant, and this may lead to use of the wrong antibiotic and failure of the treatment."

DAVID: As I've previously noted, many bacterial populations have a variety of resistant and non-resistant individuals, so that group will survive on their own without gene transfer, which is another mechanism.

Maybe the mechanism is not “spontaneous”, and maybe resistance/non-resistance depends on what you would call each bacterium’s “own operating system” for interpreting information and acting on it, i.e. “single cells change their metabolic pathways"… and “learn” and “create instructions on the hoof”, as proposed in the article you initially agreed with. The expansion of resistant bacteria would then take time because those bacteria which work out the solution to the new problems would have to pass on the new information.

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8966 views

DAVID: Again, I don't believe the large steps required in rearranging a species into a new one is simply cell adaptation. It requires a new design only a designer can create.

dhw: I have never said speciation was “simply cell adaptation”. But it is sometimes difficult to draw a borderline between adaptation and innovation, as in legs becoming flippers. And I have repeated ad nauseam that we do not know if cell communities can innovate (= take the necessary large steps), which is why my hypothesis is an unproven hypothesis, as is your own.

The problem for you is you accept the necessity for design but not the designer.

DAVID: The use of 'life' or 'living organisms' is all the same to me, although your quibble is technically correct. My point is living organisms run on information stored in the genome, much of which had to be pre-programmed for life to have formed at all. Inorganic matter does not have functional information, which means as life started from the inorganic, information had to be GIVEN from someone.

dhw: Once again you scurry back to the origin of life, whereas my point is that living organisms do NOT run on information stored in the genome but – in your own words – they run on their “own operating system” for interpreting that information and acting on it. Information without the means to interpret and act on it would be no use to any organism. But having told us that organisms must have their own operating system, you still insist that they don’t – all their actions are apparently the result of your God’s dabbles or their automatic, non-interpreting, non-decision-making obedience to instructions passed down by the first living cells through 3.8 billion years’ worth of innovations, lifestyles and natural wonders.

Just like Darwin (as usual) you avoid the origin of life, the worst problem for naturalism, which exists in a continuum with further evolution and most always be part of the discussion.

dhw: Under “Bacterial antibiotic resistance”

QUOTES: “No research to date has explained the underlying mechanisms of heteroresistance. “

“A range of genetic investigations also enabled the researchers to show that the underlying mechanism of heteroresistance was often spontaneous occurrence of gene amplifications of various antibiotic resistance genes.”

“These gene amplifications are unstable, and as a result, antibiotic-resistant bacteria can rapidly revert to susceptibility again. This instability makes heteroresistance difficult to detect and study[…]. Accordingly, bacteria can be classified as susceptible although they are actually resistant, and this may lead to use of the wrong antibiotic and failure of the treatment."

DAVID: As I've previously noted, many bacterial populations have a variety of resistant and non-resistant individuals, so that group will survive on their own without gene transfer, which is another mechanism.

dhw: Maybe the mechanism is not “spontaneous”, and maybe resistance/non-resistance depends on what you would call each bacterium’s “own operating system” for interpreting information and acting on it, i.e. “single cells change their metabolic pathways"… and “learn” and “create instructions on the hoof”, as proposed in the article you initially agreed with. The expansion of resistant bacteria would then take time because those bacteria which work out the solution to the new problems would have to pass on the new information.

The one percent who have resistance multiply every 20 minutes. Not much time to take. Lenski's E.coli show this.

Post reply

9015 views

DAVID: Again, I don't believe the large steps required in rearranging a species into a new one is simply cell adaptation. [...]

dhw: I have never said speciation was “simply cell adaptation”. But it is sometimes difficult to draw a borderline between adaptation and innovation, as in legs becoming flippers. And I have repeated ad nauseam that we do not know if cell communities can innovate (= take the necessary large steps), which is why my hypothesis is an unproven hypothesis, as is your own.

DAVID: The problem for you is you accept the necessity for design but not the designer.

That is why I am an agnostic and do not confine my hypotheses to a single, top-down designer. But we are discussing the process of evolution, not my agnosticism.

DAVID: My point is living organisms run on information stored in the genome, much of which had to be pre-programmed for life to have formed at all. Inorganic matter does not have functional information, which means as life started from the inorganic, information had to be GIVEN from someone.

dhw: Once again you scurry back to the origin of life, whereas my point is that living organisms do NOT run on information stored in the genome but – in your own words – they run on their “own operating system” for interpreting that information and acting on it. Information without the means to interpret and act on it would be no use to any organism. But having told us that organisms must have their own operating system, you still insist that they don’t – all their actions are apparently the result of your God’s dabbles or their automatic, non-interpreting, non-decision-making obedience to instructions passed down by the first living cells through 3.8 billion years’ worth of innovations, lifestyles and natural wonders.

DAVID: Just like Darwin (as usual) you avoid the origin of life, the worst problem for naturalism, which exists in a continuum with further evolution and most always be part of the discussion.

Why “must” it be? In our discussions I have accepted the possibility that your God designed the first living organisms. (So, by the way, did the agnostic Darwin.) Our disagreement concerns Chapter 2: if your God exists, and if – as we both believe – evolution took place, then what were his purposes and methods?

Dhw (re bacterial resistance): Maybe the mechanism is not “spontaneous”, and maybe resistance/non-resistance depends on what you would call each bacterium’s “own operating system” for interpreting information and acting on it, i.e. “single cells change their metabolic pathways"… and “learn” and “create instructions on the hoof”, as proposed in the article you initially agreed with. The expansion of resistant bacteria would then take time because those bacteria which work out the solution to the new problems would have to pass on the new information.

DAVID: The one percent who have resistance multiply every 20 minutes. Not much time to take. Lenski's E.coli show this.

Time is not the main point here, as we are discussing the mechanisms that enable resistance: your 3.8-billion year old library of information and instructions, or an autonomously intelligent “own operating system” in which bacteria create their own instructions. I mentioned time because it can take a while before antibiotics become ineffective.
xxxxx

Under “new axons may make local decisions”:

DAVID: A new study strongly suggests that newly developing axons have some degree of self-control […] (dhw’s bold)

If distant parts of the system have a degree of self-control, doesn't this suggest to you that the central part of the system itself also has self-control or, in your own words, its "own operating system".

https://medicalxpress.com/news/2019-02-nerve-cells-foot-soldier-axon.html

QUOTES (dhw’s bold):
"We are not the first to think that there has to be some autonomy…"

"This finding [...] proposes a more intricate web of decision-making and the existence of semi-independent units far from central command."

"What our results suggest is that growth cones are capable of taking in information from the outside world, making signaling decisions locally, and functioning semi-autonomously without the cell body," he said.

Macklis proposes that the cell body may be like a server connected to smart PCs that have the capability to interface with the world.

[NB: we should not forget that PC’s are a form of artificial intelligence. The PC is therefore used as an image for natural intelligence.]

DAVID: The findings open up part of the black box of how complex regions of the human brain can develop into five cooperative layers in the frontal cortex. My thought is the nucleus of the neuron tells the axon what to look for in a set of connections and the axon finds them on its own, as the article suggests, growing toward what it senses, far away from the body of the neuron. This was evolved when the first complex set of neurons made an early form of the brain, by design.

Thank you once more for your integrity in presenting yet more evidence that cells and cell communities are run by independent, decision-making intelligence, as bolded. In this context, I take “semi-autonomous” to mean that some decisions are taken independently of the main control system (the nucleus and cell body).

Post reply

8975 views

DAVID: Just like Darwin (as usual) you avoid the origin of life, the worst problem for naturalism, which exists in a continuum with further evolution and most always be part of the discussion.

dhw: Why “must” it be? In our discussions I have accepted the possibility that your God designed the first living organisms. (So, by the way, did the agnostic Darwin.) Our disagreement concerns Chapter 2: if your God exists, and if – as we both believe – evolution took place, then what were his purposes and methods?

How can you avoid the origin of life in our discussions. We can assume that the genome at the very beginning had all or many of the characteristics that we debate when we debate how itv all works.

Dhw (re bacterial resistance): Maybe the mechanism is not “spontaneous”, and maybe resistance/non-resistance depends on what you would call each bacterium’s “own operating system” for interpreting information and acting on it, i.e. “single cells change their metabolic pathways"… and “learn” and “create instructions on the hoof”, as proposed in the article you initially agreed with. The expansion of resistant bacteria would then take time because those bacteria which work out the solution to the new problems would have to pass on the new information.

DAVID: The one percent who have resistance multiply every 20 minutes. Not much time to take. Lenski's E.coli show this.

dhw: Time is not the main point here, as we are discussing the mechanisms that enable resistance: your 3.8-billion year old library of information and instructions, or an autonomously intelligent “own operating system” in which bacteria create their own instructions. I mentioned time because it can take a while before antibiotics become ineffective.

If one percent are already resistant, there are no new instructions.

xxxxx

Under “new axons may make local decisions”:

DAVID: A new study strongly suggests that newly developing axons have some degree of self-control […] (dhw’s bold)

dhw: If distant parts of the system have a degree of self-control, doesn't this suggest to you that the central part of the system itself also has self-control or, in your own words, its "own operating system".

https://medicalxpress.com/news/2019-02-nerve-cells-foot-soldier-axon.html

QUOTES (dhw’s bold):
"We are not the first to think that there has to be some autonomy…"

"This finding [...] proposes a more intricate web of decision-making and the existence of semi-independent units far from central command."

"What our results suggest is that growth cones are capable of taking in information from the outside world, making signaling decisions locally, and functioning semi-autonomously without the cell body," he said.

Macklis proposes that the cell body may be like a server connected to smart PCs that have the capability to interface with the world.

[NB: we should not forget that PC’s are a form of artificial intelligence. The PC is therefore used as an image for natural intelligence.]

DAVID: The findings open up part of the black box of how complex regions of the human brain can develop into five cooperative layers in the frontal cortex. My thought is the nucleus of the neuron tells the axon what to look for in a set of connections and the axon finds them on its own, as the article suggests, growing toward what it senses, far away from the body of the neuron. This was evolved when the first complex set of neurons made an early form of the brain, by design.

dhw: Thank you once more for your integrity in presenting yet more evidence that cells and cell communities are run by independent, decision-making intelligence, as bolded. In this context, I take “semi-autonomous” to mean that some decisions are taken independently of the main control system (the nucleus and cell body).

I view it as the growing ends of the axon branches respond to local stimuli and either grow toward or away automatically according to instructions it carries.

Post reply

8968 views

DAVID: How can you avoid the origin of life in our discussions. We can assume that the genome at the very beginning had all or many of the characteristics that we debate when we debate how it all works.

I have not ignored the origin of life! Over and over again I have emphasized that the mechanisms for life and evolution may have been created by your God. The dispute, then, is confined to what your God put in those first cells: you insist that it was a library with all the information and instructions necessary for evolution (other than those he dabbled), including the slug’s defensive glue, the pre-baleen whale’s toothlessness, and the weaverbird’s nest, whereas I suggest it was the intelligence to process both old and new information and then to create new instructions.

Dhw (re bacterial resistance): Maybe the mechanism is not “spontaneous”, and maybe resistance/non-resistance depends on what you would call each bacterium’s “own operating system” for interpreting information and acting on it, i.e. “single cells change their metabolic pathways"… and “learn” and “create instructions on the hoof”, as proposed in the article you initially agreed with. The expansion of resistant bacteria would then take time because those bacteria which work out the solution to the new problems would have to pass on the new information.

DAVID : The one percent who have resistance multiply every 20 minutes. Not much time to take. Lenski's E.coli show this.

dhw: Time is not the main point here, as we are discussing the mechanisms that enable resistance: your 3.8-billion year old library of information and instructions, or an autonomously intelligent “own operating system” in which bacteria create their own instructions. I mentioned time because it can take a while before antibiotics become ineffective.

DAVID: If one percent are already resistant , there are no new instructions.

There is no way of telling whether the one per cent are already resistant (having presumably been given special instructions 3.8 billion years ago) or have worked out a way of resisting.

Under “new axons may make local decisions”:

DAVID: A new study strongly suggests that newly developing axons have some degree of self-control […] (dhw’s bold)

dhw: If distant parts of the system have a degree of self-control, doesn't this suggest to you that the central part of the system itself also has self-control or, in your own words, its "own operating system".

https://medicalxpress.com/news/2019-02-nerve-cells-foot-soldier-axon.html

dhw: Thank you once more for your integrity in presenting yet more evidence that cells and cell communities are run by independent, decision-making intelligence, as bolded. In this context, I take “semi-autonomous” to mean that some decisions are taken independently of the main control system (the nucleus and cell body).

DAVID: I view it as the growing ends of the axon branches respond to local stimuli and either grow toward or away automatically according to instructions it carries.

The article, as I bolded (but I shan’t repeat all the relevant quotes here), suggests not only that the axons can take their own decisions, but also that generally instructions come from the main control centre (“central command”/the “cell body”). Self-control, decision-making, autonomy, semi-autonomy, semi-independent are not synonymous with “automatic”. Thank you again for providing scientific evidence that contradicts your view of automaticity – or do you now wish to claim that these scientists too are fakers only interested in getting grants?

Post reply

8950 views

DAVID: How can you avoid the origin of life in our discussions. We can assume that the genome at the very beginning had all or many of the characteristics that we debate when we debate how it all works.

dhw: I have not ignored the origin of life! Over and over again I have emphasized that the mechanisms for life and evolution may have been created by your God. The dispute, then, is confined to what your God put in those first cells: you insist that it was a library with all the information and instructions necessary for evolution (other than those he dabbled), including the slug’s defensive glue, the pre-baleen whale’s toothlessness, and the weaverbird’s nest, whereas I suggest it was the intelligence to process both old and new information and then to create new instructions.

We cannot really dispute what is in the first cells. We only have suppositions. I'm still awaiting Behe's book on deletions which would support my points.

Dhw (re bacterial resistance): Maybe the mechanism is not “spontaneous”, and maybe resistance/non-resistance depends on what you would call each bacterium’s “own operating system” for interpreting information and acting on it, i.e. “single cells change their metabolic pathways"… and “learn” and “create instructions on the hoof”, as proposed in the article you initially agreed with. The expansion of resistant bacteria would then take time because those bacteria which work out the solution to the new problems would have to pass on the new information.

DAVID : The one percent who have resistance multiply every 20 minutes. Not much time to take. Lenski's E.coli show this.

dhw: Time is not the main point here, as we are discussing the mechanisms that enable resistance: your 3.8-billion year old library of information and instructions, or an autonomously intelligent “own operating system” in which bacteria create their own instructions. I mentioned time because it can take a while before antibiotics become ineffective.

DAVID: If one percent are already resistant , there are no new instructions.

dhw: There is no way of telling whether the one per cent are already resistant (having presumably been given special instructions 3.8 billion years ago) or have worked out a way of resisting.

Are you disputing science finds one percent are already resistant before the antibiotic is given?

Under “new axons may make local decisions”:

DAVID: A new study strongly suggests that newly developing axons have some degree of self-control […] (dhw’s bold)

dhw: If distant parts of the system have a degree of self-control, doesn't this suggest to you that the central part of the system itself also has self-control or, in your own words, its "own operating system".

https://medicalxpress.com/news/2019-02-nerve-cells-foot-soldier-axon.html

dhw: Thank you once more for your integrity in presenting yet more evidence that cells and cell communities are run by independent, decision-making intelligence, as bolded. In this context, I take “semi-autonomous” to mean that some decisions are taken independently of the main control system (the nucleus and cell body).

DAVID: I view it as the growing ends of the axon branches respond to local stimuli and either grow toward or away automatically according to instructions it carries.

dhw: The article, as I bolded (but I shan’t repeat all the relevant quotes here), suggests not only that the axons can take their own decisions, but also that generally instructions come from the main control centre (“central command”/the “cell body”). Self-control, decision-making, autonomy, semi-autonomy, semi-independent are not synonymous with “automatic”. Thank you again for providing scientific evidence that contradicts your view of automaticity – or do you now wish to claim that these scientists too are fakers only interested in getting grants?

They are not fakers. I view the final steps in reaching a connection are automatic molecular reactions. This earlier steps are as you describe.

Post reply

8970 views

dhw: I have not ignored the origin of life! Over and over again I have emphasized that the mechanisms for life and evolution may have been created by your God. The dispute, then, is confined to what your God put in those first cells: you insist that it was a library with all the information and instructions necessary for evolution (other than those he dabbled), including the slug’s defensive glue, the pre-baleen whale’s toothlessness, and the weaverbird’s nest, whereas I suggest it was the intelligence to process both old and new information and then to create new instructions.

DAVID: We cannot really dispute what is in the first cells. We only have suppositions. I'm still awaiting Behe's book on deletions which would support my points.

Since we cannot dispute it, we should at least remain open-minded, as you appear to be when you accept my “possibilities”, but as you refuse to be when you reject them.

Dhw (re "bacterial resistance"): Maybe the mechanism is not “spontaneous”, and maybe resistance/non-resistance depends on what you would call each bacterium’s “own operating system” for interpreting information and acting on it, i.e. “single cells change their metabolic pathways"… and “learn” and “create instructions on the hoof”, as proposed in the article you initially agreed with.
[…]
DAVID: If one percent are already resistant , there are no new instructions.

dhw: There is no way of telling whether the one per cent are already resistant (having presumably been given special instructions 3.8 billion years ago) or have worked out a way of resisting.

DAVID: Are you disputing science finds one percent are already resistant before the antibiotic is given?

Are you disputing science when it finds that cells learn, create instructions on the hoof, create instructions de novo? You have complete faith in scientists who appear to confirm your conclusions, but if they disagree with you they are hyperbolic fakers.

Under “new axons may make local decisions”:

DAVID: I view it as the growing ends of the axon branches respond to local stimuli and either grow toward or away automatically according to instructions it carries.

dhw: […] Self-control, decision-making, autonomy, semi-autonomy, semi-independent are not synonymous with “automatic”. Thank you again for providing scientific evidence that contradicts your view of automaticity – or do you now wish to claim that these scientists too are fakers only interested in getting grants?

DAVID: They are not fakers. I view the final steps in reaching a connection are automatic molecular reactions. This earlier steps are as you describe.

The “earlier steps” are the processing of information, the taking of decisions, and the issuing of instructions. Then of course the final steps are automatic – otherwise the decisions and instructions would not be implemented! Thank you for at last accepting the possibility that the earlier steps are not automatic but are the product of cellular self-control and autonomous decision-making.

Post reply

8922 views

DAVID: We cannot really dispute what is in the first cells. We only have suppositions. I'm still awaiting Behe's book on deletions which would support my points.

dhw; Since we cannot dispute it, we should at least remain open-minded, as you appear to be when you accept my “possibilities”, but as you refuse to be when you reject them.

I am allowed to admit your possibilities are possible in view of the facts we know, But I have consistent conclusions which I feel are better. I will consider mine better until proven otherwise. Be content with my admission

Dhw (re "bacterial resistance"): Maybe the mechanism is not “spontaneous”, and maybe resistance/non-resistance depends on what you would call each bacterium’s “own operating system” for interpreting information and acting on it, i.e. “single cells change their metabolic pathways"… and “learn” and “create instructions on the hoof”, as proposed in the article you initially agreed with.
[…]
DAVID: If one percent are already resistant , there are no new instructions.

dhw: There is no way of telling whether the one per cent are already resistant (having presumably been given special instructions 3.8 billion years ago) or have worked out a way of resisting.

DAVID: Are you disputing science finds one percent are already resistant before the antibiotic is given?

dhw: Are you disputing science when it finds that cells learn, create instructions on the hoof, create instructions de novo? You have complete faith in scientists who appear to confirm your conclusions, but if they disagree with you they are hyperbolic fakers.

No answer to my statement. Science finds one percent are resistant to start with in many cases! In other cases they use gene transfer. How can that happen if the bacteria have to invent resistance by your favorite theory. Because antibodies are natural in nature and bacteria, molds and fungi use them all the time, resistance has naturally developed in the past. Penicillin, discovered in 1927 by Fleming, comes from the blue cheese mold!

Under “new axons may make local decisions”:

DAVID: I view it as the growing ends of the axon branches respond to local stimuli and either grow toward or away automatically according to instructions it carries.

dhw: […] Self-control, decision-making, autonomy, semi-autonomy, semi-independent are not synonymous with “automatic”. Thank you again for providing scientific evidence that contradicts your view of automaticity – or do you now wish to claim that these scientists too are fakers only interested in getting grants?

DAVID: They are not fakers. I view the final steps in reaching a connection are automatic molecular reactions. This earlier steps are as you describe.

dhw: The “earlier steps” are the processing of information, the taking of decisions, and the issuing of instructions. Then of course the final steps are automatic – otherwise the decisions and instructions would not be implemented! Thank you for at last accepting the possibility that the earlier steps are not automatic but are the product of cellular self-control and autonomous decision-making.

I think the decision-making is coded into the genome of each neuron cell. Information/ instructions all prepared for use by the designer.

Post reply

8952 views

DAVID: I am allowed to admit your possibilities are possible in view of the facts we know, But I have consistent conclusions which I feel are better. I will consider mine better until proven otherwise. Be content with my admission.

I am content with your admission. I am not content when you make admissions one day, and then rescind them the next, as with the various evolutionary hypotheses, survival as a driving force, and your rejection of cellular intelligence.

DAVID: [..] I view the final steps in reaching a connection are automatic molecular reactions. This earlier steps are as you describe.

dhw: The “earlier steps” are the processing of information, the taking of decisions, and the issuing of instructions. Then of course the final steps are automatic – otherwise the decisions and instructions would not be implemented! Thank you for at last accepting the possibility that the earlier steps are not automatic but are the product of cellular self-control and autonomous decision-making.

DAVID: I think the decision-making is coded into the genome of each neuron cell. Information/ instructions all prepared for use by the designer.

In other words, you do not think the earlier steps are as I describe, but your God provided the first cells with a library of information and instructions for every undabbled innovation, lifestyle and natural wonder in life's history, including instructions to bacteria on how to resist new antibiotics.

DAVID: Are you disputing science finds one percent are already resistant before the antibiotic is given?

dhw: Are you disputing science when it finds that cells learn, create instructions on the hoof, create instructions de novo?

DAVID: No answer to my statement. Science finds one percent are resistant to start with in many cases! In other cases they use gene transfer. How can that happen if the bacteria have to invent resistance by your favorite theory. Because antibodies are natural in nature and bacteria, molds and fungi use them all the time, resistance has naturally developed in the past. Penicillin, discovered in 1927 by Fleming, comes from the blue cheese mold!

Of course resistance has naturally developed in the past, as bacteria have learned to change themselves in accordance with new conditions! And of course they can use gene transfer to pass the new solutions on. Here is an (edited) article which seems to me to explain your one per cent and to support the view that bacteria work out their own ways of survival. I have bolded the bits that need no comment:

Some Bacteria Completely Immune To All Antibiotics
https://naturalon.com/some-bacteria-completely-immune-to-all...

A new study out of China had some very scary results. Some types of bacteria have actually breached our last walls of antibiotic defense. This study found that one gene in a strain of Escherichia coli (known to most of us as E. Coli) had no reaction to one of the last antibiotics that we have available to fight it.

Please note that the study refers only to one gene in one strain of E. coli. It is, therefore, an exception.

Researchers in this study found this gene, called mcr-1, in samples that were taken from infected people, pork products, and pigs. This gene protects the bacteria from the one antibiotic we have that still works against E. coli called colistin.
Mcr-1 was the most common gene found in samples taken from animals, which suggests that this mutation began in livestock. In China, it is common to administer the antibiotic colistin to their livestock animals.

Please note the proposal that the mutation had a beginning. The researchers are not suggesting that the beginning was instructions from 3.8 billion years ago.

Unfortunately, by giving animals antibiotics constantly, bacteria have learned to mutate and are no longer responding as they used to in the past.

Scientists have known for quite some time, and have been warning the public, that the overuse of antibiotics only stimulates bacteria to do what they have done for the past 3 billion years: Mutate and survive.

Yes indeed, the purpose or driving force of all these mutations is survival – whether your God designed the mechanisms or not.

The ability of bacteria to change and evolve outpaces our ability to create new antibiotics, says Dr. Amesh Adalja, who is an infectious disease specialist at the University of Pittsburg Medical Center.

When it comes to protecting themselves, bacteria are really good at what they do. Bacteria has been around for billions of years and they have been fine-tuning their defenses against other microbes that could harm or destroy them. Many of the antibiotics we have created began as microorganisms, which means that we are playing in the stadium owned by bacteria.

No mention of automaticity, or of a 3.8-billion-year old library of information and instructions. Bacteria fine-tune their defences, and even the one example (a strain of E.coli) that is already resistant to new bacteria is believed to have originated on a farm in China.

Post reply

8906 views

DAVID: Are you disputing science finds one percent are already resistant before the antibiotic is given?

dhw: Are you disputing science when it finds that cells learn, create instructions on the hoof, create instructions de novo?

DAVID: No answer to my statement. Science finds one percent are resistant to start with in many cases! In other cases they use gene transfer. How can that happen if the bacteria have to invent resistance by your favorite theory. Because antibodies are natural in nature and bacteria, molds and fungi use them all the time, resistance has naturally developed in the past. Penicillin, discovered in 1927 by Fleming, comes from the blue cheese mold!

dhw: Of course resistance has naturally developed in the past, as bacteria have learned to change themselves in accordance with new conditions! And of course they can use gene transfer to pass the new solutions on. Here is an (edited) article which seems to me to explain your one per cent and to support the view that bacteria work out their own ways of survival. I have bolded the bits that need no comment:

Some Bacteria Completely Immune To All Antibiotics
https://naturalon.com/some-bacteria-completely-immune-to-all...

A new study out of China had some very scary results. Some types of bacteria have actually breached our last walls of antibiotic defense. This study found that one gene in a strain of Escherichia coli (known to most of us as E. Coli) had no reaction to one of the last antibiotics that we have available to fight it.

Please note that the study refers only to one gene in one strain of E. coli. It is, therefore, an exception.

Researchers in this study found this gene, called mcr-1, in samples that were taken from infected people, pork products, and pigs. This gene protects the bacteria from the one antibiotic we have that still works against E. coli called colistin.
Mcr-1 was the most common gene found in samples taken from animals, which suggests that this mutation began in livestock. In China, it is common to administer the antibiotic colistin to their livestock animals.

Please note the proposal that the mutation had a beginning. The researchers are not suggesting that the beginning was instructions from 3.8 billion years ago.

Unfortunately, by giving animals antibiotics constantly, bacteria have learned to mutate and are no longer responding as they used to in the past.

Scientists have known for quite some time, and have been warning the public, that the overuse of antibiotics only stimulates bacteria to do what they have done for the past 3 billion years: Mutate and survive.

Yes indeed, the purpose or driving force of all these mutations is survival – whether your God designed the mechanisms or not.

The ability of bacteria to change and evolve outpaces our ability to create new antibiotics, says Dr. Amesh Adalja, who is an infectious disease specialist at the University of Pittsburg Medical Center.

When it comes to protecting themselves, bacteria are really good at what they do. Bacteria has been around for billions of years and they have been fine-tuning their defenses against other microbes that could harm or destroy them. Many of the antibiotics we have created began as microorganisms, which means that we are playing in the stadium owned by bacteria.[/b] (David's bold)

No mention of automaticity, or of a 3.8-billion-year old library of information and instructions. Bacteria fine-tune their defences, and even the one example (a strain of E.coli) that is already resistant to new bacteria is believed to have originated on a farm in China.

The bolded above that I created is a typo. " Many of the antibiotics we have created began as [creations by the] microorganisms, which means that we are playing in the stadium owned by bacteria" should read as I corrected it.

You may be surprised but this article is exactly like all the ones I've read about bacterial resistance. The bacteria are here for 3.5+ billion years as the basis of future advances in evolution, and now actively play a modifying role in the human biome. A recent study suggest schizophrenia have a relationship to bacteria in our guts!

I've not changed any of my views from having reviewed it. Note again, E. coli are still E.coli. They have solved as immediate solution for their immediate survival. Survival does not cause speciation. Survival does not drive evolution. Evolution requires design.

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8940 views

DAVID: (re “bacterial resistance”) Science finds one percent are resistant to start with in many cases! In other cases they use gene transfer. How can that happen if the bacteria have to invent resistance by your favorite theory. Because antibodies are natural in nature and bacteria, molds and fungi use them all the time, resistance has naturally developed in the past. Penicillin, discovered in 1927 by Fleming, comes from the blue cheese mold!

dhw: Of course resistance has naturally developed in the past, as bacteria have learned to change themselves in accordance with new conditions! And of course they can use gene transfer to pass the new solutions on. Here is an (edited) article which seems to me to explain your one per cent and to support the view that bacteria work out their own ways of survival. I have bolded the bits that need no comment:

Some Bacteria Completely Immune To All Antibiotics
https://naturalon.com/some-bacteria-completely-immune-to-all...

dhw: Please note that the study refers only to one gene in one strain of E. coli. It is, therefore, an exception.

dhw: Please note the proposal that the mutation had a beginning. The researchers are not suggesting that the beginning was instructions from 3.8 billion years ago.

Unfortunately, by giving animals antibiotics constantly, bacteria have learned to mutate and are no longer responding as they used to in the past.

dhw:Yes indeed, the purpose or driving force of all these mutations is survival – whether your God designed the mechanisms or not.
[…]
When it comes to protecting themselves, bacteria are really good at what they do. Bacteria has been around for billions of years and they have been fine-tuning their defenses against other microbes that could harm or destroy them.[/b] (dhw’s bold) Many of the antibiotics we have created began as microorganisms, which means that we are playing in the stadium owned by bacteria. (David's bold)

dhw: No mention of automaticity, or of a 3.8-billion-year old library of information and instructions. Bacteria fine-tune their defences, and even the one example (a strain of E.coli) that is already resistant to new bacteria is believed to have originated on a farm in China.

DAVID: The bolded above that I created is a typo. " Many of the antibiotics we have created began as [creations by the] microorganisms, which means that we are playing in the stadium owned by bacteria" should read as I corrected it.

I have reproduced the article as written. In any case, I don’t see that your addition changes the argument for bacterial intelligence.

DAVID: You may be surprised but this article is exactly like all the ones I've read about bacterial resistance. The bacteria are here for 3.5+ billion years as the basis of future advances in evolution, and now actively play a modifying role in the human biome. A recent study suggest schizophrenia have a relationship to bacteria in our guts!

I am not in the least surprised. I have reproduced the article to support my contention and that of the earlier article that bacteria have continually created their own instructions on the hoof,"de novo", as opposed to your contention that 3.8 billion years ago your God provided them with a library of information and instructions to deal with every new situation for the rest of time. Why have you changed the subject?

DAVID: I've not changed any of my views from having reviewed it. Note again, E. coli are still E.coli. They have solved as immediate solution for their immediate survival. Survival does not cause speciation. Survival does not drive evolution. Evolution requires design.

Article after article points out that bacteria solve their own problems, but you have not changed your views and you prefer to ignore all the evidence which you kindly present to us. Instead you revert to the issue of survival which we are discussing on the “Big brain evolution” thread. Once again, please stop pretending that an “immediate driving force” (your own description of survival) is not a driving force and that the hypothesis of (possibly God-given) cellular intelligence excludes design.

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Articl: Scientists have known for quite some time, and have been warning the public, that the overuse of antibiotics only stimulates bacteria to do what they have done for the past 3 billion years: Mutate and survive.

dhw: Yes indeed, the purpose or driving force of all these mutations is survival – whether your God designed the mechanisms or not. (my bold)
[…]
When it comes to protecting themselves, bacteria are really good at what they do. Bacteria has been around for billions of years and they have been fine-tuning their defenses against other microbes that could harm or destroy them.[/b] (dhw’s bold) Many of the antibiotics we have created began as microorganisms, which means that we are playing in the stadium owned by bacteria. (David's bold)

dhw: No mention of automaticity, or of a 3.8-billion-year old library of information and instructions. Bacteria fine-tune their defences, and even the one example (a strain of E.coli) that is already resistant to new bacteria is believed to have originated on a farm in China.

DAVID: The bolded above that I created is a typo. " Many of the antibiotics we have created began as [creations by the] microorganisms, which means that we are playing in the stadium owned by bacteria" should read as I corrected it.

dhw; I have reproduced the article as written. In any case, I don’t see that your addition changes the argument for bacterial intelligence.

DAVID: You may be surprised but this article is exactly like all the ones I've read about bacterial resistance. The bacteria are here for 3.5+ billion years as the basis of future advances in evolution, and now actively play a modifying role in the human biome. A recent study suggest schizophrenia have a relationship to bacteria in our guts!

dhw: I am not in the least surprised. I have reproduced the article to support my contention and that of the earlier article that bacteria have continually created their own instructions on the hoof,"de novo", as opposed to your contention that 3.8 billion years ago your God provided them with a library of information and instructions to deal with every new situation for the rest of time. Why have you changed the subject?

DAVID: I've not changed any of my views from having reviewed it. Note again, E. coli are still E.coli. They have solved as immediate solution for their immediate survival. Survival does not cause speciation. Survival does not drive evolution. Evolution requires design.

dhw: Article after article points out that bacteria solve their own problems, but you have not changed your views and you prefer to ignore all the evidence which you kindly present to us. Instead you revert to the issue of survival which we are discussing on the “Big brain evolution” thread. Once again, please stop pretending that an “immediate driving force” (your own description of survival) is not a driving force and that the hypothesis of (possibly God-given) cellular intelligence excludes design.

First of all I did not 'switch to survival' as you claim. Look at the first comment of yours in this iteration of our discussion I've edited. You returned to the subject: 'switch to survival' as you put it by noting the quote in the article above your quote. You are quoting Darwinian scientists who wrote the article. I carefully watch the obvious background thinking of those who write whatever. It always has great influence on interpretation of results. I fully agree with you: bacteria can solve immediate problems. You and I are in complete disagreement as to how that happens. Our divisions of thought will not change. I've always known , as stated in my first book, only the realization of the magnitude of extreme complexity of living beings through scientific research, will it then drive most of us to accept God, the designer. Thus I continue to present the science delving into the complexities of living biology.

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8957 views

To further my thoughts about the value of science I've introduced an article by a philosopher on the value of science in theological attempts to prove God. See below.

dhw: Article after article points out that bacteria solve their own problems, but you have not changed your views and you prefer to ignore all the evidence which you kindly present to us. Instead you revert to the issue of survival which we are discussing on the “Big brain evolution” thread. Once again, please stop pretending that an “immediate driving force” (your own description of survival) is not a driving force and that the hypothesis of (possibly God-given) cellular intelligence excludes design.

David First of all I did not 'switch to survival' as you claim. Look at the first comment of yours in this iteration of our discussion I've edited. You returned to the subject: 'switch to survival' as you put it by noting the quote in the article above your quote. You are quoting Darwinian scientists who wrote the article. I carefully watch the obvious background thinking of those who write whatever. It always has great influence on interpretation of results. I fully agree with you: bacteria can solve immediate problems. You and I are in complete disagreement as to how that happens. Our divisions of thought will not change. I've always known , as stated in my first book, only the realization of the magnitude of extreme complexity of living beings through scientific research, will it then drive most of us to accept God, the designer. Thus I continue to present the science delving into the complexities of living biology. (my bold)

http://brianhuffling.com/2018/03/13/why-philosophical-proofs-for-god-are-better-than-sc...

"I am very familiar with the intelligent design arguments from cosmology and biology. They are all very good and very convincing. So what’s the issue? Well, for one, natural science alone can’t prove God. It needs philosophy.Then what makes the scientific arguments good? They are good because they show that the chances for the design (not existence) of the universe and life due to random events are essentially zero. But the jump from probability to cause is a philosophical one. Science, does after all, require the use of philosophy. As someone once said, philosophy is unavoidable. Science can give us probability, mathematics, and descriptions of how things are. However, by definition natural science studies nature and thus cannot make the move beyond nature to the supernatural. Again, that is a philosophical move.

His conclusion: "I hope that I have been clear that I believe theistic proofs that involve natural science are strong, but limited. Natural science alone cannot make a case for God. Further, such arguments are not as conclusive as philosophical ones, nor do they give us the God of classical theism which we can discover through philosophy. I agree with Ed Feser when he says, “To be sure, this is not to deny that considerations from modern cosmology—or from other natural sciences, for that matter—can be useful to the natural theologian; the kalam cosmological argument, I concede, shows that much. But I maintain that such considerations can never be sufficient, and that recourse to the philosophy of nature is necessary to get from the world to the God of classical theism'”

I'm sorry not to have given some excerpts, but the entire article is long, too dense and too important in its entirely to not be read in full. It illustrates my point from above in the last entry in this series; my bold:

only the realization of the magnitude of extreme complexity of living beings through scientific research, will it then drive most of us to accept God, the designer.

I know I can 't provide absolute proof with science, but will continue so it comes over like a tidal wave.

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Interpreting the source of articles is very important as I previously noted in this series earlier today:

" You are quoting Darwinian scientists who wrote the article. I carefully watch the obvious background thinking of those who write whatever. It always has great influence on interpretation of results." You need to read the following article to understand my point of view:

https://darwins-god.blogspot.com/2019/02/finally-details-of-how-proteins-evolve.html

Please read entirely: it is brief but it shows the inventiveness of Darwinian scientists' suppositions. Look up the original report if you wish. Hunter is directly quoting it. And his complaints are right on. Nothing of what they describe as real evolution in DNA is proven, It is call guess work as to what might have happened.

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8891 views

DAVID: I've not changed any of my views from having reviewed [the article]. Note again, E. coli are still E.coli. They have solved as immediate solution for their immediate survival. Survival does not cause speciation. Survival does not drive evolution. Evolution requires design.

dhw: Article after article points out that bacteria solve their own problems, but you have not changed your views and you prefer to ignore all the evidence which you kindly present to us. Instead you revert to the issue of survival which we are discussing on the “Big brain evolution” thread. Once again, please stop pretending that an “immediate driving force” (your own description of survival) is not a driving force and that the hypothesis of (possibly God-given) cellular intelligence excludes design.

DAVID: First of all I did not 'switch to survival' as you claim. Look at the first comment of yours in this iteration of our discussion I've edited. You returned to the subject: 'switch to survival' as you put it by noting the quote in the article above your quote.

Fair comment (I overlooked that one quote and comment), but you then proceeded to ignore the main reason why I reproduced the article, which was the autonomous decision-making of bacteria (as opposed to your insistence that every decision was preprogrammed 3.8 billion years ago).

DAVID: You are quoting Darwinian scientists who wrote the article. I carefully watch the obvious background thinking of those who write whatever. It always has great influence on interpretation of results.

They would say exactly the same about your interpretation of results. But in any case, cellular intelligence has absolutely nothing to do with "Darwinian" science, and I wish you would stop blaming Darwin(ism) for any science you don’t like.

DAVID: I fully agree with you: bacteria can solve immediate problems. You and I are in complete disagreement as to how that happens. Our divisions of thought will not change. I've always known, as stated in my first book, only the realization of the magnitude of extreme complexity of living beings through scientific research, will it then drive most of us to accept God, the designer. Thus I continue to present the science delving into the complexities of living biology.

Yet again you revert to the design argument, which I keep accepting. It is your interpretation of your God’s purposes and methods that I question, but the alternative hypothesis – that evolution proceeds and immediate problems are solved through design by (possibly God-given) cellular intelligence, as opposed to a 3.8 billion-year-old computer programme for every undabbled solution, innovation, lifestyle and natural wonder – clearly depends on the concept of cellular intelligence! That is why I object to your continually ignoring or attempting to discredit the evidence offered by earlier scientists as well as by scientists working today.

http://brianhuffling.com/2018/03/13/why-philosophical-proofs-for-god-are-better-than-sc...

QUOTE: "I am very familiar with the intelligent design arguments from cosmology and biology. They are all very good and very convincing. So what’s the issue? Well, for one, natural science alone can’t prove God. It needs philosophy.Then what makes the scientific arguments good? They are good because they show that the chances for the design (not existence) of the universe and life due to random events are essentially zero. But the jump from probability to cause is a philosophical one. Science, does after all, require the use of philosophy. As someone once said, philosophy is unavoidable. Science can give us probability, mathematics, and descriptions of how things are. However, by definition natural science studies nature and thus cannot make the move beyond nature to the supernatural. Again, that is a philosophical move.”

Of course it is. I have already recently quoted my own “Limitations of Science”, written about 12 years ago, from the "brief guide", expressing the same ideas. And how often must I repeat that I have always accepted the strength of your design argument, and the weakness of the randomness argument. That is one major reason why I cannot embrace atheism.

https://darwins-god.blogspot.com/2019/02/finally-details-of-how-proteins-evolve.html
DAVID: Please read entirely: it is brief but it shows the inventiveness of Darwinian scientists' suppositions. Look up the original report if you wish. Hunter is directly quoting it. And his complaints are right on. Nothing of what they describe as real evolution in DNA is proven, It is call guess work as to what might have happened.

I agree. Their whole hypothesis is based on random mutations, which you and I have long since rejected. There is no more evidence for their claims than there is for the claim that an unknown, sourceless, eternal mind set out to design the brain of H. sapiens, and in order to do so spent 3.5+ billion years specially designing billions of problem-solutions, life forms, lifestyles and natural wonders, including anti-freeze for fish. When will you ever understand that the root of my agnosticism lies in my inability to choose one just-so story in preference to another?

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8928 views

DAVID: You are quoting Darwinian scientists who wrote the article. I carefully watch the obvious background thinking of those who write whatever. It always has great influence on interpretation of results.

dhw: They would say exactly the same about your interpretation of results. But in any case, cellular intelligence has absolutely nothing to do with "Darwinian" science, and I wish you would stop blaming Darwin(ism) for any science you don’t like.

Answered below in the on point C. Hunter article below.

DAVID: I fully agree with you: bacteria can solve immediate problems. You and I are in complete disagreement as to how that happens. Our divisions of thought will not change. I've always known, as stated in my first book, only the realization of the magnitude of extreme complexity of living beings through scientific research, will it then drive most of us to accept God, the designer. Thus I continue to present the science delving into the complexities of living biology.

dhw: Yet again you revert to the design argument, which I keep accepting. It is your interpretation of your God’s purposes and methods that I question, but the alternative hypothesis – that evolution proceeds and immediate problems are solved through design by (possibly God-given) cellular intelligence, as opposed to a 3.8 billion-year-old computer programme for every undabbled solution, innovation, lifestyle and natural wonder – clearly depends on the concept of cellular intelligence! That is why I object to your continually ignoring or attempting to discredit the evidence offered by earlier scientists as well as by scientists working today.

Yet you have agreed with me what cells do requires interpretation. I like mine and the odds are still 50/50, since we sit on the outside of cells as we see them respond to stimuli. Once again, kidney cells act in lockstep making urine. Shapiro's bacterial studies are on whole animals responses to needs. Different breed of cats.

http://brianhuffling.com/2018/03/13/why-philosophical-proofs-for-god-are-better-than-sc...

QUOTE: "I am very familiar with the intelligent design arguments from cosmology and biology. They are all very good and very convincing. So what’s the issue? Well, for one, natural science alone can’t prove God. It needs philosophy.Then what makes the scientific arguments good? They are good because they show that the chances for the design (not existence) of the universe and life due to random events are essentially zero. But the jump from probability to cause is a philosophical one. Science, does after all, require the use of philosophy. As someone once said, philosophy is unavoidable. Science can give us probability, mathematics, and descriptions of how things are. However, by definition natural science studies nature and thus cannot make the move beyond nature to the supernatural. Again, that is a philosophical move.”

dhw: Of course it is. I have already recently quoted my own “Limitations of Science”, written about 12 years ago, from the "brief guide", expressing the same ideas. And how often must I repeat that I have always accepted the strength of your design argument, and the weakness of the randomness argument. That is one major reason why I cannot embrace atheism.

https://darwins-god.blogspot.com/2019/02/finally-details-of-how-proteins-evolve.html
DAVID: Please read entirely: it is brief but it shows the inventiveness of Darwinian scientists' suppositions. Look up the original report if you wish. Hunter is directly quoting it. And his complaints are right on. Nothing of what they describe as real evolution in DNA is proven, It is call guess work as to what might have happened.

dhw: I agree. Their whole hypothesis is based on random mutations, which you and I have long since rejected. There is no more evidence for their claims than there is for the claim that an unknown, sourceless, eternal mind set out to design the brain of H. sapiens, and in order to do so spent 3.5+ billion years specially designing billions of problem-solutions, life forms, lifestyles and natural wonders, including anti-freeze for fish. When will you ever understand that the root of my agnosticism lies in my inability to choose one just-so story in preference to another?

And I publish here to present the complexity of life that cannot have appeared naturally, and to show the fallacies of relying on Darwin-interpreting scientists, as they strain to explain their results. I thank you for saying the is "no... evidence for their claims".

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8951 views

In the last entry bias in interpretation of scientific studies results was discussed. I've mentioned before the problem of overenthusiastic reporting by science writers:

https://www.sciencedaily.com/releases/2019/02/190213132309.htm

Note the intro:

"Biology textbooks teach us that adult cell types remain fixed in the identity they have acquired upon differentiation. By inducing non-insulin-producing human pancreatic cells to modify their function to produce insulin in a sustainable way, researchers show for the first time that the adaptive capacity of our cells is much greater than previously thought. Moreover, this plasticity would not be exclusive to human pancreatic cells."

Comment: sounds like the cells can do what they want to do. No Way:

"To explore whether human cells have this ability to adapt, Geneva scientists used islets of Langerhans from both diabetic and non-diabetic donors. They first sorted the different cell types to study two of them in particular: α cells (glucagon producers) and ϒ cells (pancreatic polypeptide cells). "We divided our cells into two groups: one where we introduced only a fluorescent cell tracer, and the other where, in addition, we added genes that produce insulin transcription factors specific to β cells," explains Pedro Herrera.

"The researchers then reconstructed "pseudo-islets," with only one cell type at a time to accurately study their behaviour. "First observation: the simple fact of aggregating cells, even into monotypic pseudo-islets, stimulates the expression of certain genes linked to insulin production, as if the "non-β" cells naturally detected the absence of their "sisters." However, in order for the cells to start producing insulin, we had to artificially stimulate the expression of one or two key β cell genes," says Kenichiro Furuyama, a researcher in the Department of Genetic Medicine at the Faculty of Medicine of the UNIGE and the first author of this work. One week after the experiment began, 30% of the α cells were producing and secreting insulin in response to glucose. ϒ-Cells, under the same treatment, were even more effective and numerous in converting and secreting insulin in response to glucose."

Comment: sure the cells can BE changed by human manipulation! NOT NATURALLY as the opening intro seems to state. Beware of what you read.

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8904 views

DAVID: You are quoting Darwinian scientists who wrote the article. I carefully watch the obvious background thinking of those who write whatever. It always has great influence on interpretation of results.

dhw: They would say exactly the same about your interpretation of results. But in any case, cellular intelligence has absolutely nothing to do with "Darwinian" science, and I wish you would stop blaming Darwin(ism) for any science you don’t like.

DAVID: Answered below in the on point C. Hunter article below.

Not answered at all. The hypothesis of cellular intelligence plays no role whatsoever in Darwin, and interpretation of results is no more and no less influenced by theism than it is by atheism.

dhw: Yet again you revert to the design argument, which I keep accepting. It is your interpretation of your God’s purposes and methods that I question, but the alternative hypothesis – that evolution proceeds and immediate problems are solved through design by (possibly God-given) cellular intelligence, as opposed to a 3.8 billion-year-old computer programme for every undabbled solution, innovation, lifestyle and natural wonder – clearly depends on the concept of cellular intelligence! That is why I object to your continually ignoring or attempting to discredit the evidence offered by earlier scientists as well as by scientists working today.

DAVID: Yet you have agreed with me what cells do requires interpretation. I like mine and the odds are still 50/50, since we sit on the outside of cells as we see them respond to stimuli.

Of course I agree. And if you see the odds as 50/50, then I don’t see how you can categorically dismiss the interpretation you don’t like.

DAVID: Once again, kidney cells act in lockstep making urine. Shapiro's bacterial studies are on whole animals responses to needs. Different breed of cats.

I keep agreeing with you that once an innovation has proved successful, the cells must act automatically for it to survive. Bacteria only change their behaviour when there are new problems for them to solve, and the same applies to our human cells.

https://darwins-god.blogspot.com/2019/02/finally-details-of-how-proteins-evolve.html

DAVID: Please read entirely: it is brief but it shows the inventiveness of Darwinian scientists' suppositions. Look up the original report if you wish. Hunter is directly quoting it. And his complaints are right on. Nothing of what they describe as real evolution in DNA is proven, It is call guess work as to what might have happened.

dhw: I agree. Their whole hypothesis is based on random mutations, which you and I have long since rejected. There is no more evidence for their claims than there is for the claim that an unknown, sourceless, eternal mind set out to design the brain of H. sapiens, and in order to do so spent 3.5+ billion years specially designing billions of problem-solutions, life forms, lifestyles and natural wonders, including anti-freeze for fish. When will you ever understand that the root of my agnosticism lies in my inability to choose one just-so story in preference to another?

DAVID: And I publish here to present the complexity of life that cannot have appeared naturally, and to show the fallacies of relying on Darwin-interpreting scientists, as they strain to explain their results. I thank you for saying the is "no... evidence for their claims".

No need to thank me. This website came into being because of my opposition to Dawkins’ version of life’s history, which for me is every bit as “just-so” as your own version of life’s history. When we started up, one critic even thought it was a disguised advert for ID! We agnostics get stick from both sides. Fair enough, since one of the two must be closer to the truth than the other. Ah, but which one?

David: In the last entry bias in interpretation of scientific studies results was discussed. I've mentioned before the problem of overenthusiastic reporting by science writers:
https://www.sciencedaily.com/releases/2019/02/190213132309.htm

QUOTE: "Biology textbooks teach us that adult cell types remain fixed in the identity they have acquired upon differentiation. By inducing non-insulin-producing human pancreatic cells to modify their function to produce insulin in a sustainable way, researchers show for the first time that the adaptive capacity of our cells is much greater than previously thought. Moreover, this plasticity would not be exclusive to human pancreatic cells."

DAVID: sounds like the cells can do what they want to do. No Way.

Not quite. There have to be limits. These people are simply saying that our cells can adapt more than we previously thought. That is the great question for my hypothesis: just how much can they change?

DAVID: sure the cells can BE changed by human manipulation! NOT NATURALLY as the opening intro seems to state. Beware of what you read.

According to you they can be changed either by your God's 3.8-billion-year-old computer programme, or by your God popping in to do a dabble. Maybe they can also be changed by their own innate intelligence, which may originally have been designed by your God. That would then be “natural”, since if your God exists, he created Nature. (If your God does not exist, then of course the process would also be natural.)

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8943 views

DAVID: Yet you have agreed with me what cells do requires interpretation. I like mine and the odds are still 50/50, since we sit on the outside of cells as we see them respond to stimuli.

dhw; Of course I agree. And if you see the odds as 50/50, then I don’t see how you can categorically dismiss the interpretation you don’t like.

Since the options number two, the truth is either or. But I have a plethora of biochemical reasons to propose only one.

DAVID: And I publish here to present the complexity of life that cannot have appeared naturally, and to show the fallacies of relying on Darwin-interpreting scientists, as they strain to explain their results. I thank you for saying the is "no... evidence for their claims".

dhw: No need to thank me. This website came into being because of my opposition to Dawkins’ version of life’s history, which for me is every bit as “just-so” as your own version of life’s history. When we started up, one critic even thought it was a disguised advert for ID! We agnostics get stick from both sides. Fair enough, since one of the two must be closer to the truth than the other. Ah, but which one?

David: In the last entry bias in interpretation of scientific studies results was discussed. I've mentioned before the problem of overenthusiastic reporting by science writers:
https://www.sciencedaily.com/releases/2019/02/190213132309.htm

QUOTE: "Biology textbooks teach us that adult cell types remain fixed in the identity they have acquired upon differentiation. By inducing non-insulin-producing human pancreatic cells to modify their function to produce insulin in a sustainable way, researchers show for the first time that the adaptive capacity of our cells is much greater than previously thought. Moreover, this plasticity would not be exclusive to human pancreatic cells." (my bold)

DAVID: sounds like the cells can do what they want to do. No Way.

dhw: Not quite. There have to be limits. These people are simply saying that our cells can adapt more than we previously thought. That is the great question for my hypothesis: just how much can they change?

DAVID: sure the cells can BE changed by human manipulation! NOT NATURALLY as the opening intro seems to state. Beware of what you read.[/i]

dhw: According to you they can be changed either by your God's 3.8-billion-year-old computer programme, or by your God popping in to do a dabble. Maybe they can also be changed by their own innate intelligence, which may originally have been designed by your God. That would then be “natural”, since if your God exists, he created Nature. (If your God does not exist, then of course the process would also be natural.)

Very fine point: the article starts by stating that cells have the ability to change. All the article shows is that several designed manipulations can cause them to act differently by the actions of intelligent designers manipulating from outside the cell. That cells that can do it themselves is not proven. Note my bold in the quote. The implied meaning of the statement is that the cells can do it on their own. Not what was proven in the study. I would again point out, science writers portray hopeful interpretations well beyond what they are describing in the facts of the story.

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8913 views

DAVID: Yet you have agreed with me what cells do requires interpretation. I like mine and the odds are still 50/50, since we sit on the outside of cells as we see them respond to stimuli.

dhw: Of course I agree. And if you see the odds as 50/50, then I don’t see how you can categorically dismiss the interpretation you don’t like.

DAVID: Since the options number two, the truth is either or. But I have a plethora of biochemical reasons to propose only one.

And I have no doubt that biologists such as Margulis, McClintock, Buehler, Shapiro have a plethora of science-based reasons for proposing the other. 50/50 should at least allow for a degree of open-mindedness.

David: In the last entry bias in interpretation of scientific studies results was discussed. I've mentioned before the problem of overenthusiastic reporting by science writers:
https://www.sciencedaily.com/releases/2019/02/190213132309.htm

QUOTE: "Biology textbooks teach us that adult cell types remain fixed in the identity they have acquired upon differentiation. By inducing non-insulin-producing human pancreatic cells to modify their function to produce insulin in a sustainable way, researchers show for the first time that the adaptive capacity of our cells is much greater than previously thought. Moreover, this plasticity would not be exclusive to human pancreatic cells." (David’s bold)

DAVID: sounds like the cells can do what they want to do. No Way.

dhw: Not quite. There have to be limits. These people are simply saying that our cells can adapt more than we previously thought. That is the great question for my hypothesis: just how much can they change?

DAVID: sure the cells can BE changed by human manipulation! NOT NATURALLY as the opening intro seems to state. Beware of what you read.

dhw: According to you they can be changed either by your God's 3.8-billion-year-old computer programme, or by your God popping in to do a dabble. Maybe they can also be changed by their own innate intelligence, which may originally have been designed by your God. That would then be “natural”, since if your God exists, he created Nature. (If your God does not exist, then of course the process would also be natural.)

DAVID: Very fine point: the article starts by stating that cells have the ability to change. All the article shows is that several designed manipulations can cause them to act differently by the actions of intelligent designers manipulating from outside the cell. That cells that can do it themselves is not proven. Note my bold in the quote. The implied meaning of the statement is that the cells can do it on their own. Not what was proven in the study. I would again point out, science writers portray hopeful interpretations well beyond what they are describing in the facts of the story.

And there you go again with your “not proven”. If anything is proven, it becomes a fact as opposed to a hypothesis or theory. NONE of our hypotheses are proven, and that is why these discussions go on. You propose hypotheses that range from the existence of God to his special design of slug glue as a means of enabling him to produce the brain of H. sapiens. Not proven, and yet your belief is fixed.

DAVID (under “Biological complexity”):Recent research reveals a huge variety of different parts of living organisms produce an enormous number if different hormones so every part communicates with all the other parts through the circulatory system:
https://aeon.co/essays/the-revolutionary-idea-revealing-the-bodys-hormonal-democracy?ut...

QUOTES: "Karsenty and others eventually confirmed that bones secrete hormones essential for an animal’s health. And with that finding, the skeleton joined a growing list of tissues shown to participate in a body-wide conversation between organs. The traditional concept of the endocrine system as a second-command system working in tandem with the nervous system – and largely directed by the brain – is being replaced with a more autonomous view of interorgan communication, one in which most, if not all, organs have a voice. (dhw’s bold)

"Perrimon and Droujinine have written that it might be as fundamental as going back to the advent of early multicellular life.[/b] (David’s bold) As organisms became more complex, and different types of cells evolved to have specialised functions within a cellular collective, there was a need to coordinate those functions. […] it’s now clear that the hormonal link – and the autonomous character of peripheral tissues – never went away. As specialised populations of cells evolved, the total organism benefitted from individual tissues broadcasting their status to modulate other organs. As Karsenty puts it, ‘no organ is an island in our body.’ (dhw’s bold)

DAVID: Wow. There is no end to unearthing the real complexity of living beings. Only a designer can create this.

Wow indeed. Yet another article laying emphasis on the autonomous cooperation between cell communities (which you try to ridicule by calling them “committees”). And your bold suggests that precisely the same process of autonomous cellular communication underlay multicellularity. NB: This still allows for your God as the inventor of the mechanism that gave rise to these different autonomous, cooperating, decision-making cell communities.

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9012 views

dhw: Of course I agree. And if you see the odds as 50/50, then I don’t see how you can categorically dismiss the interpretation you don’t like.

DAVID: Since the options number two, the truth is either or. But I have a plethora of biochemical reasons to propose only one.

dhw: And I have no doubt that biologists such as Margulis, McClintock, Buehler, Shapiro have a plethora of science-based reasons for proposing the other. 50/50 should at least allow for a degree of open-mindedness.

They can't know the truth any more than I can. I'll stick to my view as much more probable.

dhw: According to you they can be changed either by your God's 3.8-billion-year-old computer programme, or by your God popping in to do a dabble. Maybe they can also be changed by their own innate intelligence, which may originally have been designed by your God. That would then be “natural”, since if your God exists, he created Nature. (If your God does not exist, then of course the process would also be natural.)

DAVID: Very fine point: the article starts by stating that cells have the ability to change. All the article shows is that several designed manipulations can cause them to act differently by the actions of intelligent designers manipulating from outside the cell. That cells that can do it themselves is not proven. Note my bold in the quote. The implied meaning of the statement is that the cells can do it on their own. Not what was proven in the study. I would again point out, science writers portray hopeful interpretations well beyond what they are describing in the facts of the story.

dhw: And there you go again with your “not proven”. If anything is proven, it becomes a fact as opposed to a hypothesis or theory. NONE of our hypotheses are proven, and that is why these discussions go on. You propose hypotheses that range from the existence of God to his special design of slug glue as a means of enabling him to produce the brain of H. sapiens. Not proven, and yet your belief is fixed.

And your non-belief is fixed! All the article shows is cells can be manipulated from outside to make the cells do something they don't normally do. The 'no proof' is that no one knows if cells can do this on their own initiative (your pet theory). You neatly skip over my point!

DAVID (under “Biological complexity”):Recent research reveals a huge variety of different parts of living organisms produce an enormous number if different hormones so every part communicates with all the other parts through the circulatory system:
https://aeon.co/essays/the-revolutionary-idea-revealing-the-bodys-hormonal-democracy?ut...

QUOTES: "Karsenty and others eventually confirmed that bones secrete hormones essential for an animal’s health. And with that finding, the skeleton joined a growing list of tissues shown to participate in a body-wide conversation between organs. The traditional concept of the endocrine system as a second-command system working in tandem with the nervous system – and largely directed by the brain – is being replaced with a more autonomous view of interorgan communication, one in which most, if not all, organs have a voice. (dhw’s bold)

"Perrimon and Droujinine have written that it might be as fundamental as going back to the advent of early multicellular life.[/b] (David’s bold) As organisms became more complex, and different types of cells evolved to have specialised functions within a cellular collective, there was a need to coordinate those functions. […] it’s now clear that the hormonal link – and the autonomous character of peripheral tissues – never went away. As specialised populations of cells evolved, the total organism benefitted from individual tissues broadcasting their status to modulate other organs. As Karsenty puts it, ‘no organ is an island in our body.’ (dhw’s bold)

DAVID: Wow. There is no end to unearthing the real complexity of living beings. Only a designer can create this.

dhw: Wow indeed. Yet another article laying emphasis on the autonomous cooperation between cell communities (which you try to ridicule by calling them “committees”). And your bold suggests that precisely the same process of autonomous cellular communication underlay multicellularity. NB: This still allows for your God as the inventor of the mechanism that gave rise to these different autonomous, cooperating, decision-making cell communities.

Life appears/emerges from all these biochemical interactions of thousands of communicating processes all working in concert. Cells in each organ have necessarily fixed roles to play. A bacterium has to do it all in one cell. The earliest chordate fish in the Cambrian had this degree of complexity with a variety of organs. No one knows how speciation occurs from the history we have. Now that we see so many multicellular organisms in so many branches, with cells in fixed roles, we don't know how they can modify themselves while still doing their necessary work.

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8891 views

dhw: […] if you see the odds as 50/50, then I don’t see how you can categorically dismiss the interpretation you don’t like.

DAVID: Since the options number two, the truth is either or. But I have a plethora of biochemical reasons to propose only one.

dhw: And I have no doubt that biologists such as Margulis, McClintock, Buehler, Shapiro have a plethora of science-based reasons for proposing the other. 50/50 should at least allow for a degree of open-mindedness.

DAVID: They can't know the truth any more than I can. I'll stick to my view as much more probable.

Just to clarify, then: you tell us the odds are 50/50, but your view is that the odds are not 50/50. And for good measure you think it is more probable that cellular behaviour is governed by a divine 3.8-billion-year-old computer programme of instructions for every undabbled life form, lifestyle, and natural wonder in the history of life than that your God could have designed cells with an innate ability to “create instructions on the hoof”.

dhw: NONE of our hypotheses are proven, and that is why these discussions go on. You propose hypotheses that range from the existence of God to his special design of slug glue as a means of enabling him to produce the brain of H. sapiens. Not proven, and yet your belief is fixed.

DAVID: And your non-belief is fixed! All the article shows is cells can be manipulated from outside to make the cells do something they don't normally do. The 'no proof' is that no one knows if cells can do this on their own initiative (your pet theory). You neatly skip over my point!

The above is a response to your point: an acknowledgement that NONE of these hypotheses are proven, because if they were, they would not be hypotheses but facts. Non-belief (as opposed to disbelief) = open-mindedness, although I must confess that there are some hypotheses to which I do close my mind (remember Bertrand Russell’s example of the invisible teapot circling the sun?), as specified on the “Big brain” thread.

DAVID (under “Biological complexity”): Recent research reveals a huge variety of different parts of living organisms produce an enormous number if different hormones so every part communicates with all the other parts through the circulatory system:
https://aeon.co/essays/the-revolutionary-idea-revealing-the-bodys-hormonal-democracy?ut...

dhw: Yet another article laying emphasis on the autonomous cooperation between cell communities (which you try to ridicule by calling them “committees”). And your bold suggests that precisely the same process of autonomous cellular communication underlay multicellularity. NB: This still allows for your God as the inventor of the mechanism that gave rise to these different autonomous, cooperating, decision-making cell communities.

DAVID: Life appears/emerges from all these biochemical interactions of thousands of communicating processes all working in concert. Cells in each organ have necessarily fixed roles to play. A bacterium has to do it all in one cell. The earliest chordate fish in the Cambrian had this degree of complexity with a variety of organs. No one knows how speciation occurs from the history we have. Now that we see so many multicellular organisms in so many branches, with cells in fixed roles, we don't know how they can modify themselves while still doing their necessary work.

An excellent summary of the mystery of speciation. We don’t know how it works. Some evolutionists attribute it to chance (via random mutations); a dear friend of mine attributes it to divine dabbling or a divine 3.8-billion-year-old computer programme for every undabbled life form, lifestyle and natural wonder in the history of life; and I have proposed cellular intelligence (possibly God-given) responding to changing conditions. The articles you keep quoting seem to support the last of these rather than the first two. Here is another:

DAVID (under “how plants construct cells”): Again a very complex system which requires very specific molecules to direct the work. Not by chance. This process is inherited from the very first bacteria of life.

Yes, it would seem to support the concept of common descent and the idea that all the members of different cell communities cooperate to produce the varying complexities of living organisms. For three alternative explanations of how this system might work, see above.

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8908 views

DAVID: They can't know the truth any more than I can. I'll stick to my view as much more probable.

dhw: Just to clarify, then: you tell us the odds are 50/50, but your view is that the odds are not 50/50. And for good measure you think it is more probable that cellular behaviour is governed by a divine 3.8-billion-year-old computer programme of instructions for every undabbled life form, lifestyle, and natural wonder in the history of life than that your God could have designed cells with an innate ability to “create instructions on the hoof”.

My usual answer. God is in control and if he created such a mechanism, as you imagine, it would contain guidelines.

DAVID: And your non-belief is fixed! All the article shows is cells can be manipulated from outside to make the cells do something they don't normally do. The 'no proof' is that no one knows if cells can do this on their own initiative (your pet theory). You neatly skip over my point!

dhw: The above is a response to your point: an acknowledgement that NONE of these hypotheses are proven, because if they were, they would not be hypotheses but facts. Non-belief (as opposed to disbelief) = open-mindedness, although I must confess that there are some hypotheses to which I do close my mind (remember Bertrand Russell’s example of the invisible teapot circling the sun?), as specified on the “Big brain” thread.

DAVID (under “Biological complexity”): Recent research reveals a huge variety of different parts of living organisms produce an enormous number if different hormones so every part communicates with all the other parts through the circulatory system:
https://aeon.co/essays/the-revolutionary-idea-revealing-the-bodys-hormonal-democracy?ut...

dhw: Yet another article laying emphasis on the autonomous cooperation between cell communities (which you try to ridicule by calling them “committees”). And your bold suggests that precisely the same process of autonomous cellular communication underlay multicellularity. NB: This still allows for your God as the inventor of the mechanism that gave rise to these different autonomous, cooperating, decision-making cell communities.

DAVID: Life appears/emerges from all these biochemical interactions of thousands of communicating processes all working in concert. Cells in each organ have necessarily fixed roles to play. A bacterium has to do it all in one cell. The earliest chordate fish in the Cambrian had this degree of complexity with a variety of organs. No one knows how speciation occurs from the history we have. Now that we see so many multicellular organisms in so many branches, with cells in fixed roles, we don't know how they can modify themselves while still doing their necessary work.

dhw: An excellent summary of the mystery of speciation. We don’t know how it works. Some evolutionists attribute it to chance (via random mutations); a dear friend of mine attributes it to divine dabbling or a divine 3.8-billion-year-old computer programme for every undabbled life form, lifestyle and natural wonder in the history of life; and I have proposed cellular intelligence (possibly God-given) responding to changing conditions. The articles you keep quoting seem to support the last of these rather than the first two. Here is another:

DAVID (under “how plants construct cells”): Again a very complex system which requires very specific molecules to direct the work. Not by chance. This process is inherited from the very first bacteria of life.

dhw: Yes, it would seem to support the concept of common descent and the idea that all the members of different cell communities cooperate to produce the varying complexities of living organisms. For three alternative explanations of how this system might work, see above.

And see my objections to cellular capabilities to speciate above. Cells have fixed roles. Cells have ability to invent. They can slightly modify their outputs when given sightly different instructions by nerves or hormones.

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8955 views

DAVID: They can't know the truth any more than I can. I'll stick to my view as much more probable.

dhw: Just to clarify, then: you tell us the odds are 50/50, but your view is that the odds are not 50/50. And for good measure you think it is more probable that cellular behaviour is governed by a divine 3.8-billion-year-old computer programme of instructions for every undabbled life form, lifestyle, and natural wonder in the history of life than that your God could have designed cells with an innate ability to “create instructions on the hoof”.

DAVID: My usual answer. God is in control and if he created such a mechanism, as you imagine, it would contain guidelines.

You agree the odds are 50/50, but in your view they are not 50/50. As for your guidelines, they have turned out to be a 3.8-billion-year-old library of information and instructions for every undabbled innovation, lifestyle and natural wonder in the history of life. The exact opposite of the autonomous mechanism I am proposing.

dhw: An excellent summary of the mystery of speciation. We don’t know how it works. Some evolutionists attribute it to chance (via random mutations); a dear friend of mine attributes it to divine dabbling or a divine 3.8-billion-year-old computer programme for every undabbled life form, lifestyle and natural wonder in the history of life; and I have proposed cellular intelligence (possibly God-given) responding to changing conditions. The articles you keep quoting seem to support the last of these rather than the first two. Here is another:
DAVID (under “how plants construct cells”): Again a very complex system which requires very specific molecules to direct the work. Not by chance. This process is inherited from the very first bacteria of life.

dhw: Yes, it would seem to support the concept of common descent and the idea that all the members of different cell communities cooperate to produce the varying complexities of living organisms. For three alternative explanations of how this system might work, see above.

DAVID: And see my objections to cellular capabilities to speciate above. Cells have fixed roles. Cells have ability to invent.

Cells have fixed roles once an innovation has proved to be successful. Then it is only when new conditions arise that they take on new roles. I presume your last sentence is meant to read cells do NOT have the ability to invent. That is the big question, and that is why my proposal remains a hypothesis, as does your own. But if in your view cells have a 50/50 chance of being autonomously intelligent and hence of creating instructions “on the hoof” or “de novo”, as believed by some scientists in the field, then clearly it is a hypothesis that demands serious consideration even by you - and without the condition of “guidelines” which = God’s instructions.

Post reply

8925 views

DAVID: They can't know the truth any more than I can. I'll stick to my view as much more probable.

dhw: Just to clarify, then: you tell us the odds are 50/50, but your view is that the odds are not 50/50. And for good measure you think it is more probable that cellular behaviour is governed by a divine 3.8-billion-year-old computer programme of instructions for every undabbled life form, lifestyle, and natural wonder in the history of life than that your God could have designed cells with an innate ability to “create instructions on the hoof”.

DAVID: My usual answer. God is in control and if he created such a mechanism, as you imagine, it would contain guidelines.

dhw: You agree the odds are 50/50, but in your view they are not 50/50. As for your guidelines, they have turned out to be a 3.8-billion-year-old library of information and instructions for every undabbled innovation, lifestyle and natural wonder in the history of life. The exact opposite of the autonomous mechanism I am proposing.

And which I continue to reject. You like a slightly impotent God.

DAVID: Life appears/emerges from all these biochemical interactions of thousands of communicating processes all working in concert. Cells in each organ have necessarily fixed roles to play. A bacterium has to do it all in one cell. The earliest chordate fish in the Cambrian had this degree of complexity with a variety of organs. No one knows how speciation occurs from the history we have. Now that we see so many multicellular organisms in so many branches, with cells in fixed roles, we don't know how they can modify themselves while still doing their necessary work.

dhw: An excellent summary of the mystery of speciation. We don’t know how it works. Some evolutionists attribute it to chance (via random mutations); a dear friend of mine attributes it to divine dabbling or a divine 3.8-billion-year-old computer programme for every undabbled life form, lifestyle and natural wonder in the history of life; and I have proposed cellular intelligence (possibly God-given) responding to changing conditions. The articles you keep quoting seem to support the last of these rather than the first two. Here is another:
DAVID (under “how plants construct cells”): Again a very complex system which requires very specific molecules to direct the work. Not by chance. This process is inherited from the very first bacteria of life.

dhw: Yes, it would seem to support the concept of common descent and the idea that all the members of different cell communities cooperate to produce the varying complexities of living organisms. For three alternative explanations of how this system might work, see above.

DAVID: And see my objections to cellular capabilities to speciate above. Cells have fixed roles. Cells have no ability to invent.

dhw: Cells have fixed roles once an innovation has proved to be successful. Then it is only when new conditions arise that they take on new roles. I presume your last sentence is meant to read cells do NOT have the ability to invent. That is the big question, and that is why my proposal remains a hypothesis, as does your own. But if in your view cells have a 50/50 chance of being autonomously intelligent and hence of creating instructions “on the hoof” or “de novo”, as believed by some scientists in the field, then clearly it is a hypothesis that demands serious consideration even by you - and without the condition of “guidelines” which = God’s instructions.

What all cells can do according to your scientists and mine is that cells can modify responses as necessary, but they still remain the same cells,. Lenski's E. coli have made minor metabolic changes, but are still E. coli after 20,000+ generations. Based on those facts and the many requirements to jump from Ediacaran to Cambrian, Ediacaran cells did not invent Cambrian forms. That is what your hypothesis logically proposes! I can't seriously consider it any more than I can accept an inventive mechanism without God's guidelines.

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8921 views

DAVID: God is in control and if he created such a mechanism, as you imagine, it would contain guidelines.

dhw: You agree the odds [for cellular intelligence] are 50/50, but in your view they are not 50/50. As for your guidelines, they have turned out to be a 3.8-billion-year-old library of information and instructions for every undabbled innovation, lifestyle and natural wonder in the history of life. The exact opposite of the autonomous mechanism I am proposing.

DAVID: And which I continue to reject. You like a slightly impotent God.

As explained under “Big brain evolution”, there is no impotence involved if God chooses to give evolution free rein through his design of an autonomous mechanism (cellular intelligence), as opposed to providing a 3.8-billion-year-old library of information and instructions for every single undabbled life form, lifestyle and natural wonder, plus solutions for every single problem that bacteria would have to solve for the rest of time.

DAVID: Cells have fixed roles. Cells have no ability to invent.

dhw: Cells have fixed roles once an innovation has proved to be successful. Then it is only when new conditions arise that they take on new roles. [The ability to invent] is the big question, and that is why my proposal remains a hypothesis, as does your own. But if in your view cells have a 50/50 chance of being autonomously intelligent and hence of creating instructions “on the hoof” or “de novo”, as believed by some scientists in the field, then clearly it is a hypothesis that demands serious consideration even by you - and without the condition of “guidelines” which = God’s instructions.

DAVID: What all cells can do according to your scientists and mine is that cells can modify responses as necessary, but they still remain the same cells,. Lenski's E. coli have made minor metabolic changes, but are still E. coli after 20,000+ generations. Based on those facts and the many requirements to jump from Ediacaran to Cambrian, Ediacaran cells did not invent Cambrian forms. That is what your hypothesis logically proposes! I can't seriously consider it any more than I can accept an inventive mechanism without God's guidelines.

We only know what cells/cell communities do after the fact of speciation. Nobody knows how the innovations occurred. I accept your rational doubts about cells’ ability to invent – it is a hypothesis – just as we both rationally doubt the efficacy of random mutations as the driving force. But for the life of me I cannot understand how you can stick to your irrational fixed belief that although your God’s one and only purpose was to specially design the brain of H. sapiens, he chose to create a now 3.8-billion-year-old library with precise instructions for flippers, slug glue, cuttlefish camouflage, dragonfly reproduction systems and the weaverbird’s nest, plus every other undabbled life form extinct and extant.

Post reply

8923 views

DAVID: God is in control and if he created such a mechanism, as you imagine, it would contain guidelines.

dhw: You agree the odds [for cellular intelligence] are 50/50, but in your view they are not 50/50. As for your guidelines, they have turned out to be a 3.8-billion-year-old library of information and instructions for every undabbled innovation, lifestyle and natural wonder in the history of life. The exact opposite of the autonomous mechanism I am proposing.

DAVID: And which I continue to reject. You like a slightly impotent God.

dhw: As explained under “Big brain evolution”, there is no impotence involved if God chooses to give evolution free rein through his design of an autonomous mechanism (cellular intelligence), as opposed to providing a 3.8-billion-year-old library of information and instructions for every single undabbled life form, lifestyle and natural wonder, plus solutions for every single problem that bacteria would have to solve for the rest of time.

You do not see a purposeful God as I do. If He is driven to achieve certain goals He will keep tight control.

DAVID: Cells have fixed roles. Cells have no ability to invent.

dhw: Cells have fixed roles once an innovation has proved to be successful. Then it is only when new conditions arise that they take on new roles. [The ability to invent] is the big question, and that is why my proposal remains a hypothesis, as does your own. But if in your view cells have a 50/50 chance of being autonomously intelligent and hence of creating instructions “on the hoof” or “de novo”, as believed by some scientists in the field, then clearly it is a hypothesis that demands serious consideration even by you - and without the condition of “guidelines” which = God’s instructions.

DAVID: What all cells can do according to your scientists and mine is that cells can modify responses as necessary, but they still remain the same cells,. Lenski's E. coli have made minor metabolic changes, but are still E. coli after 20,000+ generations. Based on those facts and the many requirements to jump from Ediacaran to Cambrian, Ediacaran cells did not invent Cambrian forms. That is what your hypothesis logically proposes! I can't seriously consider it any more than I can accept an inventive mechanism without God's guidelines.

dhw: We only know what cells/cell communities do after the fact of speciation. Nobody knows how the innovations occurred. I accept your rational doubts about cells’ ability to invent – it is a hypothesis – just as we both rationally doubt the efficacy of random mutations as the driving force. But for the life of me I cannot understand how you can stick to your irrational fixed belief that although your God’s one and only purpose was to specially design the brain of H. sapiens, he chose to create a now 3.8-billion-year-old library with precise instructions for flippers, slug glue, cuttlefish camouflage, dragonfly reproduction systems and the weaverbird’s nest, plus every other undabbled life form extinct and extant.

We can stop this vein of discussion. I don't know how God did it but He drove evolution and all the bushiness we see. Behe's book is finally out next week and it looks at deletion of DNA causing advances in form! Don't spend your life worrying about my logical conclusions. You know my points.

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More about his book:

https://uncommondescent.com/intelligent-design/darwinism-like-every-other-natural-proce...

"Although every other known natural (unintelligent) process tends to turn order into disorder, Darwinists have always believed that natural selection is the one natural process which can create spectacular order out of disorder. In my 2012 video Evolution is a Natural Process Running Backward I cited examples (beginning at the 10:50 mark) from Behe’s 2007 book The Edge of Evolution, to show that despite all the claims about the creative powers of natural selection, those creative powers have never actually been observed. Behe looks in detail at “the thrust and parry of human-malaria evolution” and concludes that it “did not build anything—it only destroyed things.” He reviews the results from Richard Lenski’s decades long E. Coli experiment, which a New Scientist article claims was “the first time evolution has been caught in the act,” and concludes that natural selection can only be credited with “breaking some genes and turning others off.” Thus, I concluded in the video, “it seems that perhaps natural selection of random mutations is like every other unintelligent cause in the universe after all, and tends to create disorder out of order and not vice-versa.”

"As another illustration that natural selection of random mutations can only degrade, in this German TV interview, retired geneticist Wolf-Ekkehard Loennig recounts (minutes 24:00 to 28:00, turn on English subtitles if you don’t speak German) the well-funded attempts at, among other places, his own Max Planck Institute for Plant Breeding Research, to speed up evolution in plants using radiation and advanced artificial selection techniques. Loennig reports that only devolution occurred: the only progress observed before this effort was given up was that the genes that made some plants toxic were damaged, making these plants more useful as animal fodder. Who would have predicted that bombarding genes with radiation would not lead to major agricultural advances!

"Behe’s new book expands greatly on this theme and concludes that natural selection of random mutations occasionally makes species better adapted to their environment by destroying things, but it never creates. So it is not, after all, the one natural process in the universe that can make Nature “run backward.” To understand what I mean by Nature running backward, you’ll have to watch the video."

Comment: Soon!

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8967 views

DAVID: Cells have fixed roles. Cells have no ability to invent.

dhw: We only know what cells/cell communities do after the fact of speciation. Nobody knows how the innovations occurred. I accept your rational doubts about cells’ ability to invent – it is a hypothesis – just as we both rationally doubt the efficacy of random mutations as the driving force. But for the life of me I cannot understand how you can stick to your irrational fixed belief that although your God’s one and only purpose was to specially design the brain of H. sapiens, he chose to create a now 3.8-billion-year-old library with precise instructions for flippers, slug glue, cuttlefish camouflage, dragonfly reproduction systems and the weaverbird’s nest, plus every other undabbled life form extinct and extant.

DAVID: We can stop this vein of discussion. I don't know how God did it but He drove evolution and all the bushiness we see.

I fully understand your desire to drop it, but so long as you continue to push your own inexplicable hypotheses, and to denigrate research that points to cellular intelligence, the discussion will go on.

QUOTE: "Behe’s new book […] concludes that natural selection of random mutations occasionally makes species better adapted to their environment by destroying things, but it never creates. So it is not, after all, the one natural process in the universe that can make Nature “run backward.” [..]

Behe is about ten years behind us then. You and I have long since rejected random mutations as a driving force, and have pointed out that natural selection never created anything – it simply explains why some organisms survive and others don’t. Let's hope the rest of the book comes up with something more enlightening.

Under “De novo genes”
QUOTE: “Taxonomically restricted (i.e., orphan) genes have contributed to the evolution of unique tissues and organs in a number of animals."

Fits in nicely with the idea that cells produce instructions “on the hoof” or “de novo”, as opposed to magically and automatically picking out their new instructions from a 3.8-billion-year-old library of instructions for the whole of evolution.

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8937 views

dhw: We only know what cells/cell communities do after the fact of speciation. Nobody knows how the innovations occurred. I accept your rational doubts about cells’ ability to invent – it is a hypothesis – just as we both rationally doubt the efficacy of random mutations as the driving force. But for the life of me I cannot understand how you can stick to your irrational fixed belief that although your God’s one and only purpose was to specially design the brain of H. sapiens, he chose to create a now 3.8-billion-year-old library with precise instructions for flippers, slug glue, cuttlefish camouflage, dragonfly reproduction systems and the weaverbird’s nest, plus every other undabbled life form extinct and extant.

DAVID: We can stop this vein of discussion. I don't know how God did it but He drove evolution and all the bushiness we see.

dhw: I fully understand your desire to drop it, but so long as you continue to push your own inexplicable hypotheses, and to denigrate research that points to cellular intelligence, the discussion will go on.

I will enter a very clear paper today, later on how genes don't matter anymore in understanding life, but don't explain evolution.

QUOTE: "Behe’s new book […] concludes that natural selection of random mutations occasionally makes species better adapted to their environment by destroying things, but it never creates. So it is not, after all, the one natural process in the universe that can make Nature “run backward.” [..]

dhw: Behe is about ten years behind us then. You and I have long since rejected random mutations as a driving force, and have pointed out that natural selection never created anything – it simply explains why some organisms survive and others don’t. Let's hope the rest of the book comes up with something more enlightening.

Under “De novo genes”
QUOTE: “Taxonomically restricted (i.e., orphan) genes have contributed to the evolution of unique tissues and organs in a number of animals."

dhw: Fits in nicely with the idea that cells produce instructions “on the hoof” or “de novo”, as opposed to magically and automatically picking out their new instructions from a 3.8-billion-year-old library of instructions for the whole of evolution.

In running existing life, that is true for what exists today. The programming through God and His dabbles has produced His goal. I view evolution as completed.

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8857 views

A great article on changing concepts on the true role of genes. To set the scene b e sure to read the very learned concepts, especially this one:

Yelloguy: "I think the article makes a very good case of flipping the old way of thinking that the genes are the blueprint to an organism's development, to a new way of thinking that genes are a small subset of the database available, and that the blueprint lies elsewhere." I think he uses the term 'blueprint' broadly to imply information and controls.

http://nautil.us//issue/68/context/its-the-end-of-the-gene-as-we-know-it

"We’ve all seen the stark headlines: “Being Rich and Successful Is in Your DNA” (Guardian, July 12); “A New Genetic Test Could Help Determine Children’s Success” (Newsweek, July 10); “Our Fortunetelling Genes” make us (Wall Street Journal, Nov. 16); and so on.

"The problem is, many of these headlines are not discussing real genes at all, but a crude statistical model of them, involving dozens of unlikely assumptions. Now, slowly but surely, that whole conceptual model of the gene is being challenged.

"We have reached peak gene, and passed it.

***

"In a famous paper in 1911, Wilhelm Johannsen warned against doing that. We do not know, he said, how those inferred, but invisible, factors can possibly carry such complex information. But Johannsen was ignored, for reasons, as it turned out, more to do with ideology than biology.

***

"So the accepted “central dogma” could be conceived as the one-way flow of information from the code in the gene:

"DNA template → proteins → developing characteristics;

as if production of the words alone is tantamount to writing the whole “book” of a complex being.

***

"So the hype now pouring out of the mass media is popularizing what has been lurking in the science all along: a gene-god as an entity with almost supernatural powers. Today it’s the gene that, in the words of the Anglican hymn, “makes us high and lowly and orders our estate.”

"In her 1984 book, The Ontogeny of Information, the philosopher of science Susan Oyama warned, “Just as traditional thought placed biological forms in the mind of God, so modern thought finds ways of endowing the genes with ultimate formative power.”

"The long-suppressed logic of Johansenn that has stalked the gene-god for decades has come home to roost. Scientists now understand that the information in the DNA code can only serve as a template for a protein. It cannot possibly serve as instructions for the more complex task of putting the proteins together into a fully functioning being, no more than the characters on a typewriter can produce a story.

***
"Genes are used as templates for making vital resources, of course. But directions and outcomes of the system are not controlled by genes. Like colonies of ants or bees, there are deeper dynamical laws at work in the development of forms and variations.

***

"It is most stunningly displayed in early development. Within hours, the fertilized egg becomes a ball of identical cells—all with the same genome, of course. But the cells are already talking to each other with storms of chemical signals. Through the statistical patterns within the storms, instructions are, again, created de novo. The cells, all with the same genes, multiply into hundreds of starkly different types, moving in a glorious ballet to find just the right places at the right times. That could not have been specified in the fixed linear strings of DNA.

"So it has been dawning on us is that there is no prior plan or blueprint for development: Instructions are created on the hoof, far more intelligently than is possible from dumb DNA. That is why today’s molecular biologists are reporting “cognitive resources” in cells; “bio-information intelligence”; “cell intelligence”; “metabolic memory”; and “cell knowledge”—all terms appearing in recent literature.1,2 “Do cells think?” is the title of a 2007 paper in the journal Cellular and Molecular Life Sciences.3 On the other hand the assumed developmental “program” coded in a genotype has never been described.

"It is such discoveries that are turning our ideas of genetic causation inside out. We have traditionally thought of cell contents as servants to the DNA instructions. But, as the British biologist Denis Noble insists in an interview with the writer Suzan Mazur,1 “The modern synthesis has got causality in biology wrong … DNA on its own does absolutely nothing until activated by the rest of the system … DNA is not a cause in an active sense. I think it is better described as a passive data base which is used by the organism to enable it to make the proteins that it requires.” (my bold)

Comment: See next entry to continue. My bias has had me skip his references to RNA world beginning. My bold above is my agreement with Noble.

Post reply

8870 views

Second part of the article just presented:

"All of this provides a fraught background for modern gene association studies. What’s more, the statistical analyses that power these studies are, themselves, full of pitfalls. First, the methods for computing polygenic scores, in which millions of variables are analyzed by statistical manipulation, provides huge opportunities for false positives. Very large databases—even randomly generated ones—can contain large numbers of meaningless correlations; and statistical significance values can be hugely inflated by invalid assumptions.

'In polygenic score estimations, for example, it is assumed that SNP associations [single nucleotide polymorphisms] can be simply added together, as if beans in a bag, with no effects on each other, or from the environment. Then, as the National Institute of Health website reminds us, the majority of SNPs are functionally irrelevant anyway.

***

"Another wrench in the works has been the discovery that a gene product typically undergoes rearrangements before being put to use. It means that different proteins, with potentially widely different functions, can be produced from the same gene: not one for one, as the central dogma has told us. Again, the instructions for such rearrangements are not in the genes themselves.

"More startling has been the realization that less than 5 percent of the genome is used to make proteins at all. Most produce a vast range of different factors (RNAs) regulating, through the network, how the other genes are used.

"Increasingly, we are finding that, in complex evolved traits—like human minds—there is little prediction from DNA variation through development to individual differences. The genes are crucial, of course, but nearly all genetic variations are dealt with in the way you can vary your journey from A to B: by constructing alternative routes. “Multiple alternative pathways … are the rule rather than the exception,” reported a paper in the journal BioSystems in 2007.

"Conversely, it is now well known that a group of genetically identical individuals, reared in identical environments—as in pure-bred laboratory animals—do not become identical adults. Rather, they develop to exhibit the full range of bodily and functional variations found in normal, genetically-variable, groups. In a report in Science in 2013, Julia Fruend and colleagues observed this effect in differences in developing brain structures.

"In the same vein, we can now understand why the same genetic resources can be used in many different ways in different organs and tissues. Genes now utilized in the development of our arms and legs, first appeared in organisms that have neither. Genes used in fruit flies for gonad development are now used in the development of human brains. And most genes are used in several different tissues for different purposes at the same time.

"So it is, in a review in the journal Genetics in 2017, that the geneticists Petter Portin and Adam Wilkins question “the utility of the concept of a basic ‘unit of inheritance’ and the long implicit belief that genes are autonomous agents.” They show that “the classic molecular definition [is] obsolete.'”

Comment: Goodbye Dawkins' Selfish Gene. Shapiro's work on bacteria surely shows how embryology must work, a wild concert of genes, structural forces, hormones and transcriptional distortions all arriving somehow as a reproduced organism. What has been obvious to me is that we have not found an underlying informational control mechanism. It is still a black box, but somehow a massive set of continues coordinated processes produce an emergence of living beings. And it had to be designed, which, obviously, the author does not believe. Again please review comments. They are very thoughtful, especially as they bring information agreeing and disagreeing.

Post reply

8942 views

Under “De novo genes”
QUOTE: “Taxonomically restricted (i.e., orphan) genes have contributed to the evolution of unique tissues and organs in a number of animals."

dhw: Fits in nicely with the idea that cells produce instructions “on the hoof” or “de novo”, as opposed to magically and automatically picking out their new instructions from a 3.8-billion-year-old library of instructions for the whole of evolution.

DAVID: In running existing life, that is true for what exists today. The programming through God and His dabbles has produced His goal. I view evolution as completed.

Ah, so cells today are intelligent and produce their own instructions, but in the past they could only read selected volumes from God’s 3.8-billion-year-old library.

DAVID: We can stop this vein of discussion. I don't know how God did it but He drove evolution and all the bushiness we see.

dhw: I fully understand your desire to drop it, but so long as you continue to push your own inexplicable hypotheses, and to denigrate research that points to cellular intelligence, the discussion will go on.

DAVID: I will enter a very clear paper today, later on how genes don't matter anymore in understanding life, but don't explain evolution.

The paper is an extended version of the one which you quoted at the very beginning of this thread, on 14 January at 13.35, and which you have been trying to discredit ever since. I will repeat some of my bolded quotes, plus a couple of new ones:

Scientists now understand that the information in the DNA code can only serve as a template for a protein. It cannot possibly serve as instructions for the more complex task of putting the proteins together into a fully functioning being, no more than the characters on a typewriter can produce a story.

"Through the statistical patterns within the storms, instructions are, again, created de novo. The cells, all with the same genes, multiply into hundreds of starkly different types, moving in a glorious ballet to find just the right places at the right times. That could not have been specified in the fixed linear strings of DNA.

Perhaps the most graphic of them all:

So it has been dawning on us is that there is no prior plan or blueprint for development: Instructions are created on the hoof, far more intelligently than is possible from dumb DNA. That is why today’s molecular biologists are reporting “cognitive resources” in cells; “bio-information intelligence”; “cell intelligence”; “metabolic memory”; and “cell knowledge”—all terms appearing in recent literature. “Do cells think?” is the title of a 2007 paper in the journal Cellular and Molecular Life Sciences. On the other hand the assumed developmental “program” coded in a genotype has never been described.[/i]

You could hardly have a clearer endorsement of the thinking cell hypothesis, as opposed to your hypothesis of programming through a library of instructions.

"DNA on its own does absolutely nothing until activated by the rest of the system … DNA is not a cause in an active sense. I think it is better described as a passive data base which is used by the organism to enable it to make the proteins that it requires.”

Contrary to your comment above, this paper does offer an explanation of evolution: intelligent cells utilize the same genetic resources to develop new organs.

"In a paper in Physics of Life Reviews in 2013, James Shapiro describes how cells and organisms are capable of “natural genetic engineering.” That is, they frequently alter their own DNA sequences, rewriting their own genomes throughout life. The startling implication is that the gene as popularly conceived—a blueprint on a strand of DNA, determining development and its variations—does not really exist.

DAVID: […] What has been obvious to me is that we have not found an underlying informational control mechanism. It is still a black box, but somehow a massive set of continues coordinated processes produce an emergence of living beings. And it had to be designed, which, obviously, the author does not believe.

The quotes could hardly be clearer: these scientists agree with Shapiro that the underlying informational control mechanism is cellular intelligence, and that is what coordinates the massive set of processes. They have not said how this mechanism might have come into being in the first place, but I have consistently proposed that a possible source is your God. Of course none of this provides the conclusive evidence you are looking for in any hypothesis that contradicts your own unproven hypothesis, but I must thank you for illustrating yet again the fact that there are lots of modern scientists who now support the concept of cellular intelligence as the mechanism that runs evolution – as opposed to your 3.8 billion-year-old library of instructions.

Post reply

8918 views

Under “De novo genes”
QUOTE: “Taxonomically restricted (i.e., orphan) genes have contributed to the evolution of unique tissues and organs in a number of animals."

dhw: Fits in nicely with the idea that cells produce instructions “on the hoof” or “de novo”, as opposed to magically and automatically picking out their new instructions from a 3.8-billion-year-old library of instructions for the whole of evolution.

DAVID: In running existing life, that is true for what exists today. The programming through God and His dabbles has produced His goal. I view evolution as completed.

dhw: Ah, so cells today are intelligent and produce their own instructions, but in the past they could only read selected volumes from God’s 3.8-billion-year-old library.

That is your conclusion, not mine,

DAVID: I will enter a very clear paper today, later on how genes don't matter anymore in understanding life, but don't explain evolution.

dhw: The paper is an extended version of the one which you quoted at the very beginning of this thread, on 14 January at 13.35, and which you have been trying to discredit ever since. I will repeat some of my bolded quotes, plus a couple of new ones:

Scientists now understand that the information in the DNA code can only serve as a template for a protein. It cannot possibly serve as instructions for the more complex task of putting the proteins together into a fully functioning being, no more than the characters on a typewriter can produce a story.

"Through the statistical patterns within the storms, instructions are, again, created de novo. The cells, all with the same genes, multiply into hundreds of starkly different types, moving in a glorious ballet to find just the right places at the right times. That could not have been specified in the fixed linear strings of DNA.

Perhaps the most graphic of them all:

So it has been dawning on us is that there is no prior plan or blueprint for development: Instructions are created on the hoof, far more intelligently than is possible from dumb DNA. That is why today’s molecular biologists are reporting “cognitive resources” in cells; “bio-information intelligence”; “cell intelligence”; “metabolic memory”; and “cell knowledge”—all terms appearing in recent literature. “Do cells think?” is the title of a 2007 paper in the journal Cellular and Molecular Life Sciences. On the other hand the assumed developmental “program” coded in a genotype has never been described.[/i]

You could hardly have a clearer endorsement of the thinking cell hypothesis, as opposed to your hypothesis of programming through a library of instructions.

"DNA on its own does absolutely nothing until activated by the rest of the system … DNA is not a cause in an active sense. I think it is better described as a passive data base which is used by the organism to enable it to make the proteins that it requires.”

"In the same vein, we can now understand why the same genetic resources can be used in many different ways in different organs and tissues. Genes now utilized in the development of our arms and legs, first appeared in organisms that have neither. [/b]

Contrary to your comment above, this paper does offer an explanation of evolution: intelligent cells utilize the same genetic resources to develop new organs.

We know speciation occurs. Your statement is a guess. We don't know how genes achieve results.

dhw: "In a paper in Physics of Life Reviews in 2013, James Shapiro describes how cells and organisms are capable of “natural genetic engineering.” That is, they frequently alter their own DNA sequences, rewriting their own genomes throughout life. The startling implication is that the gene as popularly conceived—a blueprint on a strand of DNA, determining development and its variations—does not really exist.

DAVID: […] What has been obvious to me is that we have not found an underlying informational control mechanism. It is still a black box, but somehow a massive set of continues coordinated processes produce an emergence of living beings. And it had to be designed, which, obviously, the author does not believe.

dhw: The quotes could hardly be clearer: these scientists agree with Shapiro that the underlying informational control mechanism is cellular intelligence, and that is what coordinates the massive set of processes. They have not said how this mechanism might have come into being in the first place, but I have consistently proposed that a possible source is your God. Of course none of this provides the conclusive evidence you are looking for in any hypothesis that contradicts your own unproven hypothesis, but I must thank you for illustrating yet again the fact that there are lots of modern scientists who now support the concept of cellular intelligence as the mechanism that runs evolution – as opposed to your 3.8 billion-year-old library of instructions.

And they are all materialists. Us ID folks will always disagree as to the correct interpretations.

Post reply

8910 views

Under “De novo genes”
QUOTE: “Taxonomically restricted (i.e., orphan) genes have contributed to the evolution of unique tissues and organs in a number of animals."

DAVID: In running existing life, that is true for what exists today. The programming through God and His dabbles has produced His goal. I view evolution as completed.

dhw: Ah, so cells today are intelligent and produce their own instructions, but in the past they could only read selected volumes from God’s 3.8-billion-year-old library.

DAVID: That is your conclusion, not mine.

Then I don’t understand your answer to my comment that cells produce instructions “de novo”. You said “that is true for what exists today”. If so, it means cells are intelligent today. You go on to say that before evolution was “completed” (I envy your foreknowledge of events over the next few billion years), it was all preprogramming and dabbles, which can only mean cells were not intelligent then.

QUOTE: "In the same vein, we can now understand why the same genetic resources can be used in many different ways in different organs and tissues. Genes now utilized in the development of our arms and legs, first appeared in organisms that have neither. [/b]

dhw: Contrary to your comment above, this paper does offer an explanation of evolution: intelligent cells utilize the same genetic resources to develop new organs.

DAVID: We know speciation occurs. Your statement is a guess. We don't know how genes achieve results.

You claimed that the paper did not offer an explanation of evolution. It does – it clearly sides with Shapiro. But of course the explanation is a hypothesis or “guess”. And it’s a totally different guess from your own.

dhw: The quotes could hardly be clearer: these scientists agree with Shapiro that the underlying informational control mechanism is cellular intelligence, and that is what coordinates the massive set of processes. They have not said how this mechanism might have come into being in the first place, but I have consistently proposed that a possible source is your God. Of course none of this provides the conclusive evidence you are looking for in any hypothesis that contradicts your own unproven hypothesis, but I must thank you for illustrating yet again the fact that there are lots of modern scientists who now support the concept of cellular intelligence as the mechanism that runs evolution – as opposed to your 3.8 billion-year-old library of instructions.

DAVID: And they are all materialists. Us ID folks will always disagree as to the correct interpretations.

I thought you told us that Shapiro was a practising Jew, but it makes no difference at all. The idea that the underlying informational control mechanism is cellular intelligence does not in any way exclude God or intelligent design, and in your discussions with me, your attempts to equate it with atheism and materialism are out of order. I am neither an atheist nor a materialist.

QUOTE: So it has been dawning on us is that there is no prior plan or blueprint for development: Instructions are created on the hoof, far more intelligently than is possible from dumb DNA. That is why today’s molecular biologists are reporting “cognitive resources” in cells; “bio-information intelligence”; “cell intelligence”; “metabolic memory”; and “cell knowledge”—all terms appearing in recent literature. “Do cells think?” is the title of a 2007 paper in the journal Cellular and Molecular Life Sciences. On the other hand the assumed developmental “program” coded in a genotype has never been described.[/i]

I am repeating this quote because time and again you have told me that only a small minority of scientists (I always name Margulis, McClintock, Buehler and Shapiro as my examples) support the concept of cellular intelligence, and everyone else is on your side. Apparently “today’s molecular scientists” are not on your side. But I must thank you yet again for your integrity in presenting papers which support my arguments.

Post reply

8850 views

dhw: Then I don’t understand your answer to my comment that cells produce instructions “de novo”. You said “that is true for what exists today”. If so, it means cells are intelligent today. You go on to say that before evolution was “completed” (I envy your foreknowledge of events over the next few billion years), it was all preprogramming and dabbles, which can only mean cells were not intelligent then.

dhw: Contrary to your comment above, this paper does offer an explanation of evolution: intelligent cells utilize the same genetic resources to develop new organs.

dhw: You claimed that the paper did not offer an explanation of evolution. It does – it clearly sides with Shapiro. But of course the explanation is a hypothesis or “guess”. And it’s a totally different guess from your own.

dhw: The quotes could hardly be clearer: these scientists agree with Shapiro that the underlying informational control mechanism is cellular intelligence, and that is what coordinates the massive set of processes. They have not said how this mechanism might have come into being in the first place, but I have consistently proposed that a possible source is your God. Of course none of this provides the conclusive evidence you are looking for in any hypothesis that contradicts your own unproven hypothesis, but I must thank you for illustrating yet again the fact that there are lots of modern scientists who now support the concept of cellular intelligence as the mechanism that runs evolution – as opposed to your 3.8 billion-year-old library of instructions.

dhw: The idea that the underlying informational control mechanism is cellular intelligence does not in any way exclude God or intelligent design, and in your discussions with me, your attempts to equate it with atheism and materialism are out of order. I am neither an atheist nor a materialist.

QUOTE: So it has been dawning on us is that there is no prior plan or blueprint for development: Instructions are created on the hoof, far more intelligently than is possible from dumb DNA. That is why today’s molecular biologists are reporting “cognitive resources” in cells; “bio-information intelligence”; “cell intelligence”; “metabolic memory”; and “cell knowledge”—all terms appearing in recent literature. “Do cells think?” is the title of a 2007 paper in the journal Cellular and Molecular Life Sciences. On the other hand the assumed developmental “program” coded in a genotype has never been described.[/i]

dhw: I am repeating this quote because time and again you have told me that only a small minority of scientists (I always name Margulis, McClintock, Buehler and Shapiro as my examples) support the concept of cellular intelligence, and everyone else is on your side. Apparently “today’s molecular scientists” are not on your side. But I must thank you yet again for your integrity in presenting papers which support my arguments.

I present this material because it can support either view, that is chance or design, which is exactly, in a sense, equal to my 50/50 interpretation of the cells activities independent decisions or designed responses. You have chosen as a middle road, cells are intelligent in and of themselves. This is a mental compromise which allows you to stand on both pillars, chance and design all at once. In your mind this allows chance cells to appear (somehow) on the scene, develop (somehow) the ability to design for the future and therefore facilitate speciation. Nice sidestep to my thinking. You get to keep chance and design without losing either.

I view chance and design as absolutely either/or. I throw out chance absolutely. Life had to be started by design. Cells can not design their own future, recognizing the giant changes required in form and physiology as shown by the huge gaps in the fossil record.

But in the current evolution stage we do see cells that appear to design. It is in immune and embryological processes. In immunity, B cells change their DNA to code for antibody production. Do they follow rigid protocols or make independent decisions? For me they follow dictated procedures or they might make fatal errors in judgment.

And in embryology the cells of the zygote reproduced accurately resultant progeny which are mostly exact replicas of parents. I've alluded to all the various factors: chemical, structural pressures, DNA input, etc., all working in a frantic mixture. The process reproduces human copies accurately by design. In humans we can find variations which are minor as shown in Grey's Anatomy, such as variations in vessel routes. I have a misplaced artery in the palm of my left hand, of no importance. If in the melee of fetus formation free-form decisions are not allowed to happen. Mistakes do happens as shown in the ' human monsters' that do appear at birth, but are generally caused by some environmental insult in the uterus. underlying design instructions are required. Somehow zygote cells follow directions in the factors listed as well as others.

So Shapiro et al are not wrong. Their conclusions are open to debate as I've described. They offer you a safe shore to row to so as to get away from the very specific either/or approach that I follow in these discussions.

Post reply

8966 views

This group looked at modifiers of genes with general comments:

https://medicalxpress.com/news/2019-02-genes-onoff.html

"It takes just 2 percent of the human genome to code for all of the proteins that make cellular functions—from producing energy to repairing tissues—possible.

"So what does the other 98 percent do?

"A large portion of this so-called noncoding DNA controls the expression of genes, switching them on and off. This regulation is essential because every cell has the same DNA.

"In other words, the only thing that makes a muscle cell different from a brain cell is which genes are activated.

***

"'In a new paper in the journal Genetics, they compare five types of regulatory regions that have been identified in the past few years in an effort to figure out how the regions behave in different types of cells.

"'When people try to look at how gene regulation occurs, they look at different epigenomic information using sequencing, trying to understand molecular profiles," says lead author Arushi Varshney, a Ph.D. candidate in human genetics.

"Epigenomics refers to changes in the organization of genes caused by factors other than the DNA sequence.

"For example, researchers have recently discovered that genetic variants—the slight variations in DNA that make us unique—that are associated with diseases tend to lie in areas of the genome that act as gene regulatory elements called enhancers and promoters.

"Enhancers boost the rate of transcription of a gene, much like the accelerator in a car, and promoters initiate transcription of a gene, like a car's ignition.

"'There were a number of papers coming out describing different classes of gene regulatory elements, and it was not clear how they are related," explains Stephen Parker, Ph.D., assistant professor of computational medicine and bioinformatics and of human genetics.

"'Our paper was the first to really compare them," Parker says. "One of the things that came out is that they're all different and act differently in different cell types."

"However, the U-M team also discovered that genetic variants in the more cell type-specific enhancers have relatively small effects on their target genes. This could spell trouble for scientists who are comparing thousands of people's genomes to try to locate genetic variation associated with disease traits.

"The U-M authors suggest that these genes are so important for a cell's function that their transcription is tightly regulated under normal conditions. (my bold)

***

"Varshney, Parker and their colleagues suggest that enhancers and promoters that are cell-specific—meaning they have bigger effects in certain types of cells—could make it easier for transcription to occur under certain environmental conditions.

"They appear to do this by making the cell's chromatin, the dense protein molecules that the DNA wraps around inside the nucleus of a cell, more accessible."

Comment: 3-D DNA is a key to this. Little is 'junk'. Note my bold. Cells are tightly regulated in how the genes are activated in organisms that are as fully evolved as we are.

Post reply

8926 views

dhw: I am repeating this quote because time and again you have told me that only a small minority of scientists (I always name Margulis, McClintock, Buehler and Shapiro as my examples) support the concept of cellular intelligence, and everyone else is on your side. Apparently “today’s molecular scientists” are not on your side. But I must thank you yet again for your integrity in presenting papers which support my arguments.

DAVID: I present this material because it can support either view, that is chance or design, which is exactly, in a sense, equal to my 50/50 interpretation of the cells activities independent decisions or designed responses. You have chosen as a middle road, cells are intelligent in and of themselves. This is a mental compromise which allows you to stand on both pillars, chance and design all at once. In your mind this allows chance cells to appear (somehow) on the scene, develop (somehow) the ability to design for the future and therefore facilitate speciation. Nice sidestep to my thinking. You get to keep chance and design without losing either.

What a cop-out! You have persistently maintained that only a minority of scientists believe in cellular intelligence. According to the article you have presented to us, there are lots of scientists who now believe that cells are intelligent. So you switch from whether cells are intelligent to the either/or of chance and design. The context of cellular intelligence is our discussion of how evolution works: you say divine preprogramming and/or dabbling; I propose cellular intelligence, the very idea of which you have pooh-poohed. I am NOT proposing that this appeared by chance. For the purposes of our discussion I have offered nothing but theistic hypotheses, and I have even asked you if you think your God is incapable of designing such a mechanism. But (let us now exchange personal attempts at mind-reading) you wish to change the subject because (a) you can’t explain your own combination of hypotheses, and (b) you cannot bear the thought that your God might have given that mechanism free rein, thereby achieving his goal – or at least one of his goals (I don’t exclude the idea of humans as a goal) – of an ever changing spectacle which you yourself are sure he enjoys, like a painter enjoying his paintings.

Apart from your final comment, the rest of your post acknowledges the appearance of cellular design, rejects chance, and categorically rejects the idea that cellular intelligence might be capable of invention (Shapiro’s “natural genetic engineering”) before this - somewhat surprising - conclusion:

DAVID: So Shapiro et al are not wrong. Their conclusions are open to debate as I've described. They offer you a safe shore to row to so as to get away from the very specific either/or approach that I follow in these discussions.

Having stated categorically that “cells cannot design their own future”, you agree that Shapiro et al are not wrong! Of course their conclusions are open to debate. So are yours. That is why we have all these discussions. But if we are discussing my hypotheses and yours concerning how evolution works, please don’t pretend that we are discussing chance v. design. My hypotheses (and Shapiro’s) simply allow for a different design from the one you have fixed in your mind, and those I have offered you are all theistic.

xxxxx

The U-M authors suggest that these genes are so important for a cell's function that their transcription is tightly regulated under normal conditions. (David’s bold)

DAVID: : 3-D DNA is a key to this. Little is 'junk'. Note my bold. Cells are tightly regulated in how the genes are activated in organisms that are as fully evolved as we are.

Of course they are tightly regulated. Once a system has been invented and is successful, it must repeat its actions – and these will only change if conditions change.

David (under “Biological complexity”): This study supports the article I presented about the place of DNA in the control of life's processes. it is a tiny part of the controls

So I’d better add the relevant quotes from earlier, to be coupled with the quote at the start of this post.

"Scientists now understand that the information in the DNA code can only serve as a template for a protein. It cannot possibly serve as instructions for the more complex task of putting the proteins together into a fully functioning being, no more than the characters on a typewriter can produce a story."

"Through the statistical patterns within the storms, instructions are, again, created de novo. The cells, all with the same genes, multiply into hundreds of starkly different types, moving in a glorious ballet to find just the right places at the right times. That could not have been specified in the fixed linear strings of DNA."

Post reply

8905 views

DAVID: I present this material because it can support either view, that is chance or design, which is exactly, in a sense, equal to my 50/50 interpretation of the cells activities independent decisions or designed responses. You have chosen as a middle road, cells are intelligent in and of themselves. This is a mental compromise which allows you to stand on both pillars, chance and design all at once. In your mind this allows chance cells to appear (somehow) on the scene, develop (somehow) the ability to design for the future and therefore facilitate speciation. Nice sidestep to my thinking. You get to keep chance and design without losing either.

dhw: What a cop-out! You have persistently maintained that only a minority of scientists believe in cellular intelligence. According to the article you have presented to us, there are lots of scientists who now believe that cells are intelligent. So you switch from whether cells are intelligent to the either/or of chance and design. The context of cellular intelligence is our discussion of how evolution works: you say divine preprogramming and/or dabbling; I propose cellular intelligence, the very idea of which you have pooh-poohed. I am NOT proposing that this appeared by chance.

So how did it appear?

dhw: For the purposes of our discussion I have offered nothing but theistic hypotheses, and I have even asked you if you think your God is incapable of designing such a mechanism. But (let us now exchange personal attempts at mind-reading) you wish to change the subject because (a) you can’t explain your own combination of hypotheses,

I've explained my hypotheses so well to myself I changed from agnostic to theistic!

dhw; Apart from your final comment, the rest of your post acknowledges the appearance of cellular design, rejects chance, and categorically rejects the idea that cellular intelligence might be capable of invention (Shapiro’s “natural genetic engineering”) before this - somewhat surprising - conclusion:

DAVID: So Shapiro et al are not wrong. Their conclusions are open to debate as I've described. They offer you a safe shore to row to so as to get away from the very specific either/or approach that I follow in these discussions.

dhw: Having stated categorically that “cells cannot design their own future”, you agree that Shapiro et al are not wrong! Of course their conclusions are open to debate. So are yours. That is why we have all these discussions. But if we are discussing my hypotheses and yours concerning how evolution works, please don’t pretend that we are discussing chance v. design. My hypotheses (and Shapiro’s) simply allow for a different design from the one you have fixed in your mind, and those I have offered you are all theistic.

Without a belief in God. Shapiro is describing single cells in charge of their own fate. In our stage of evolution our cells are tightly controlled by feedback looks to achieve exact results.

xxxxx

The U-M authors suggest that these genes are so important for a cell's function that their transcription is tightly regulated under normal conditions. (David’s bold)

DAVID: : 3-D DNA is a key to this. Little is 'junk'. Note my bold. Cells are tightly regulated in how the genes are activated in organisms that are as fully evolved as we are.

dhw; Of course they are tightly regulated. Once a system has been invented and is successful, it must repeat its actions – and these will only change if conditions change.

David (under “Biological complexity”): This study supports the article I presented about the place of DNA in the control of life's processes. it is a tiny part of the controls

dhw: So I’d better add the relevant quotes from earlier, to be coupled with the quote at the start of this post.

"Scientists now understand that the information in the DNA code can only serve as a template for a protein. It cannot possibly serve as instructions for the more complex task of putting the proteins together into a fully functioning being, no more than the characters on a typewriter can produce a story."

"Through the statistical patterns within the storms, instructions are, again, created de novo. The cells, all with the same genes, multiply into hundreds of starkly different types, moving in a glorious ballet to find just the right places at the right times. That could not have been specified in the fixed linear strings of DNA."

Shapiro studies bacteria which are responsible for their own survival. Our cells function at a different level. There are controls we do not know see clearly at this point. Some of that is seen in B cells making DNA instructions for new antibodies on the fly and the wild machinations of embryological development resulting in almost exact reproductions.

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dhw: You have persistently maintained that only a minority of scientists believe in cellular intelligence. According to the article you have presented to us, there are lots of scientists who now believe that cells are intelligent. So you switch from whether cells are intelligent to the either/or of chance and design. The context of cellular intelligence is our discussion of how evolution works: you say divine preprogramming and/or dabbling; I propose cellular intelligence, the very idea of which you have pooh-poohed. I am NOT proposing that this appeared by chance.

DAVID: So how did it appear?

Nobody knows, but I for one am not prepared to dismiss the theory that there is a God who made it appear.

dhw: For the purposes of our discussion I have offered nothing but theistic hypotheses, and I have even asked you if you think your God is incapable of designing such a mechanism. But (let us now exchange personal attempts at mind-reading) you wish to change the subject because (a) you can’t explain your own combination of hypotheses […]

DAVID: I've explained my hypotheses so well to myself I changed from agnostic to theistic!

I have no problem at all with your belief in God. This discussion focuses on your interpretation of your God’s purposes and methods, and in particular on your insistence that the unknown mechanism that leads to speciation cannot possibly be cellular intelligence – although many modern scientists are coming round to the belief that cells really are intelligent. Instead you have a fixed belief that your God either intervened personally (dabbled) or the cell communities automatically chose the correct instructions from a 3.8-billion-year-old library of information and instructions that was stored in their genome, detailing every single innovation, lifestyle and natural wonder in the history of life. And all for the sake of delaying his design of the only thing he wanted to design: you and me.

DAVID: So Shapiro et al are not wrong. Their conclusions are open to debate as I've described. They offer you a safe shore to row to so as to get away from the very specific either/or approach that I follow in these discussions.

dhw: Having stated categorically that “cells cannot design their own future”, you agree that Shapiro et al are not wrong! Of course their conclusions are open to debate. So are yours. That is why we have all these discussions. But if we are discussing my hypotheses and yours concerning how evolution works, please don’t pretend that we are discussing chance v. design. My hypotheses (and Shapiro’s) simply allow for a different design from the one you have fixed in your mind, and those I have offered you are all theistic.

DAVID: Without a belief in God. Shapiro is describing single cells in charge of their own fate. In our stage of evolution our cells are tightly controlled by feedback looks to achieve exact results.

Yes, as I have agreed repeatedly, once an innovation is successful, it has to be tightly controlled in order to ensure that it survives intact. There is absolutely no reason why belief in autonomous cellular intelligence should entail not believing in God – hence my answer to your question “how did it appear?”

DAVID: Shapiro studies bacteria which are responsible for their own survival. Our cells function at a different level. There are controls we do not know see clearly at this point. Some of that is seen in B cells making DNA instructions for new antibodies on the fly and the wild machinations of embryological development resulting in almost exact reproductions.

I’m delighted at your agreement that bacteria are responsible for their own survival, as opposed to following instructions issued 3.8 billion years ago. They are individual living organisms. Our cell communities are parts of immensely complex living organisms, and must cooperate if the overall community is to survive. Since single cells, you now agree, have the intelligence to work out their own ways of survival, why is it so difficult for you to imagine that communities of single cells might also have the intelligence to work out their own ways of survival? Once a method has been established, the cell communities must repeat their actions in order to survive – until new conditions arise, and then the communities will respond, just as bacteria do, by making changes to themselves. But as I keep agreeing, we do not know whether they are capable of the innovations which result in speciation. That is why, just like your library and your divine dabbling, it is a hypothesis and not a fact.

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dhw: I have no problem at all with your belief in God. This discussion focuses on your interpretation of your God’s purposes and methods, and in particular on your insistence that the unknown mechanism that leads to speciation cannot possibly be cellular intelligence – although many modern scientists are coming round to the belief that cells really are intelligent. Instead you have a fixed belief that your God either intervened personally (dabbled) or the cell communities automatically chose the correct instructions from a 3.8-billion-year-old library of information and instructions that was stored in their genome, detailing every single innovation, lifestyle and natural wonder in the history of life. And all for the sake of delaying his design of the only thing he wanted to design: you and me.

Your thoughts about my thoughts of God are very confused. My conclusions about God's actions are based on the reasons why I accepted that God exists, and all follow logically from my original conclusions. These are your problems as you study the concept of God from the outside.

DAVID: Without a belief in God. Shapiro is describing single cells in charge of their own fate. In our stage of evolution our cells are tightly controlled by feedback looks to achieve exact results.

Yes, as I have agreed repeatedly, once an innovation is successful, it has to be tightly controlled in order to ensure that it survives intact. There is absolutely no reason why belief in autonomous cellular intelligence should entail not believing in God – hence my answer to your question “how did it appear?”

DAVID: Shapiro studies bacteria which are responsible for their own survival. Our cells function at a different level. There are controls we do not know see clearly at this point. Some of that is seen in B cells making DNA instructions for new antibodies on the fly and the wild machinations of embryological development resulting in almost exact reproductions.

dhw: I’m delighted at your agreement that bacteria are responsible for their own survival, as opposed to following instructions issued 3.8 billion years ago. They are individual living organisms.

My view of bacteria differs: They have a library of possible responses as threats and environmental changes appear. Their survival ability depends upon choosing the correct responses, which they obviously can do, having survived since the start of life.

dhw: Our cell communities are parts of immensely complex living organisms, and must cooperate if the overall community is to survive. Since single cells, you now agree, have the intelligence to work out their own ways of survival, why is it so difficult for you to imagine that communities of single cells might also have the intelligence to work out their own ways of survival? Once a method has been established, the cell communities must repeat their actions in order to survive – until new conditions arise, and then the communities will respond, just as bacteria do, by making changes to themselves. But as I keep agreeing, we do not know whether they are capable of the innovations which result in speciation. That is why, just like your library and your divine dabbling, it is a hypothesis and not a fact.

Yes, it fills in for God, and admits something must design the future steps. To me God represents a specific purpose. Do cell committees have purpose other than immediate adaptability?

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dhw: I have no problem at all with your belief in God. This discussion focuses on your interpretation of your God’s purposes and methods, and in particular on your insistence that the unknown mechanism that leads to speciation cannot possibly be cellular intelligence – although many modern scientists are coming round to the belief that cells really are intelligent. Instead you have a fixed belief that your God either intervened personally (dabbled) or the cell communities automatically chose the correct instructions from a 3.8-billion-year-old library of information and instructions that was stored in their genome, detailing every single innovation, lifestyle and natural wonder in the history of life. And all for the sake of delaying his design of the only thing he wanted to design: you and me.

DAVID: Your thoughts about my thoughts of God are very confused. My conclusions about God's actions are based on the reasons why I accepted that God exists, and all follow logically from my original conclusions. These are your problems as you study the concept of God from the outside.

Nobody can study the concept of God from the inside. Your belief that God exists is based on logical arguments for design, but they provide no justification for the beliefs summarized above.

DAVID: Shapiro studies bacteria which are responsible for their own survival.

dhw: I’m delighted at your agreement that bacteria are responsible for their own survival, as opposed to following instructions issued 3.8 billion years ago. They are individual living organisms.

DAVID: My view of bacteria differs: They have a library of possible responses as threats and environmental changes appear. Their survival ability depends upon choosing the correct responses, which they obviously can do, having survived since the start of life.

Ah, so they are only responsible for looking into the 3.8-billion-year-old library of instructions for the whole history of undabbled life, and for picking out the one set of instructions for their new situation – which apparently they do automatically because they are also preprogrammed to pick out the right programme. Isn’t it possible that their survival ability depends on their working out their own solutions, i.e. “being responsible for their own survival” using the (perhaps God-given) intelligence that Shapiro’s research suggests?

dhw: …as I keep agreeing, we do not know whether they [cells/cell communities] are capable of the innovations which result in speciation. That is why, just like your library and your divine dabbling, it is a hypothesis and not a fact.

DAVID: Yes, it fills in for God, and admits something must design the future steps. To me God represents a specific purpose. Do cell committees have purpose other than immediate adaptability?

In my hypothesis they are not future steps but intelligent responses to current conditions. There is no “filling in for God” if God created the inventive mechanism in the first place. As I have repeated ad nauseam, if God exists then of course he had a purpose in creating life and the mechanism (cellular intelligence in my hypothesis) that led to evolution. But the only purpose you allow him is the production of H. sapiens (except when you are sure that he enjoys his own creations). You have agreed that his immediate driving force in designing flippers, camouflage and migration routes would have been to enable those organisms to survive; I also believe the purpose of cell communities is to ensure survival and, in my hypothesis, to improve chances of survival through innovation. That does not mean that the only reason they had to survive was to give your God 3.5+ billion years to design humans.

DAVID (under “Human evolution”: this an obvious transitional fossil, but full blown speciation requiring design. I don't believe the cells of the common ancestor of chimps and humans could conceive of how to design a foot and spine and pelvis for bipedal movement.

Hurray for all these transitional fossils, though I can’t help wondering why an always-in-control God should need to take 3.5+ billion years before specially designing big toes, spines and pelvises on the way to his sole aim of specially designing us. However, it is not inconceivable that improvements might gradually emerge as generation after generation of cell communities come up with new ideas. Just a hypothesis.

DAVID (under “Egnor”): And again, if there was no awareness of a large portion of reality how did cell committees know to create brains/minds. Cell committees can't create evolved new forms.

Opinion stated as fact. Yet again: nobody knows how new forms evolved. One theory is random mutations, and another is the inventiveness of intelligent cells (perhaps designed by your God – or do you think your God is incapable of designing inventive “minds” other than those of H. sapiens?). Now please tell us how immaterial “pure energy” - as you have described your God - knew how to create and presumably perceive materially generated sound, sight, smell, taste, touch if they had never existed before. How indeed can pure energy even be conscious of itself? The history of evolution only shows us what has been invented – not how it was invented. That is a mystery which you “solve” by creating an even greater mystery. But you may be right. I am an agnostic.

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dhw: I have no problem at all with your belief in God. This discussion focuses on your interpretation of your God’s purposes and methods, and in particular on your insistence that the unknown mechanism that leads to speciation cannot possibly be cellular intelligence – Instead you have a fixed belief that your God either intervened personally (dabbled) or the cell communities automatically chose the correct instructions from a 3.8-billion-year-old library of information and instructions that was stored in their genome, detailing every single innovation, lifestyle and natural wonder in the history of life. And all for the sake of delaying his design of the only thing he wanted to design: you and me.

DAVID: Your thoughts about my thoughts of God are very confused. My conclusions about God's actions are based on the reasons why I accepted that God exists, and all follow logically from my original conclusions. These are your problems as you study the concept of God from the outside.

dhw: Nobody can study the concept of God from the inside. Your belief that God exists is based on logical arguments for design, but they provide no justification for the beliefs summarized above.

I'm simply proposing likely ways God controlled the process.

DAVID: Shapiro studies bacteria which are responsible for their own survival.

dhw: I’m delighted at your agreement that bacteria are responsible for their own survival, as opposed to following instructions issued 3.8 billion years ago. They are individual living organisms.

DAVID: My view of bacteria differs: They have a library of possible responses as threats and environmental changes appear. Their survival ability depends upon choosing the correct responses, which they obviously can do, having survived since the start of life.

dhw: Ah, so they are only responsible for looking into the 3.8-billion-year-old library of instructions for the whole history of undabbled life, and for picking out the one set of instructions for their new situation – which apparently they do automatically because they are also preprogrammed to pick out the right programme. Isn’t it possible that their survival ability depends on their working out their own solutions, i.e. “being responsible for their own survival” using the (perhaps God-given) intelligence that Shapiro’s research suggests?

They have a few simple things they sense, listed in the past.

dhw: …as I keep agreeing, we do not know whether they [cells/cell communities] are capable of the innovations which result in speciation. That is why, just like your library and your divine dabbling, it is a hypothesis and not a fact.

DAVID: Yes, it fills in for God, and admits something must design the future steps. To me God represents a specific purpose. Do cell committees have purpose other than immediate adaptability?

In my hypothesis they are not future steps but intelligent responses to current conditions. ... I also believe the purpose of cell communities is to ensure survival and, in my hypothesis, to improve chances of survival through innovation. That does not mean that the only reason they had to survive was to give your God 3.5+ billion years to design humans.

That doesn't explain why we are here. We were never necessary as a logical step. The difference of Man theory.

DAVID (under “Human evolution”: this an obvious transitional fossil, but full blown speciation requiring design. I don't believe the cells of the common ancestor of chimps and humans could conceive of how to design a foot and spine and pelvis for bipedal movement.

dhw: Hurray for all these transitional fossils, though I can’t help wondering why an always-in-control God should need to take 3.5+ billion years before specially designing big toes, spines and pelvises on the way to his sole aim of specially designing us. However, it is not inconceivable that improvements might gradually emerge as generation after generation of cell communities come up with new ideas. Just a hypothesis.

Itty-bitty steps again. if we could only find the your hypotheses about cell inventions might have some credence. Mind the gaps!

DAVID (under “Egnor”): And again, if there was no awareness of a large portion of reality how did cell committees know to create brains/minds. Cell committees can't create evolved new forms.

dhw: Opinion stated as fact. Yet again: nobody knows how new forms evolved. One theory is random mutations, and another is the inventiveness of intelligent cells (perhaps designed by your God – or do you think your God is incapable of designing inventive “minds” other than those of H. sapiens?). Now please tell us how immaterial “pure energy” - as you have described your God - knew how to create and presumably perceive materially generated sound, sight, smell, taste, touch if they had never existed before. How indeed can pure energy even be conscious of itself? The history of evolution only shows us what has been invented – not how it was invented. That is a mystery which you “solve” by creating an even greater mystery. But you may be right. I am an agnostic.

I view God as pure energy forming the most brilliant mind around! Consciousness cannot appear de novo from gasses, rocks and minerals. I am conscious and I believe your are.

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DAVID: (Under “Egnor”): My point was if nothing is mental in the universe how do cells know to create a mental capacity? Just another logical attack on your beloved cell groups.

Of course there has to be something mental in the universe. The question is whether there was something mental BEFORE the universe, or something mental evolved within the universe.

DAVID: I view God as pure energy forming the most brilliant mind around! Consciousness cannot appear de novo from gasses, rocks and minerals. I am conscious and I believe you are.

I too believe we are conscious. I know how you view God, and I gave you an answer last time which you have completely ignored, so here it is again: I don’t know how consciousness can evolve de novo from gases, rocks and minerals. Nor do I know how “pure energy” can simply BE conscious and can know all about materially generated life, sound, sight, smell, taste, touch even before the materials exist. The history of evolution only shows us what has been invented – not how it was invented. That is a mystery which you “solve” by creating an even greater mystery. But you may be right. I am an agnostic.

DAVID: […] My conclusions about God's actions are based on the reasons why I accepted that God exists, and all follow logically from my original conclusions. These are your problems as you study the concept of God from the outside.

dhw: Nobody can study the concept of God from the inside. Your belief that God exists is based on logical arguments for design, but they provide no justification for the beliefs summarized above.

DAVID: I'm simply proposing likely ways God controlled the process.

I have offered you several logical options concerning ways God controlled the process, but you have a fixed belief in the only one which you cannot explain.

DAVID: Shapiro studies bacteria which are responsible for their own survival.

dhw: I’m delighted at your agreement that bacteria are responsible for their own survival, as opposed to following instructions issued 3.8 billion years ago. They are individual living organisms.

Opinion stated as fact. So please explain how they select the one set of relevant instructions from the 3.8-billion-year-old library of instructions for every life form and every situation in the history of life past, present and future.

DAVID: Yes, it fills in for God, and admits something must design the future steps. To me God represents a specific purpose. Do cell committees have purpose other than immediate adaptability?

dhw: In my hypothesis they are not future steps but intelligent responses to current conditions. ... I also believe the purpose of cell communities is to ensure survival and, in my hypothesis, to improve chances of survival through innovation. That does not mean that the only reason they had to survive was to give your God 3.5+ billion years to design humans.

DAVID: That doesn't explain why we are here. We were never necessary as a logical step. The difference of Man theory.

Usual slither away from the fact that NO multicellular form of life was “necessary” as a logical step, since bacteria have survived perfectly well.

dhw: Hurray for all these transitional fossils, though I can’t help wondering why an always-in-control God should need to take 3.5+ billion years before specially designing big toes, spines and pelvises on the way to his sole aim of specially designing us. However, it is not inconceivable that improvements might gradually emerge as generation after generation of cell communities come up with new ideas. Just a hypothesis.

DAVID: Itty-bitty steps again. if we could only find the your hypotheses about cell inventions might have some credence. Mind the gaps!

It is you who have drawn attention to the itty-bitty steps. Specially designed big toes, spines, pelvises, legs and mini-to-maxi brains as apes turn into hominins turn into humans turn into H. sapiens. There's a gap in your sentence: “If we could only find the your hypotheses”...but perhaps you meant the transitional fossils which indicate itty-bitty steps. Amazingly, it seems that we are finding more and more of them, all specially designed according to you, as your always-in-control God for some inexplicable reason, after 3.5+ billion years of specially designing anything but H. sapiens, now specially designs the itty bits which will eventually become parts of H. sapiens, which is the only thing he ever wanted to specially design in the first place.

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DAVID: (Under “Egnor”): My point was if nothing is mental in the universe how do cells know to create a mental capacity? Just another logical attack on your beloved cell groups.

dhw: Of course there has to be something mental in the universe. The question is whether there was something mental BEFORE the universe, or something mental evolved within the universe.

I still believe in a first cause which has to b e eternal.

DAVID: I view God as pure energy forming the most brilliant mind around! Consciousness cannot appear de novo from gasses, rocks and minerals. I am conscious and I believe you are.

dhw: I too believe we are conscious. I know how you view God, and I gave you an answer last time which you have completely ignored, so here it is again: I don’t know how consciousness can evolve de novo from gases, rocks and minerals. Nor do I know how “pure energy” can simply BE conscious and can know all about materially generated life, sound, sight, smell, taste, touch even before the materials exist. The history of evolution only shows us what has been invented – not how it was invented. That is a mystery which you “solve” by creating an even greater mystery. But you may be right. I am an agnostic.

And you accept that consciousness might have appeared from rocks uncaused.

DAVID: My view of bacteria differs: They have a library of possible responses as threats and environmental changes appear. Their survival ability depends upon choosing the correct responses, which they obviously can do, having survived since the start of life.
And:
DAVID: They have a few simple things they sense, listed in the past.

dhw: Opinion stated as fact. So please explain how they select the one set of relevant instructions from the 3.8-billion-year-old library of instructions for every life form and every situation in the history of life past, present and future.

Not opinion , bacteria have need of very few responses.

DAVID (under “Human evolution”: this an obvious transitional fossil, but full blown speciation requiring design. I don't believe the cells of the common ancestor of chimps and humans could conceive of how to design a foot and spine and pelvis for bipedal movement.

dhw: Hurray for all these transitional fossils, though I can’t help wondering why an always-in-control God should need to take 3.5+ billion years before specially designing big toes, spines and pelvises on the way to his sole aim of specially designing us. However, it is not inconceivable that improvements might gradually emerge as generation after generation of cell communities come up with new ideas. Just a hypothesis.

DAVID: Itty-bitty steps again. if we could only find the your hypotheses about cell inventions might have some credence. Mind the gaps!

dhw: It is you who have drawn attention to the itty-bitty steps. Specially designed big toes, spines, pelvises, legs and mini-to-maxi brains as apes turn into hominins turn into humans turn into H. sapiens. There's a gap in your sentence: “If we could only find the your hypotheses”...but perhaps you meant the transitional fossils which indicate itty-bitty steps. Amazingly, it seems that we are finding more and more of them, all specially designed according to you, as your always-in-control God for some inexplicable reason, after 3.5+ billion years of specially designing anything but H. sapiens, now specially designs the itty bits which will eventually become parts of H. sapiens, which is the only thing he ever wanted to specially design in the first place.

What the sentence should say 'is if we could only find the cellular mechanism to support your hypothesis'. It is all hypothesis based on the fact that cells operate automatically in very intelligent ways.

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Paul Davies in wracking his brain to explain the ghost in the machine:

https://www.theguardian.com/science/2019/jan/26/i-predict-great-revolution-physicists-d...

"Rather than biology, some scientists are now looking to physics for answers, in particular the physics of information. Buried in the rules that shape information lie the secrets of life and perhaps even the reason for our existence.

"That, at least, is the bold proposal from Paul Davies, a prominent physicist who explores the idea in his forthcoming book, The Demon in the Machine.

***

“'The basic hypothesis is this,” Davies says. “We have fundamental laws of information that bring life into being from an incoherent mish-mash of chemicals. The remarkable properties we associate with life are not going to come about by accident.”

"The proposal takes some unpacking. Davies believes that the laws of nature as we know them today are insufficient to explain what life is and how it came about. We need to find new laws, he says, or at least new principles, which describe how information courses around living creatures. Those rules may not only nail down what life is, but actively favour its emergence.

"To understand what bothers Davies, consider a hypothetical device: a life meter. Wave it over a sterile rock and the dial stays at zero. Wave it over a purring cat and it swings over to 100. But what if you dunked it in the primordial soup, or held it over a dying person? At what point does complex chemistry become life, and when does life revert to mere matter? Between an atom and an amoeba lies something profound and perplexing.

"Davies suspects that information is the answer because it seems increasingly fundamental to both physics and biology. In recent years, physicists have shown that information is more than the bits and bytes that course through computers. Information can be converted into energy, for example, such that physicists now build little information engines and information-powered refrigerators, if not with the appearance their names suggest.

"Similar machines are found in biology. Constructed from proteins, they chunter away inside living cells where they manipulate information at the nanoscale. “What we’re seeing in the lab is these two worlds colliding in a very practical way,” he says. “The physics is really connecting with the biology and that’s why I think we’re on the verge of this great new revolution.”

"Davies believes that life will turn out to bear telltale patterns of information processing that distinguish it from non-life. Few people would argue that a computer is alive no matter how the ones and zeroes zip around inside it. What Davies suspects is that life exploits, and arises from, particular patterns of information flow.

***

"He concedes: “It is wishful thinking because at this stage I can’t demonstrate it. But if we live in a universe in which the emergence of life is built into it in a fundamental way then we can feel more at home in the universe.

Rob Shelton responds:

https://uncommondescent.com/intelligent-design/physicist-rob-sheldon-on-paul-davies-lif...

"Recently, we quoted Paul Davies writing on the information content of life forms in New Scientist, in The Demon in the Machine, to the effect that the really tough question is how life’s hardware can write its own software.

***

" If information is a conserved quantity, then the ability to increase the information flow leads to faster and faster complexity. This is a property of feedback-enabled or “bootstrap” systems

***

" Davies is suggesting that the way to pack more information into a smaller volume is effectively to make information hierarchical. It is as if we take a text, compress it with PKZIP, add some more zipped files, and then pack them all in a library file. When we need the information, we read the header in the library file, extract the file that we want, and then unzip it. This packing and zipping can be done again and again, putting libraries inside libraries inside libraries, as much as is needed, so that an incredible video game with great graphics displaying Terabytes of information can be shipped in a file of 1 Gbyte.

" But what Davies perhaps doesn’t recognize is that the header files, the directories must be “above” the information level of the files. Nothing in the zipped file tells you how to extract it.

" So if Davies believes that a hierarchy of information can pack more information in, and possibly explain the incredible information content of biology, then there must be something “outside” or “above” the biology that is responsible for the compression algorithm. That information cannot arise from inside the cell any more than a self-extracting program can exist without the operating system/hardware outside it.

"The only thing Davies hasn’t done is name this attribute.

"Should we suggest a name? How about … intelligent design?

Comment: Material Life runs an immaterial information.

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QUOTE: So if Davies believes that a hierarchy of information can pack more information in, and possibly explain the incredible information content of biology, then there must be something “outside” or “above” the biology that is responsible for the compression algorithm. That information cannot arise from inside the cell any more than a self-extracting program can exist without the operating system/hardware outside it.

"The only thing Davies hasn’t done is name this attribute.
"Should we suggest a name? How about … intelligent design?

DAVID: Material Life runs an immaterial information.

I find the whole argument unnecessarily complex and irritatingly nebulous, but perhaps Davies defines “information” elsewhere in a manner that would make more sense to me. My response to the above response to Davies is that information on its own is useless. It does indeed need require something “outside” or “above” itself to absorb it, process it, and decide how to use it. But intelligent design is the product, not the user. We are talking here about how life operates, so in life what might the user or “operating system” be? In the biological world, I propose that the answer is intelligent minds. And so I would suggest that material life runs on intelligent minds using information – all the way from single-celled bacteria through to the vast cell communities that combine to form humans. Information comes from both inside and outside the cell(s), but the absorbing, processing, decision-making “mind” is inside it (them). The source of these intelligent minds may be your God, or may be a chance combination of materials that evolved into increasingly complex intelligences, or may be a form of panpsychism inherent in materials and again evolving. I find all three explanations equally difficult to believe.

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QUOTE: So if Davies believes that a hierarchy of information can pack more information in, and possibly explain the incredible information content of biology, then there must be something “outside” or “above” the biology that is responsible for the compression algorithm. That information cannot arise from inside the cell any more than a self-extracting program can exist without the operating system/hardware outside it.

"The only thing Davies hasn’t done is name this attribute.
"Should we suggest a name? How about … intelligent design?

DAVID: Material Life runs an immaterial information.

dhw; I find the whole argument unnecessarily complex and irritatingly nebulous, but perhaps Davies defines “information” elsewhere in a manner that would make more sense to me. My response to the above response to Davies is that information on its own is useless. It does indeed need require something “outside” or “above” itself to absorb it, process it, and decide how to use it. But intelligent design is the product, not the user. We are talking here about how life operates, so in life what might the user or “operating system” be? In the biological world, I propose that the answer is intelligent minds. And so I would suggest that material life runs on intelligent minds using information – all the way from single-celled bacteria through to the vast cell communities that combine to form humans. Information comes from both inside and outside the cell(s), but the absorbing, processing, decision-making “mind” is inside it (them). The source of these intelligent minds may be your God, or may be a chance combination of materials that evolved into increasingly complex intelligences, or may be a form of panpsychism inherent in materials and again evolving. I find all three explanations equally difficult to believe.

I believe Davies recognizes life's processes run under a complex set of instructions/information which are the ghost in the machine. as in the above quote. It is equivalent to ID without the designer. You are correct. Information does nothing. It must acted upon. Only then can living organisms appear.

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DAVID: Material Life runs an immaterial information.

dhw; I find the whole argument unnecessarily complex and irritatingly nebulous, but perhaps Davies defines “information” elsewhere in a manner that would make more sense to me. My response to the above response to Davies is that information on its own is useless. It does indeed need require something “outside” or “above” itself to absorb it, process it, and decide how to use it. But intelligent design is the product, not the user. We are talking here about how life operates, so in life what might the user or “operating system” be? In the biological world, I propose that the answer is intelligent minds. And so I would suggest that material life runs on intelligent minds using information – all the way from single-celled bacteria through to the vast cell communities that combine to form humans. Information comes from both inside and outside the cell(s), but the absorbing, processing, decision-making “mind” is inside it (them). The source of these intelligent minds may be your God, or may be a chance combination of materials that evolved into increasingly complex intelligences, or may be a form of panpsychism inherent in materials and again evolving. I find all three explanations equally difficult to believe.

DAVID: I believe Davies recognizes life's processes run under a complex set of instructions/information which are the ghost in the machine, as in the above quote. It is equivalent to ID without the designer. You are correct. Information does nothing. It must acted upon. Only then can living organisms appear.

And only then can living organisms function. I don't see information as the ghost in the machine. The ghost in the machine is whatever uses the information. You say it’s a 3.8-billion-year old computer programme (which your God installed in the first living cells) with instructions for every single undabbled life form, econiche, lifestyle and natural wonder in the history of life. I suggest it’s intelligence, and in my post I offered three alternative and, for me, equally mysterious sources of that intelligence, one of which is your God.

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QUOTE: So if Davies believes that a hierarchy of information can pack more information in, and possibly explain the incredible information content of biology, then there must be something “outside” or “above” the biology that is responsible for the compression algorithm. That information cannot arise from inside the cell any more than a self-extracting program can exist without the operating system/hardware outside it.
"The only thing Davies hasn’t done is name this attribute.
"Should we suggest a name? How about … intelligent design?

DAVID: Material Life runs an immaterial information.

dhw; I find the whole argument unnecessarily complex and irritatingly nebulous, but perhaps Davies defines “information” elsewhere in a manner that would make more sense to me. My response to the above response to Davies is that information on its own is useless. It does indeed need require something “outside” or “above” itself to absorb it, process it, and decide how to use it. But intelligent design is the product, not the user. We are talking here about how life operates, so in life what might the user or “operating system” be? In the biological world, I propose that the answer is intelligent minds. And so I would suggest that material life runs on intelligent minds using information – all the way from single-celled bacteria through to the vast cell communities that combine to form humans. Information comes from both inside and outside the cell(s), but the absorbing, processing, decision-making “mind” is inside it (them). The source of these intelligent minds may be your God, or may be a chance combination of materials that evolved into increasingly complex intelligences, or may be a form of panpsychism inherent in materials and again evolving. I find all three explanations equally difficult to believe.

DAVID: I believe Davies recognizes life's processes run under a complex set of instructions/information which are the ghost in the machine, as in the above quote. It is equivalent to ID without the designer. You are correct. Information does nothing. It must acted upon. Only then can living organisms appear.

dhw: And only then can living organisms function. I don't see information as the ghost in the machine. The ghost in the machine is whatever uses the information. You say it’s a 3.8-billion-year old computer programme (which your God installed in the first living cells) with instructions for every single undabbled life form, econiche, lifestyle and natural wonder in the history of life. I suggest it’s intelligence, and in my post I offered three alternative and, for me, equally mysterious sources of that intelligence, one of which is your God.

You are right. Intelligent information/instructions and intelligent instructions as to how to interpret and use the instructions are all part of the ghost with all processes acting together like a giant symphony orchestra. All dssigned.

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Parts of protein molecules in life are in constant motion, and that motion is used to promote active processes:

https://phys.org/news/2019-03-gotcha-scientists-fingerprint-proteins-vibrations.html

"In the cells of every living organism—humans, birds, bees, roses and even bacteria—proteins vibrate with microscopic motions that help them perform vital tasks ranging from cell repair to photosynthesis.

***

"A team led by University at Buffalo physicist Andrea Markelz reports that it has developed a method for rapidly measuring proteins' unique vibrations.

"The advance could open new possibilities in biological research, such as studying the microscopic motions of proteins more efficiently, or leveraging vibrational patterns as "fingerprints" to quickly determine whether specific proteins are present in a laboratory sample.

"Scientists could also use the new technique to swiftly assess whether pharmaceuticals designed to inhibit a protein's vibrations are working. This would require comparing the vibrational signatures of proteins before and after the application of inhibitors.

"'Proteins are elegant and robust nanomachines that nature has developed," says Markelz, Ph.D., a professor of physics in the UB College of Arts and Sciences. "We know nature uses molecular motions to optimize these machines. By learning the underlying principles of this optimization, we can develop new biotechnology for medicine, energy harvesting and even electronics.'"

Comment: This is just the beginning of unpeeling another layer of activity and controls of processes. We'll await results and more layers.

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DAVID: (Under “Egnor”): My point was if nothing is mental in the universe how do cells know to create a mental capacity? Just another logical attack on your beloved cell groups.

dhw: Of course there has to be something mental in the universe. The question is whether there was something mental BEFORE the universe, or something mental evolved within the universe.

DAVID: I still believe in a first cause which has to be eternal.

So do I. But I can’t choose between the two equally mysterious options I have described.

DAVID: I view God as pure energy forming the most brilliant mind around! Consciousness cannot appear de novo from gasses, rocks and minerals. [..]

dhw: […] I know how you view God, and I gave you an answer last time which you have completely ignored, so here it is again: I don’t know how consciousness can evolve de novo from gases, rocks and minerals. Nor do I know how “pure energy” can simply BE conscious and can know all about materially generated life, sound, sight, smell, taste, touch even before the materials exist. The history of evolution only shows us what has been invented – not how it was invented. That is a mystery which you “solve” by creating an even greater mystery. But you may be right. I am an agnostic.

DAVID: And you accept that consciousness might have appeared from rocks uncaused.

I don’t “accept” either of the options! You have a fixed belief that “pure energy” can simply BE conscious etc., and that gases and materials cannot combine spontaneously to create consciousness. I find both hypotheses equally impossible to accept, even though one of them must be correct. That is one major reason for my agnosticism.

dhw: Opinion stated as fact. So please explain how they select the one set of relevant instructions from the 3.8-billion-year-old library of instructions for every life form and every situation in the history of life past, present and future.

DAVID: Not opinion, bacteria have need of very few responses.

They have need of responses to every single situation and environment in which they have found themselves since the beginning of life. Now please explain how they manage unthinkingly to select relevant instructions for every single situation out of your great library of instructions for the whole of life.

DAVID (under “Human evolution”): this an obvious transitional fossil, but full blown speciation requiring design. I don't believe the cells of the common ancestor of chimps and humans could conceive of how to design a foot and spine and pelvis for bipedal movement.

DAVID: Itty-bitty steps again. if we could only find the your hypotheses about cell inventions might have some credence. Mind the gaps!

dhw: There's a gap in your sentence: “If we could only find the your hypotheses”...but perhaps you meant the transitional fossils which indicate itty-bitty steps. Amazingly, it seems that we are finding more and more of them, all specially designed according to you, as your always-in-control God for some inexplicable reason, after 3.5+ billion years of specially designing anything but H. sapiens, now specially designs the itty bits which will eventually become parts of H. sapiens, which is the only thing he ever wanted to specially design in the first place.

DAVID: What the sentence should say 'is if we could only find the cellular mechanism to support your hypothesis'. It is all hypothesis based on the fact that cells operate automatically in very intelligent ways.

Sorry you couldn’t respond to the major point about your God’s itty-bitty steps. As regards my hypothesis, it is absolutely NOT a fact that cells operate automatically (although I have pointed out that they may do so once a system has been established, and will only change if conditions change). That is your opinion, which you admit has a 50/50 chance of being wrong, i.e. that their intelligent ways may be the product of autonomous intelligence. And how often do I have to repeat that my hypothesis is a hypothesis. If only we could find your God’s 3.8-billion-year-old library of instructions for the whole of life, your hypothesis might have some credence.

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DAVID: And you accept that consciousness might have appeared from rocks uncaused.

dhw: I don’t “accept” either of the options! You have a fixed belief that “pure energy” can simply BE conscious etc., and that gases and materials cannot combine spontaneously to create consciousness. I find both hypotheses equally impossible to accept, even though one of them must be correct. That is one major reason for my agnosticism.

I fully understand and appreciate your agnosticism in these discussions.

dhw: Opinion stated as fact. So please explain how they select the one set of relevant instructions from the 3.8-billion-year-old library of instructions for every life form and every situation in the history of life past, present and future.

DAVID: Not opinion, bacteria have need of very few responses.

dhw: They have need of responses to every single situation and environment in which they have found themselves since the beginning of life. Now please explain how they manage unthinkingly to select relevant instructions for every single situation out of your great library of instructions for the whole of life.

Not as complex as you would like to think to advance your pet arguments. Bacteria sense others, sense food, sense dangerous chemicals, transfer genes, join in mats, and little more. In causing disease all they are doing is finding great food to eat in the wrong place for the host. And they divide by a very complex mechanism every 20 minutes in the best of conditions. I might ask, how did they learn to divide so precisely and obviously automatically ?

DAVID (under “Human evolution”): this an obvious transitional fossil, but full blown speciation requiring design. I don't believe the cells of the common ancestor of chimps and humans could conceive of how to design a foot and spine and pelvis for bipedal movement.

dhw: Hurray for all these transitional fossils, though I can’t help wondering why an always-in-control God should need to take 3.5+ billion years before specially designing big toes, spines and pelvises on the way to his sole aim of specially designing us. However, it is not inconceivable that improvements might gradually emerge as generation after generation of cell communities come up with new ideas. Just a hypothesis.

DAVID: Itty-bitty steps again. if we could only find the your hypotheses about cell inventions might have some credence. Mind the gaps!

dhw: There's a gap in your sentence: “If we could only find the your hypotheses”...but perhaps you meant the transitional fossils which indicate itty-bitty steps. Amazingly, it seems that we are finding more and more of them, all specially designed according to you, as your always-in-control God for some inexplicable reason, after 3.5+ billion years of specially designing anything but H. sapiens, now specially designs the itty bits which will eventually become parts of H. sapiens, which is the only thing he ever wanted to specially design in the first place.

DAVID: What the sentence should say 'is if we could only find the cellular mechanism to support your hypothesis'. It is all hypothesis based on the fact that cells operate automatically in very intelligent ways.

dhw: Sorry you couldn’t respond to the major point about your God’s itty-bitty steps. As regards my hypothesis, it is absolutely NOT a fact that cells operate automatically (although I have pointed out that they may do so once a system has been established, and will only change if conditions change). That is your opinion, which you admit has a 50/50 chance of being wrong, i.e. that their intelligent ways may be the product of autonomous intelligence. And how often do I have to repeat that my hypothesis is a hypothesis. If only we could find your God’s 3.8-billion-year-old library of instructions for the whole of life, your hypothesis might have some credence.

The multitude of layers of controls over DNA expression under current discovery is slowly elucidating how it all works.

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DAVID: […] bacteria have need of very few responses.

dhw: They have need of responses to every single situation and environment in which they have found themselves since the beginning of life. Now please explain how they manage unthinkingly to select relevant instructions for every single situation out of your great library of instructions for the whole of life.

DAVID: Not as complex as you would like to think to advance your pet arguments. Bacteria sense others, sense food, sense dangerous chemicals, transfer genes, join in mats, and little more. In causing disease all they are doing is finding great food to eat in the wrong place for the host. And they divide by a very complex mechanism every 20 minutes in the best of conditions. I might ask, how did they learn to divide so precisely and obviously automatically?

It is possible that your God created the mechanism by which all cells and cell communities divide precisely until conditions change and then the cells/cell communities change themselves. Now please stop dodging my question. How do bacteria automatically select the relevant instructions from your 3.8-billion-year-old library of instructions for all conditions, life forms, lifestyles, econiches, and natural wonders in the history of life?

DAVID: Itty-bitty steps again. if we could only find the your hypotheses about cell inventions might have some credence. Mind the gaps!

dhw: There's a gap in your sentence: “If we could only find the your hypotheses…”

dhw: Sorry you couldn’t respond to the major point about your God’s itty-bitty steps. As regards my hypothesis, it is absolutely NOT a fact that cells operate automatically (although I have pointed out that they may do so once a system has been established, and will only change if conditions change). That is your opinion, which you admit has a 50/50 chance of being wrong, i.e. that their intelligent ways may be the product of autonomous intelligence. And how often do I have to repeat that my hypothesis is a hypothesis. If only we could find your God’s 3.8-billion-year-old library of instructions for the whole of life, your hypothesis might have some credence.

DAVID: The multitude of layers of controls over DNA expression under current discovery is slowly elucidating how it all works.

And we still have your God specially designing humans itty-bitty, and current discovery still hasn’t discovered a 3.8-billion-year-old computer programme for the whole of evolution, but according to several of the articles you have posted, scientists seem to be slowly coming round to the idea that cells create their own instructions “on the hoof” and “de novo”, because they are intelligent. Even you give that hypothesis a 50/50 chance.

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dhw: They have need of responses to every single situation and environment in which they have found themselves since the beginning of life. Now please explain how they manage unthinkingly to select relevant instructions for every single situation out of your great library of instructions for the whole of life.

DAVID: Not as complex as you would like to think to advance your pet arguments. Bacteria sense others, sense food, sense dangerous chemicals, transfer genes, join in mats, and little more. In causing disease all they are doing is finding great food to eat in the wrong place for the host. And they divide by a very complex mechanism every 20 minutes in the best of conditions. I might ask, how did they learn to divide so precisely and obviously automatically?

dhw: It is possible that your God created the mechanism by which all cells and cell communities divide precisely until conditions change and then the cells/cell communities change themselves. Now please stop dodging my question. How do bacteria automatically select the relevant instructions from your 3.8-billion-year-old library of instructions for all conditions, life forms, lifestyles, econiches, and natural wonders in the history of life?

I've listed above the few challenges bacteria have. Their library is small, and their constant division is fully automatic. For other responses as a food example: sense food which then causes a series of molecular reactions to move toward it, and then automatically engulf it, followed by automatic digestion.

dhw: Sorry you couldn’t respond to the major point about your God’s itty-bitty steps. As regards my hypothesis, it is absolutely NOT a fact that cells operate automatically (although I have pointed out that they may do so once a system has been established, and will only change if conditions change). That is your opinion, which you admit has a 50/50 chance of being wrong, i.e. that their intelligent ways may be the product of autonomous intelligence. And how often do I have to repeat that my hypothesis is a hypothesis. If only we could find your God’s 3.8-billion-year-old library of instructions for the whole of life, your hypothesis might have some credence.

DAVID: The multitude of layers of controls over DNA expression under current discovery is slowly elucidating how it all works.

dhw: And we still have your God specially designing humans itty-bitty, and current discovery still hasn’t discovered a 3.8-billion-year-old computer programme for the whole of evolution, but according to several of the articles you have posted, scientists seem to be slowly coming round to the idea that cells create their own instructions “on the hoof” and “de novo”, because they are intelligent. Even you give that hypothesis a 50/50 chance.

All open to interpretation.

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A new study on fluid flow and unicellular organisms shows they go with the flow:

https://phys.org/news/2019-03-microbes-mathematical.html

"Freeing thousands of microorganisms to swim in random directions in an infinite pool of liquid may not sound like a recipe for order, but eventually the swarm will go with its own flow.

"Theoretical modeling led by University of Wisconsin–Madison applied mathematician Saverio Spagnolie shows that the forces generated by different kinds of tiny swimmers will sweep them all up in predictable ways.

"'When each individual particle experiences the flows created by all the other particles, it's known that really surprising effects can naturally emerge," says Spagnolie. "The flows and orientations of the swimmers become coherent on a length scale much longer than any individual particle, resulting in huge flocks of organisms swimming in the same direction and, perhaps unintentionally, working together."

***

"The researchers worked out the relevant equations for particles that move by various means—swimmers that actively push or pull themselves through fluid, and types (like microtubules inside a cell) that push or pull themselves through molecular means without active appendages like flagella—and goosed them into motion.

"'From that perturbation there's this explosion of motion," Spagnolie says. "And then we watch how the different forces play out on different types of particles."

"While a tight colony of pulling swimmers, for example, stretches itself out in a line perpendicular to the direction they're headed, a colony of pushers stretches quickly in the direction of motion, and then bends on itself over and over in a cascade of shrinking folds.

"'That these individuals can group together passively due to their fluid interactions alone, and that this results in large-scale events and effects they can't achieve as independent particles, is relevant to many biological functions—like nutrient mixing and bacterial resistance to antibiotics in bacterial swarms and biofilms," Spagnolie says."

Comment: In this instance bacteria appear to be mostly passive.

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I am combining all the relevant posts on this subject.

dhw: How do bacteria automatically select the relevant instructions from your 3.8-billion-year-old library of instructions for all conditions, life forms, lifestyles, econiches, and natural wonders in the history of life?

DAVID: I've listed above the few challenges bacteria have. Their library is small, and their constant division is fully automatic. For other responses as a food example: sense food which then causes a series of molecular reactions to move toward it, and then automatically engulf it, followed by automatic digestion.

Your 3.8-billion-year-old library with information and instructions for every undabbled future life form, econiche, lifestyle and natural wonder has suddenly undergone an amazing transformation. Those first single cells only had a library for bacteria and instructions only for the vast number of different conditions that future bacteria would have to cope with. So where was the library for the whole future of evolution? And even if bacteria had their own special library with their own limited number of special instructions, you still haven’t explained how they chose the right ones for each situation. (And we mustn’t forget that when trying to cope with new antibiotics, millions of them die before the chosen few are istructed to pick out the right instructions). (See below)

DAVID: The multitude of layers of controls over DNA expression under current discovery is slowly elucidating how it all works.

dhw: And we still have your God specially designing humans itty-bitty, and current discovery still hasn’t discovered a 3.8-billion-year-old computer programme for the whole of evolution, but according to several of the articles you have posted, scientists seem to be slowly coming round to the idea that cells create their own instructions “on the hoof” and “de novo”, because they are intelligent. Even you give that hypothesis a 50/50 chance.

DAVID: All open to interpretation.

Like everything else we discuss. That is why some of us find it so hard to pin ourselves to a fixed belief, and why we try to test the logic of each interpretation.

dhw: And only then can living organisms function. I don't see information as the ghost in the machine. The ghost in the machine is whatever uses the information. You say it’s a 3.8-billion-year old computer programme (which your God installed in the first living cells) with instructions for every single undabbled life form, econiche, lifestyle and natural wonder in the history of life. I suggest it’s intelligence, and in my post I offered three alternative and, for me, equally mysterious sources of that intelligence, one of which is your God.

DAVID: You are right. Intelligent information/instructions and intelligent instructions as to how to interpret and use the instructions are all part of the ghost with all processes acting together like a giant symphony orchestra. All designed.

Now we have instructions on how to use instructions. I suppose that explains how bacteria use their mini-library. But hold on, how do they know which instructions they should look for when they look for instructions on how to use instructions? Somewhere amid this great tangle there has to be a decision. So maybe whenever bacteria find themselves in a tricky new situation, your God pops in and picks out the correct instructions on how to use his instructions? Oh, if only he’d given them the intelligence to work out their own solutions to each problem, he would have saved himself and us a lot of time and effort.

Under “are bacteria truly independent?”

QUOTE: The flows and orientations of the swimmers become coherent on a length scale much longer than any individual particle, resulting in huge flocks of organisms swimming in the same direction and, perhaps unintentionally, working together. (dhw’s bold)

Or perhaps intentionally.

QUOTE: "'That these individuals can group together passively due to their fluid interactions alone, and that this results in large-scale events and effects they can't achieve as independent particles, is relevant to many biological functions—like nutrient mixing and bacterial resistance to antibiotics in bacterial swarms and biofilms," Spagnolie says.

DAVID: In this instance bacteria appear to be mostly passive.

You would have thought that if individuals grouped together and thus achieved results they could not achieve as independent particles, it might be conceivable that they did so actively and intentionally. And the more often they do it, and the more successful they are, the more likely it might seem that they do it actively and intentionally.

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DAVID: I've listed above the few challenges bacteria have. Their library is small, and their constant division is fully automatic. For other responses as a food example: sense food which then causes a series of molecular reactions to move toward it, and then automatically engulf it, followed by automatic digestion.

dhw: Your 3.8-billion-year-old library with information and instructions for every undabbled future life form, econiche, lifestyle and natural wonder has suddenly undergone an amazing transformation. Those first single cells only had a library for bacteria and instructions only for the vast number of different conditions that future bacteria would have to cope with. So where was the library for the whole future of evolution? And even if bacteria had their own special library with their own limited number of special instructions, you still haven’t explained how they chose the right ones for each situation.

If God front-loaded evolutionary information, what I see is that bacteria had excess to their own small part. As for how bacteria operate, they have only a small group of stimuli and have automatic responses to each. This does not remove the God dabbling as necessary.

dhw: Sorry you couldn’t respond to the major point about your God’s itty-bitty steps. As regards my hypothesis, it is absolutely NOT a fact that cells operate automatically (although I have pointed out that they may do so once a system has been established, and will only change if conditions change). That is your opinion, which you admit has a 50/50 chance of being wrong, i.e. that their intelligent ways may be the product of autonomous intelligence. And how often do I have to repeat that my hypothesis is a hypothesis. If only we could find your God’s 3.8-billion-year-old library of instructions for the whole of life, your hypothesis might have some credence.

DAVID: You are right. Intelligent information/instructions and intelligent instructions as to how to interpret and use the instructions are all part of the ghost with all processes acting together like a giant symphony orchestra. All designed.

dhw: Now we have instructions on how to use instructions. I suppose that explains how bacteria use their mini-library. But hold on, how do they know which instructions they should look for when they look for instructions on how to use instructions? Somewhere amid this great tangle there has to be a decision. So maybe whenever bacteria find themselves in a tricky new situation, your God pops in and picks out the correct instructions on how to use his instructions? Oh, if only he’d given them the intelligence to work out their own solutions to each problem, he would have saved himself and us a lot of time and effort.

Since bacteria have simple stimuli, they have a simple set of prescribed responses. Bacterial lives are simple. What do you mean with 'tricky situations'. Bacteria live very simple lives. Tell me about a tricky event you imagine. I note you have avoided the main point I made about bacteria , the constant complex automatic cell division cell division. Lenski's E. coli are still E coli. Following exact instructions for their biggest job..

Under “are bacteria truly independent?”

QUOTE: The flows and orientations of the swimmers become coherent on a length scale much longer than any individual particle, resulting in huge flocks of organisms swimming in the same direction and, perhaps unintentionally, working together. (dhw’s bold)

Or perhaps intentionally.

QUOTE: "'That these individuals can group together passively due to their fluid interactions alone, and that this results in large-scale events and effects they can't achieve as independent particles, is relevant to many biological functions—like nutrient mixing and bacterial resistance to antibiotics in bacterial swarms and biofilms," Spagnolie says.

DAVID: In this instance bacteria appear to be mostly passive.

dhw: You would have thought that if individuals grouped together and thus achieved results they could not achieve as independent particles, it might be conceivable that they did so actively and intentionally. And the more often they do it, and the more successful they are, the more likely it might seem that they do it actively and intentionally.

Having quorum sensing allows them to flow with the group. Automatic.

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DAVID: If God front-loaded evolutionary information, what I see is that bacteria had excess to their own small part. As for how bacteria operate, they have only a small group of stimuli and have automatic responses to each. This does not remove the God dabbling as necessary.

For years now you have been telling us that your God provided the first unicellular forms of life with a computer programme for every single undabbled innovation etc. in the history of evolution. Now you are telling us that bacteria were only provided with a library for bacteria. So what happened to the library of instructions for every single undabbled innovation in the history of evolution from bacteria through to elephants, whales, humans and the duckbilled platypus? How did all the other instructions and instructions on how to use instructions bypass bacteria and their unicellular mates when they were the only forms of life on the planet? Your library theory is literally falling to pieces.

dhw: Now we have instructions on how to use instructions. I suppose that explains how bacteria use their mini-library. But hold on, how do they know which instructions they should look for when they look for instructions on how to use instructions? Somewhere amid this great tangle there has to be a decision. So maybe whenever bacteria find themselves in a tricky new situation, your God pops in and picks out the correct instructions on how to use his instructions? Oh, if only he’d given them the intelligence to work out their own solutions to each problem, he would have saved himself and us a lot of time and effort.

DAVID: Since bacteria have simple stimuli, they have a simple set of prescribed responses. Bacterial lives are simple. What do you mean with 'tricky situations'. Bacteria live very simple lives. Tell me about a tricky event you imagine. I note you have avoided the main point I made about bacteria , the constant complex automatic cell division cell division. Lenski's E. coli are still E coli. Following exact instructions for their biggest job.

I note you continue to avoid the question of how bacteria select God’s instructions on how to use his instructions – or do you really believe your God pops in to do a dabble every time they are in trouble?

Bacteria have been found in virtually every environment on earth. Each one demands special adaptation. And I am not “imagining” the health crisis that has arisen through the fact that they always find a solution to the tricky situations created by antibiotics. Millions of them die. God didn’t dabble to save them, or they didn’t receive the anti-antibiotic programme he is supposed to have installed 3.8 billion years ago. But eventually they come up with a solution. Yes, they remain themselves, and automatic cell division is an integral part of all life: once a system is successful, its accurate reproduction is essential to the survival of the system. And to anticipate your usual question, nobody knows how life, reproduction and the ability to adapt and to innovate (i.e. to restructure existing cell communities) first arose. One theory is that a universal mind we call God did the original engineering.

Under “are bacteria truly independent?”
DAVID: In this instance bacteria appear to be mostly passive.

dhw: You would have thought that if individuals grouped together and thus achieved results they could not achieve as independent particles, it might be conceivable that they did so actively and intentionally. And the more often they do it, and the more successful they are, the more likely it might seem that they do it actively and intentionally.

DAVID: Having quorum sensing allows them to flow with the group. Automatic.

Wikipedia definition: Quorum sensing is the ability to detect and to respond to cell population density by gene regulation. […] Many species of bacteria use quorum sensing to coordinate gene expression according to the density of their local population. In similar fashion, some social insects use quorum sensing to determine where to nest.

No mention of the word “automatic”. Bacteria USE quorum sensing to detect and respond, to coordinate and to determine.

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DAVID: If God front-loaded evolutionary information, what I see is that bacteria had excess to their own small part. As for how bacteria operate, they have only a small group of stimuli and have automatic responses to each. This does not remove the God dabbling as necessary.

dhw: For years now you have been telling us that your God provided the first unicellular forms of life with a computer programme for every single undabbled innovation etc. in the history of evolution. Now you are telling us that bacteria were only provided with a library for bacteria. ...Your library theory is literally falling to pieces.

Use your logic. My concept is that Bacteria are bacteria because their only genome access is the bacterial level of instructions. Different levels open up throughout evolution.

DAVID: You are right. Intelligent information/instructions and intelligent instructions as to how to interpret and use the instructions are all part of the ghost with all processes acting together like a giant symphony orchestra. All designed.

DAVID: Since bacteria have simple stimuli, they have a simple set of prescribed responses. Bacterial lives are simple. What do you mean with 'tricky situations'. Bacteria live very simple lives. Tell me about a tricky event you imagine. I note you have avoided the main point I made about bacteria , the constant complex automatic cell division cell division. Lenski's E. coli are still E coli. Following exact instructions for their biggest job.

dhw: I note you continue to avoid the question of how bacteria select God’s instructions on how to use his instructions – or do you really believe your God pops in to do a dabble every time they are in trouble?

Dabbling is always a possibility, but bacteria can only access what is meant for them to use.

dhw: Bacteria have been found in virtually every environment on earth. Each one demands special adaptation. And I am not “imagining” the health crisis that has arisen through the fact that they always find a solution to the tricky situations created by antibiotics. Millions of them die. God didn’t dabble to save them, or they didn’t receive the anti-antibiotic programme he is supposed to have installed 3.8 billion years ago. But eventually they come up with a solution. Yes, they remain themselves, and automatic cell division is an integral part of all life: once a system is successful, its accurate reproduction is essential to the survival of the system. And to anticipate your usual question, nobody knows how life, reproduction and the ability to adapt and to innovate (i.e. to restructure existing cell communities) first arose. One theory is that a universal mind we call God did the original engineering.

I agree.

Under “are bacteria truly independent?”
DAVID: In this instance bacteria appear to be mostly passive.

dhw: You would have thought that if individuals grouped together and thus achieved results they could not achieve as independent particles, it might be conceivable that they did so actively and intentionally. And the more often they do it, and the more successful they are, the more likely it might seem that they do it actively and intentionally.

DAVID: Having quorum sensing allows them to flow with the group. Automatic.

dhw: Wikipedia definition: Quorum sensing is the ability to detect and to respond to cell population density by gene regulation. […] Many species of bacteria use quorum sensing to coordinate gene expression according to the density of their local population. In similar fashion, some social insects use quorum sensing to determine where to nest.

No mention of the word “automatic”. Bacteria USE quorum sensing to detect and respond, to coordinate and to determine.

And I view it as automatic. Wikipedia is not authoritative, it is full of opinion You don 't know the background of that particular writer. Is he a Darwin follower?

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dhw: For years now you have been telling us that your God provided the first unicellular forms of life with a computer programme for every single undabbled innovation etc. in the history of evolution. Now you are telling us that bacteria were only provided with a library for bacteria. ...Your library theory is literally falling to pieces.

DAVID: Use your logic. My concept is that Bacteria are bacteria because their only genome access is the bacterial level of instructions. Different levels open up throughout evolution.

So the first living cells contained a library of programmes for every single undabbled life form etc. in the history of life, but although unicellular forms were the only life forms, they only contained the programmes pertinent to themselves. So how on earth did they manage to pass on the programmes for elephants, whales, humans and the duckbilled platypus?

dhw: I note you continue to avoid the question of how bacteria select God’s instructions on how to use his instructions – or do you really believe your God pops in to do a dabble every time they are in trouble?

DAVID: Dabbling is always a possibility, but bacteria can only access what is meant for them to use.

See above for the impossibility of bacteria passing on programmes they don’t have. You are therefore left with your God dabbling every single life form, lifestyle etc. subsequent to bacteria – and this indeed is what you frequently imply in your wonderful catalogue of Nature’s wonders, normally accompanied by the comment that these must be the product of design. You haven’t made that comment on the latest of these, but we can use it as an example:
QUOTE: Today, the transient anus may be unique to the warty comb jelly. Tamm is now looking at other species of comb jelly, but so far they appear to have permanent anuses."

DAVID: The bush of life has some strange twigs.

It certainly does. May I ask if you think the disappearing anus was programmed 3.8 billion years ago or was the result of a divine dabble, in order to keep life going for 3.5+ billion years until your God could design the only thing he wanted to design: the brain of H. sapiens? Or could this strange twig have been uniquely designed by the cell communities of the warty comb jelly?

dhw: Bacteria have been found in virtually every environment on earth. Each one demands special adaptation. And I am not “imagining” the health crisis that has arisen through the fact that they always find a solution to the tricky situations created by antibiotics. Millions of them die. God didn’t dabble to save them, or they didn’t receive the anti-antibiotic programme he is supposed to have installed 3.8 billion years ago. But eventually they come up with a solution. Yes, they remain themselves, and automatic cell division is an integral part of all life: once a system is successful, its accurate reproduction is essential to the survival of the system. And to anticipate your usual question, nobody knows how life, reproduction and the ability to adapt and to innovate (i.e. to restructure existing cell communities) first arose. One theory is that a universal mind we call God did the original engineering.

DAVID: I agree.

Then please stop harping on about simple lives, Lenski’s E-coli and cell division, as if somehow they prove that bacteria cannot be intelligent.

DAVID: Having quorum sensing allows them to flow with the group. Automatic.

dhw: Wikipedia definition: Quorum sensing is the ability to detect and to respond to cell population density by gene regulation. […] Many species of bacteria use quorum sensing to coordinate gene expression according to the density of their local population. In similar fashion, some social insects use quorum sensing to determine where to nest.
No mention of the word “automatic”. Bacteria USE quorum sensing to detect and respond, to coordinate and to determine.

DAVID: And I view it as automatic. Wikipedia is not authoritative, it is full of opinion You don 't know the background of that particular writer. Is he a Darwin follower?

What on earth does this have to do with Darwin? I don’t recall Darwin ever promoting the idea that bacteria are intelligent organisms which use quorum sensing to cooperate in making decisions. You are the one who insists that their decision-making is automatic, and for some reason you brought up quorum sensing to try and discredit the proposal that the more successful bacterial cooperation is, the more likely it is to be active and intentional.

Under “confirmation bias”:
DAVID: The worst cases are in the sociology and psychology sciences where much research cannot be confirmed. But this clearly points out skepticism is needed when reading any article with Darwin-inculcated authors.

Nobody knows the objective truth about any of the major issues we keep discussing. Therefore scepticism is needed when reading any article written by authors with fixed beliefs of whatever kind.

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dhw: For years now you have been telling us that your God provided the first unicellular forms of life with a computer programme for every single undabbled innovation etc. in the history of evolution. Now you are telling us that bacteria were only provided with a library for bacteria. ...Your library theory is literally falling to pieces.

DAVID: Use your logic. My concept is that Bacteria are bacteria because their only genome access is the bacterial level of instructions. Different levels open up throughout evolution.

dhw: So the first living cells contained a library of programmes for every single undabbled life form etc. in the history of life, but although unicellular forms were the only life forms, they only contained the programmes pertinent to themselves. So how on earth did they manage to pass on the programmes for elephants, whales, humans and the duckbilled platypus?

You do not understand what I wrote. Bacteria have a set of instructions they use, but they carry instructions for the future in a closed file (to use computer terms).

dhw:...this indeed is what you frequently imply in your wonderful catalogue of Nature’s wonders, normally accompanied by the comment that these must be the product of design. You haven’t made that comment on the latest of these, but we can use it as an example:

QUOTE: Today, the transient anus may be unique to the warty comb jelly. Tamm is now looking at other species of comb jelly, but so far they appear to have permanent anuses."

DAVID: The bush of life has some strange twigs.

dhw: It certainly does. May I ask if you think the disappearing anus was programmed 3.8 billion years ago or was the result of a divine dabble, ...Or could this strange twig have been uniquely designed by the cell communities of the warty comb jelly?

How could I answer or know?

dhw: Bacteria have been found in virtually every environment on earth. Each one demands special adaptation. And I am not “imagining” the health crisis that has arisen through the fact that they always find a solution to the tricky situations created by antibiotics. Millions of them die. God didn’t dabble to save them, or they didn’t receive the anti-antibiotic programme he is supposed to have installed 3.8 billion years ago. But eventually they come up with a solution. Yes, they remain themselves, and automatic cell division is an integral part of all life: once a system is successful, its accurate reproduction is essential to the survival of the system. And to anticipate your usual question, nobody knows how life, reproduction and the ability to adapt and to innovate (i.e. to restructure existing cell communities) first arose. One theory is that a universal mind we call God did the original engineering.

DAVID: I agree.

dhw: Then please stop harping on about simple lives, Lenski’s E-coli and cell division, as if somehow they prove that bacteria cannot be intelligent.

Lenski's E. coli, after 22,000 generations are still E. coli with minor metabolic changes.

dhw: Wikipedia definition: Quorum sensing is the ability to detect and to respond to cell population density by gene regulation. […] Many species of bacteria use quorum sensing to coordinate gene expression according to the density of their local population. In similar fashion, some social insects use quorum sensing to determine where to nest.
No mention of the word “automatic”. Bacteria USE quorum sensing to detect and respond, to coordinate and to determine.

DAVID: And I view it as automatic. Wikipedia is not authoritative, it is full of opinion You don 't know the background of that particular writer. Is he a Darwin follower?

dhw: What on earth does this have to do with Darwin? I don’t recall Darwin ever promoting the idea that bacteria are intelligent organisms which use quorum sensing to cooperate in making decisions. You are the one who insists that their decision-making is automatic, and for some reason you brought up quorum sensing to try and discredit the proposal that the more successful bacterial cooperation is, the more likely it is to be active and intentional.

I'm referencing conclusion bias. Is automatic quorum sensing automatic (/) is my point.

dhw: Under “confirmation bias”:

DAVID: The worst cases are in the sociology and psychology sciences where much research cannot be confirmed. But this clearly points out skepticism is needed when reading any article with Darwin-inculcated authors.

dhw: Nobody knows the objective truth about any of the major issues we keep discussing. Therefore scepticism is needed when reading any article written by authors with fixed beliefs of whatever kind.

Exactly my point.

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DAVID: My concept is that Bacteria are bacteria because their only genome access is the bacterial level of instructions. Different levels open up throughout evolution.

dhw: So the first living cells contained a library of programmes for every single undabbled life form etc. in the history of life, but although unicellular forms were the only life forms, they only contained the programmes pertinent to themselves. So how on earth did they manage to pass on the programmes for elephants, whales, humans and the duckbilled platypus?

DAVID: You do not understand what I wrote. Bacteria have a set of instructions they use, but they carry instructions for the future in a closed file (to use computer terms).

I understand. Once again: until now your theory has been that your God provided the first living cells with a library of programmes for the whole of undabbled evolution. How could this library have been passed on if the only living creatures had a library restricted to instructions for themselves?

QUOTE: Today, the transient anus may be unique to the warty comb jelly. Tamm is now looking at other species of comb jelly, but so far they appear to have permanent anuses."

DAVID: The bush of life has some strange twigs.

dhw: It certainly does. May I ask if you think the disappearing anus was programmed 3.8 billion years ago or was the result of a divine dabble, ...Or could this strange twig have been uniquely designed by the cell communities of the warty comb jelly?

DAVID: How could I answer or know?

But over and over again you have claimed that whale flippers, cuttlefish camouflage, monarch migration, and weaverbirds’ nests were specially designed (dabbled) or preprogrammed by your God. You deny the possibility that they could have been designed by the cell communities of the organisms themselves. How do you know?

DAVID: I agree.

dhw: Then please stop harping on about simple lives, Lenski’s E-coli and cell division, as if somehow they prove that bacteria cannot be intelligent.

DAVID: Lenski's E. coli, after 22,000 generations are still E. coli with minor metabolic changes.

A complete non sequitur. How does this prove they can’t be intelligent?

DAVID: And I view it as automatic. Wikipedia is not authoritative, it is full of opinion You don 't know the background of that particular writer. Is he a Darwin follower?

dhw: What on earth does this have to do with Darwin? I don’t recall Darwin ever promoting the idea that bacteria are intelligent organisms which use quorum sensing to cooperate in making decisions. You are the one who insists that their decision-making is automatic, and for some reason you brought up quorum sensing to try and discredit the proposal that the more successful bacterial cooperation is, the more likely it is to be active and intentional.

DAVID: I'm referencing conclusion bias. Is automatic quorum sensing automatic (/) is my point.

I’m also referencing conclusion bias, namely yours. All forms of sensing are automatic. We and our fellow animals use our automatic senses to gather information and then we make decisions. What does this have to do with Darwin, and how does it support your conclusion that bacteria are not intelligent?

dhw: Nobody knows the objective truth about any of the major issues we keep discussing. Therefore scepticism is needed when reading any article written by authors with fixed beliefs of whatever kind.

DAVID: Exactly my point.

Your point points at Darwin-inculcated authors but glaringly omits ID and religion-inculcated authors.

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DAVID: You do not understand what I wrote. Bacteria have a set of instructions they use, but they carry instructions for the future in a closed file (to use computer terms).

dhw: I understand. Once again: until now your theory has been that your God provided the first living cells with a library of programmes for the whole of undabbled evolution. How could this library have been passed on if the only living creatures had a library restricted to instructions for themselves?

Many possibilities. In computer terms: zipped files which could be opened by automatic triggers at certain point in time, opened by God, or opened when certain changes occurred in Earth's climate. This would cover Behe's theory about devolution of the genome, which uncovers one new layer at a time.

dhw: But over and over again you have claimed that whale flippers, cuttlefish camouflage, monarch migration, and weaverbirds’ nests were specially designed (dabbled) or preprogrammed by your God. You deny the possibility that they could have been designed by the cell communities of the organisms themselves. How do you know?

You know my approach. Cells don't have enough mindful ability to design advances.

dhw: Then please stop harping on about simple lives, Lenski’s E-coli and cell division, as if somehow they prove that bacteria cannot be intelligent.

DAVID: Lenski's E. coli, after 22,000 generations are still E. coli with minor metabolic changes.

dhw: A complete non sequitur. How does this prove they can’t be intelligent?

We are stuck at this point. What I am reading in Behe shows automaticity. As research proceeds, more and more automaticity is described.

DAVID: I'm referencing conclusion bias. Is automatic quorum sensing automatic (/) is my point.

dhw: I’m also referencing conclusion bias, namely yours. All forms of sensing are automatic. We and our fellow animals use our automatic senses to gather information and then we make decisions. What does this have to do with Darwin, and how does it support your conclusion that bacteria are not intelligent?

Because research into the actions of bacteria currently constantly finds automaticity as the research advances. I expect more advances will reach the point that all bacteria are shown to be automatic. We will have to wait to see which of us is correct.

Under “confirmation bias”:
DAVID: The worst cases are in the sociology and psychology sciences where much research cannot be confirmed. But this clearly points out skepticism is needed when reading any article with Darwin-inculcated authors.

dhw: Nobody knows the objective truth about any of the major issues we keep discussing. Therefore scepticism is needed when reading any article written by authors with fixed beliefs of whatever kind.

DAVID: Exactly my point.

dhw: Your point points at Darwin-inculcated authors but glaringly omits ID and religion-inculcated authors.

Yes, that is the side I am representing

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dhw: …until now your theory has been that your God provided the first living cells with a library of programmes for the whole of undabbled evolution. How could this library have been passed on if the only living creatures had a library restricted to instructions for themselves?

DAVID: Many possibilities. In computer terms: zipped files which could be opened by automatic triggers at certain point in time, opened by God, or opened when certain changes occurred in Earth's climate. This would cover Behe's theory about devolution of the genome, which uncovers one new layer at a time.

Forget about computer terms. Since you believe in common descent, your God’s programmes have to be passed on from life forms to life forms. You (and apparently Behe too) claim that every life form was preprogrammed from the beginning, and yet you claim that bacteria only had a programme for bacteria. So how did they pass on the programmes for whales and their flippers, cuttlefish and their camouflage, monarchs and their migration, and weaverbirds and their nests?

DAVID: You know my approach. Cells don't have enough mindful ability to design advances.

You say you don’t and can’t know whether the vanishing anus was divinely preprogrammed or dabbled, or designed by the warty comb jelly itself, but you apparently know that its cell communities couldn’t have done it. Ditto the other examples.

DAVID: Lenski's E. coli, after 22,000 generations are still E. coli with minor metabolic changes.

dhw: How does this prove they can’t be intelligent?

DAVID: We are stuck at this point. What I am reading in Behe shows automaticity. As research proceeds, more and more automaticity is described.

And yet we have just been discussing two articles which tell us that more and more scientists believe cells are intelligent and create instructions on the hoof, de novo. Could your view be the result of confirmation/conclusion bias?

DAVID( Under “confirmation bias”): […] this clearly points out skepticism is needed when reading any article with Darwin-inculcated authors.

DAVID: Exactly my point.

dhw: Your point points at Darwin-inculcated authors but glaringly omits ID and religion-inculcated authors.

DAVID: Yes, that is the side I am representing.

So do you or do you not agree that scepticism is also needed when reading an article by ID and religion-inculcated authors?

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dhw: …until now your theory has been that your God provided the first living cells with a library of programmes for the whole of undabbled evolution. How could this library have been passed on if the only living creatures had a library restricted to instructions for themselves?

DAVID: Many possibilities. In computer terms: zipped files which could be opened by automatic triggers at certain point in time, opened by God, or opened when certain changes occurred in Earth's climate. This would cover Behe's theory about devolution of the genome, which uncovers one new layer at a time.

dhw: Forget about computer terms. Since you believe in common descent, your God’s programmes have to be passed on from life forms to life forms. You (and apparently Behe too) claim that every life form was preprogrammed from the beginning, and yet you claim that bacteria only had a programme for bacteria. So how did they pass on the programmes for whales and their flippers, cuttlefish and their camouflage, monarchs and their migration, and weaverbirds and their nests?

Bacteria carry their program and ones for the future they cannot use for themselves but is passed on to allow multicellular forms to arrive.

DAVID: Lenski's E. coli, after 22,000 generations are still E. coli with minor metabolic changes.

dhw: How does this prove they can’t be intelligent?

DAVID: We are stuck at this point. What I am reading in Behe shows automaticity. As research proceeds, more and more automaticity is described.

dhw: And yet we have just been discussing two articles which tell us that more and more scientists believe cells are intelligent and create instructions on the hoof, de novo. Could your view be the result of confirmation/conclusion bias?

What 'more and more' scientists. You keep quoting your tiny list.

DAVID( Under “confirmation bias”): […] this clearly points out skepticism is needed when reading any article with Darwin-inculcated authors.

dhw: Nobody knows the objective truth about any of the major issues we keep discussing. Therefore scepticism is needed when reading any article written by authors with fixed beliefs of whatever kind.

DAVID: Exactly my point.

dhw: Your point points at Darwin-inculcated authors but glaringly omits ID and religion-inculcated authors.

DAVID: Yes, that is the side I am representing.

dhw: So do you or do you not agree that scepticism is also needed when reading an article by ID and religion-inculcated authors?

I certainly agree that all articles must be read with an open mind. Some of the ID stuff I do not accept.

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dhw: Since you believe in common descent, your God’s programmes have to be passed on from life forms to life forms. You (and apparently Behe too) claim that every life form was preprogrammed from the beginning, and yet you claim that bacteria only had a programme for bacteria. So how did they pass on the programmes for whales and their flippers, cuttlefish and their camouflage, monarchs and their migration, and weaverbirds and their nests?

DAVID: Bacteria carry their program and ones for the future they cannot use for themselves but is passed on to allow multicellular forms to arrive.

Thank you. So now we have the first bacteria carrying programmes for every single life form, econiche, lifestyle and natural wonder in the history of life past, present and future, and somehow knowing which programme is for them alone. I wonder what happened next. Did they squiggle through history unknowingly passing the dinosaur programme and nothing but the dinosaur programme to pre-dinosaur cells, cuttlefish and camouflage programme to pre-cuttlefish cells, weaverbird and nest programme to pre-weaverbird cells, and hominin and pelvis programme to pre-hominin cells? Wouldn’t it be fascinating to discover what programmes they are still carrying for life in, say, a thousand million years’ time! Of course you think evolution is over, but hey, you never know. ;-)

DAVID: As research proceeds, more and more automaticity is described.

dhw: And yet we have just been discussing two articles which tell us that more and more scientists believe cells are intelligent and create instructions on the hoof, de novo. Could your view be the result of confirmation/conclusion bias?

DAVID: What 'more and more' scientists. You keep quoting your tiny list.

On Monday 25 February you gave us an extended version of the article with which you opened this thread. QUOTE (my bold): “So it has been dawning on us is that there is no prior plan or blueprint for development: Instructions are created on the hoof, far more intelligently than is possible from dumb DNA. That is why today’s molecular biologists are reporting “cognitive resources” in cells; “bio-information intelligence”; “cell intelligence”; “metabolic memory”; and “cell knowledge”—all terms appearing in recent literature. “Do cells think?” is the title of a 2007 paper in the journal Cellular and Molecular Life Sciences. On the other hand the assumed developmental “program” coded in a genotype has never been described.”

Sounds like more and more scientists to me.

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dhw: Since you believe in common descent, your God’s programmes have to be passed on from life forms to life forms. You (and apparently Behe too) claim that every life form was preprogrammed from the beginning, and yet you claim that bacteria only had a programme for bacteria. So how did they pass on the programmes for whales and their flippers, cuttlefish and their camouflage, monarchs and their migration, and weaverbirds and their nests?

DAVID: Bacteria carry their program and ones for the future they cannot use for themselves but is passed on to allow multicellular forms to arrive.

dhw: Thank you. So now we have the first bacteria carrying programmes for every single life form, econiche, lifestyle and natural wonder in the history of life past, present and future, and somehow knowing which programme is for them alone. I wonder what happened next. Did they squiggle through history unknowingly passing the dinosaur programme and nothing but the dinosaur programme to pre-dinosaur cells, cuttlefish and camouflage programme to pre-cuttlefish cells, weaverbird and nest programme to pre-weaverbird cells, and hominin and pelvis programme to pre-hominin cells? Wouldn’t it be fascinating to discover what programmes they are still carrying for life in, say, a thousand million years’ time! Of course you think evolution is over, but hey, you never know.

Great response, very funny at that! It is either that or dabbling. It can't itty -bitty Darwin steps. They don't exist. Mind the gaps! They need a designer. And for both of us, you are right. There is a future in research: more and more complexity of controls and designs that naturalism cannot ever explain.

DAVID: As research proceeds, more and more automaticity is described.

dhw: And yet we have just been discussing two articles which tell us that more and more scientists believe cells are intelligent and create instructions on the hoof, de novo. Could your view be the result of confirmation/conclusion bias?

DAVID: What 'more and more' scientists. You keep quoting your tiny list.

dhw: On Monday 25 February you gave us an extended version of the article with which you opened this thread. QUOTE (my bold): “So it has been dawning on us is that there is no prior plan or blueprint for development: Instructions are created on the hoof, far more intelligently than is possible from dumb DNA. That is why today’s molecular biologists are reporting “cognitive resources” in cells; “bio-information intelligence”; “cell intelligence”; “metabolic memory”; and “cell knowledge”—all terms appearing in recent literature. “Do cells think?” is the title of a 2007 paper in the journal Cellular and Molecular Life Sciences. On the other hand the assumed developmental “program” coded in a genotype has never been described.”

dhw: Sounds like more and more scientists to me.

90% of scientists are atheists. What interpretation did you expect? Remember the chances are still either/or.

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DAVID: Bacteria carry their program and ones for the future they cannot use for themselves but is passed on to allow multicellular forms to arrive.

dhw: Thank you. So now we have the first bacteria carrying programmes for every single life form, econiche, lifestyle and natural wonder in the history of life past, present and future, and somehow knowing which programme is for them alone. I wonder what happened next. Did they squiggle through history unknowingly passing the dinosaur programme and nothing but the dinosaur programme to pre-dinosaur cells, cuttlefish and camouflage programme to pre-cuttlefish cells, weaverbird and nest programme to pre-weaverbird cells, and hominin and pelvis programme to pre-hominin cells? Wouldn’t it be fascinating to discover what programmes they are still carrying for life in, say, a thousand million years’ time! Of course you think evolution is over, but hey, you never know.

DAVID: Great response, very funny at that! It is either that or dabbling.

I’m glad you agree that your vision of bacteria unknowingly dishing out programmes to pre-dinosaurs, pre-cuttlefish, pre-weaverbirds and pre-hominins is so ridiculous as to be funny. So out goes your preprogramming hypothesis. But I disagree that this leaves nothing but dabbling, i.e. your in-full-control God separately designing every life form, econiche, lifestyle and natural wonder in the history of life, although apparently he actually wanted to design just one life form. (I find that pretty funny too.) A theistic alternative is your God specially designing a mechanism whereby cells and cell communities use the intelligence he has given them to do their own designing.

DAVID: It can't itty -bitty Darwin steps. They don't exist. Mind the gaps! They need a designer.

Itty-bitty steps are not an alternative to preprogramming and dabbling, so please don’t change the subject. And besides, you never responded when I pointed out to you that your accounts of big toe design, pelvis design, and mini-to maxi brain design constitute itty-bitty steps on the way to H. sapiens. In my hypothesis, the cells/cell communities are the designers – and one can present a very logical case that the complexities of such designers are too great to have arisen by chance, and so they in turn "need a designer”. The issue here is not the existence of God but the mechanics of evolution.

DAVID: And for both of us, you are right. There is a future in research: more and more complexity of controls and designs that naturalism cannot ever explain.

So you have no reason whatsoever to assume that future research will reveal that only large organisms are intelligent, and small organisms are automatons.

DAVID: As research proceeds, more and more automaticity is described.

DAVID: What 'more and more' scientists. You keep quoting your tiny list.

dhw: On Monday 25 February you gave us an extended version of the article with which you opened this thread. QUOTE (my bold): “So it has been dawning on us is that there is no prior plan or blueprint for development: Instructions are created on the hoof, far more intelligently than is possible from dumb DNA. That is why today’s molecular biologists are reporting “cognitive resources” in cells; “bio-information intelligence”; “cell intelligence”; “metabolic memory”; and “cell knowledge”—all terms appearing in recent literature. “Do cells think?” is the title of a 2007 paper in the journal Cellular and Molecular Life Sciences. On the other hand the assumed developmental “program” coded in a genotype has never been described.”

dhw: Sounds like more and more scientists to me.

DAVID: 90% of scientists are atheists. What interpretation did you expect? Remember the chances are still either/or.

You asked me what “more and more” scientists, and I have told you! So now you do a complete volte face and tell us that 90% of scientists reject your automaticity but let’s not listen to them because they are atheists! In any case, just like the theory of evolution, the proposal that cells/cell communities are intelligent does not in any way exclude your God, since nobody knows the origin of life or of the mechanisms that have led to evolution.

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DAVID: Bacteria carry their program and ones for the future they cannot use for themselves but is passed on to allow multicellular forms to arrive.

dhw: Thank you. So now we have the first bacteria carrying programmes for every single life form, econiche, lifestyle and natural wonder in the history of life past, present and future, and somehow knowing which programme is for them alone. I wonder what happened next. Did they squiggle through history unknowingly passing the dinosaur programme and nothing but the dinosaur programme to pre-dinosaur cells, cuttlefish and camouflage programme to pre-cuttlefish cells, weaverbird and nest programme to pre-weaverbird cells, and hominin and pelvis programme to pre-hominin cells? Wouldn’t it be fascinating to discover what programmes they are still carrying for life in, say, a thousand million years’ time! Of course you think evolution is over, but hey, you never know.

DAVID: Great response, very funny at that! It is either that or dabbling.

dhw: I’m glad you agree that your vision of bacteria unknowingly dishing out programmes to pre-dinosaurs, pre-cuttlefish, pre-weaverbirds and pre-hominins is so ridiculous as to be funny. So out goes your preprogramming hypothesis. But I disagree that this leaves nothing but dabbling, i.e. your in-full-control God separately designing every life form, econiche, lifestyle and natural wonder in the history of life, although apparently he actually wanted to design just one life form. (I find that pretty funny too.) A theistic alternative is your God specially designing a mechanism whereby cells and cell communities use the intelligence he has given them to do their own designing.

I did not throw out pre-programming as a reasonable theory. Twisted over-interpreting as usual. Dabbling is the other alternative if God creates species as I believe.

DAVID: It can't itty -bitty Darwin steps. They don't exist. Mind the gaps! They need a designer.

Itty-bitty steps are not an alternative to preprogramming and dabbling, so please don’t change the subject. And besides, you never responded when I pointed out to you that your accounts of big toe design, pelvis design, and mini-to maxi brain design constitute itty-bitty steps on the way to H. sapiens. In my hypothesis, the cells/cell communities are the designers – and one can present a very logical case that the complexities of such designers are too great to have arisen by chance, and so they in turn "need a designer”. The issue here is not the existence of God but the mechanics of evolution.

Redesigning an ape pelvis to a human pelvis is not itty-bitty, considering the birthing issues that also arise. Chimp brain (400 cc) to human (1,200 cc) in 200 cc jumps is anything but itty-bitty. You present a very skewed view of evolutionary biological changes, just to sneak in your cell committees.

dhw: Sounds like more and more scientists to me.

DAVID: 90% of scientists are atheists. What interpretation did you expect? Remember the chances are still either/or.

dhw: You asked me what “more and more” scientists, and I have told you! So now you do a complete volte face and tell us that 90% of scientists reject your automaticity but let’s not listen to them because they are atheists! In any case, just like the theory of evolution, the proposal that cells/cell communities are intelligent does not in any way exclude your God, since nobody knows the origin of life or of the mechanisms that have led to evolution.

I agree we don't know how life started or speciation occurs. At least we have gotten rid of Darwin's gradualism. And we understand that natural selection can only act on forms it is given. Since there are the unknowns you listed, interpretations have to be open to reinterpretations, the background of atheist, agnostic, and theistic thinkers considered, when reading anything each group produces. You are sitting atop your picket fence with atheists on one side and us theists on the other. Not that the metaphor implies you are in a higher (better) position, only that your feet aren't planted or grounded in anything but disbelief. I'll reinterpret as I wish.

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DAVID: Bacteria carry their program and ones for the future they cannot use for themselves but is passed on to allow multicellular forms to arrive.

dhw: So now we have the first bacteria carrying programmes for every single life form, econiche, lifestyle and natural wonder in the history of life past, present and future, and somehow knowing which programme is for them alone. I wonder what happened next. Did they squiggle through history unknowingly passing the dinosaur programme and nothing but the dinosaur programme to pre-dinosaur cells, cuttlefish and camouflage programme to pre-cuttlefish cells [etc.]

DAVID: Great response, very funny at that! It is either that or dabbling.

dhw: I’m glad you agree that your vision of bacteria unknowingly dishing out programmes to pre-dinosaurs, pre-cuttlefish, pre-weaverbirds and pre-hominins is so ridiculous as to be funny. So out goes your preprogramming hypothesis. […]

DAVID: I did not throw out pre-programming as a reasonable theory. Twisted over-interpreting as usual. Dabbling is the other alternative if God creates species as I believe.

I described how your bacteria apparently distribute programmes for the whole of evolution, and you found it very funny. If my description was inaccurate, please tell us how else they could have done it.

DAVID: It can't itty -bitty Darwin steps. They don't exist. Mind the gaps! They need a designer.

dhw: Itty-bitty steps are not an alternative to preprogramming and dabbling, so please don’t change the subject. And besides, you never responded when I pointed out to you that your accounts of big toe design, pelvis design, and mini-to maxi brain design constitute itty-bitty steps on the way to H. sapiens. In my hypothesis, the cells/cell communities are the alternative] designers […]

DAVID: Redesigning an ape pelvis to a human pelvis is not itty-bitty, considering the birthing issues that also arise. Chimp brain (400 cc) to human (1,200 cc) in 200 cc jumps is anything but itty-bitty. You present a very skewed view of evolutionary biological changes, just to sneak in your cell committees.

If, over millions of years, your God specially designed big toes, pelvises, mini brains and maxi brains and all the other bits and pieces that distinguish H. sapiens from pre-hominins, you have a stage by stage or itty-bitty design of H. sapiens. But that is a digression from the main subject - your very funny concept of preprogramming and your belief that preprogramming and dabbling are the only possibilities. Itty-bitty steps are not an alternative, but cellular intelligence is.

DAVID: 90% of scientists are atheists. What interpretation did you expect? Remember the chances are still either/or.

dhw: You asked me what “more and more” scientists, and I have told you! So now you do a complete volte face and tell us that 90% of scientists reject your automaticity but let’s not listen to them because they are atheists! In any case, just like the theory of evolution, the proposal that cells/cell communities are intelligent does not in any way exclude your God, since nobody knows the origin of life or of the mechanisms that have led to evolution.

DAVID: I agree we don't know how life started or speciation occurs. At least we have gotten rid of Darwin's gradualism. And we understand that natural selection can only act on forms it is given. Since there are the unknowns you listed, interpretations have to be open to reinterpretations, the background of atheist, agnostic, and theistic thinkers considered, when reading anything each group produces. You are sitting atop your picket fence with atheists on one side and us theists on the other. Not that the metaphor implies you are in a higher (better) position, only that your feet aren't planted or grounded in anything but disbelief. I'll reinterpret as I wish.

One digression after another. I wrote that more and more scientists accept the concept of cellular intelligence, and you asked: “What ‘more and more scientists’? You keep quoting your tiny list.” It is not a tiny list, so you decided to dismiss the findings of 90% of scientists because they are atheists. I accept what you have written above, and by all means reinterpret as you wish, but please don’t expect me to accept your reinterpretations as if they emanated from “a higher (better) position”. Do you accept that more and more scientists now favour the concept of cellular intelligence?

DAVID (under “Biological complexity”): There is lots of cross talk and communication between all parts of the cells:
https://www.nature.com/articles/d41586-019-00792-9?utm_source=Nature+Briefing&utm_c...

DAVID: All of this is automatic activity as the cell produces its products. A complex going factory. Huge article, hard to compress.

Thank you for giving us the gist- much appreciated. I keep pointing out that most cellular activity has to be automatic if a particular system is to survive intact, and intelligence will only be applied (a) when the system first comes into existence, and (b) when there are new conditions, e.g. new problems to be solved or new opportunities to be exploited. In my hypothesis, that is when cross talk and communication – essential elements of intelligent cooperation – precede intelligent decision-making, which in turn produces more automatic activity as new instructions are implemented.

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DAVID: I did not throw out pre-programming as a reasonable theory. Twisted over-interpreting as usual. Dabbling is the other alternative if God creates species as I believe.

dhw: I described how your bacteria apparently distribute programmes for the whole of evolution, and you found it very funny. If my description was inaccurate, please tell us how else they could have done it.

Bacteria don't do anything with future use of the genome. They only have access to what they are programmed to use. Whenever advances in speciation occur, it is due to activation of a portion of the genome for that advance.

DAVID: Redesigning an ape pelvis to a human pelvis is not itty-bitty, considering the birthing issues that also arise. Chimp brain (400 cc) to human (1,200 cc) in 200 cc jumps is anything but itty-bitty. You present a very skewed view of evolutionary biological changes, just to sneak in your cell committees.

dhw: If, over millions of years, your God specially designed big toes, pelvises, mini brains and maxi brains and all the other bits and pieces that distinguish H. sapiens from pre-hominins, you have a stage by stage or itty-bitty design of H. sapiens.

Yes, God deigns parts, but then H. habilis jumps to H. erectus with all those parts which have now been designed for change in place. You have tried to introduce itty-bitty where it dos not exist. You know full well all major speciation introduces gaps!

DAVID: 90% of scientists are atheists. What interpretation did you expect? Remember the chances are still either/or.

dhw: You asked me what “more and more” scientists, and I have told you! So now you do a complete volte face and tell us that 90% of scientists reject your automaticity but let’s not listen to them because they are atheists!

I will interpret sources as I evaluate their biases! Still 50/50.

dhw: One digression after another. I wrote that more and more scientists accept the concept of cellular intelligence, and you asked: “What ‘more and more scientists’? You keep quoting your tiny list.” ....Do you accept that more and more scientists now favour the concept of cellular intelligence?

The final description of a scientific theory requires a paradigm shift due to enough convincing discoveries (Kuhn) and we are obviously not at that point in the known facts. It is still 50/50 although a majority try to say that cells show intelligence in their activities. Yes, they do, but it can be automatic from intelligent instruction/information.

DAVID (under “Biological complexity”): There is lots of cross talk and communication between all parts of the cells:
https://www.nature.com/articles/d41586-019-00792-9?utm_source=Nature+Briefing&utm_c...

DAVID: All of this is automatic activity as the cell produces its products. A complex going factory. Huge article, hard to compress.

dhw: Thank you for giving us the gist- much appreciated. I keep pointing out that most cellular activity has to be automatic if a particular system is to survive intact, and intelligence will only be applied (a) when the system first comes into existence, and (b) when there are new conditions, e.g. new problems to be solved or new opportunities to be exploited. In my hypothesis, that is when cross talk and communication – essential elements of intelligent cooperation – precede intelligent decision-making, which in turn produces more automatic activity as new instructions are implemented.

As you state: intelligence will only be applied (a) when the system first comes into existence, and (b) when there are new conditions, e.g. new problems to be solved or new opportunities to be exploited. And what I can see is that you are describing the exact need for design and a designer. Our only experiences always show is that such complex systems require design and a designer.

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DAVID: I did not throw out pre-programming as a reasonable theory. […]

dhw: I described how your bacteria apparently distribute programmes for the whole of evolution, and you found it very funny. If my description was inaccurate, please tell us how else they could have done it.

DAVID: Bacteria don't do anything with future use of the genome. They only have access to what they are programmed to use. Whenever advances in speciation occur, it is due to activation of a portion of the genome for that advance.

You still haven’t told us how bacteria could have passed on billions of programmes for evolution if they only had access to their own. And I keep repeating that my hypothesis has nothing to do with FUTURE use of the genome but proposes that speciation is the result of responses to new conditions.

dhw: If, over millions of years, your God specially designed big toes, pelvises, mini brains and maxi brains and all the other bits and pieces that distinguish H. sapiens from pre-hominins, you have a stage by stage or itty-bitty design of H. sapiens.

DAVID: Yes, God designs parts, but then H. habilis jumps to H. erectus with all those parts which have now been designed for change in place. You have tried to introduce itty-bitty where it does not exist. You know full well all major speciation introduces gaps!

Of course there are gaps. But if your always-in-control God’s one and only purpose was to design the brain of Homo sapiens, and he designed a succession of mini and less mini brains before designing the maxi brain, that is itty-bitty design. Ditto all the other bits and pieces passed on from hominins to humans to H. sapiens.

DAVID: 90% of scientists are atheists. What interpretation did you expect? Remember the chances are still either/or.

DAVID: I will interpret sources as I evaluate their biases! Still 50/50.

Fine. But please stop telling me that there is only a “tiny list” of scientists who support the concept of cellular intelligence.

DAVID: The final description of a scientific theory requires a paradigm shift due to enough convincing discoveries (Kuhn) and we are obviously not at that point in the known facts. It is still 50/50 although a majority try to say that cells show intelligence in their activities. Yes, they do, but it can be automatic from intelligent instruction/information.

So when you told me I was quoting a “tiny list” of scientists, you actually meant the majority of scientists, and it is your scientists who constitute the tiny list. But I’m happy with your odds of 50/50. I’m just unhappy with your claim that science supports you.

DAVID (under “Biological complexity”): There is lots of cross talk and communication between all parts of the cells:
https://www.nature.com/articles/d41586-019-00792-9?utm_source=Nature+Briefing&utm_c...

DAVID: All of this is automatic activity as the cell produces its products. A complex going factory. Huge article, hard to compress.

dhw: […] I keep pointing out that most cellular activity has to be automatic if a particular system is to survive intact, and intelligence will only be applied (a) when the system first comes into existence, and (b) when there are new conditions, e.g. new problems to be solved or new opportunities to be exploited. In my hypothesis, that is when cross talk and communication – essential elements of intelligent cooperation – precede intelligent decision-making, which in turn produces more automatic activity as new instructions are implemented. [David’s bold]

DAVID: […] And what I can see is that you are describing the exact need for design and a designer. Our only experiences always show is that such complex systems require design and a designer.

And my proposal is that cell communities are the designers who design the design. But the cell communities themselves may have been designed by your God.

Under “Magic embryology”
QUOTES: That mounting evidence is leading some biologists to a bold hypothesis: that where information is concerned, cells might often find solutions to life’s challenges that are not just good but optimal — that cells extract as much useful information from their complex surroundings as is theoretically possible.

"How the cells do it remains a mystery. Right now, “the whole thing is kind of wonderful and magical…”

DAVID: Note the important use of information which is guiding the making of an embryo. A blueprint exists in an orchestrated mass of stimuli. As in a symphony, it has to written by a composer.

As you rightly say, it is USE of information that guides the process. Cells extract information and then USE it to find solutions to life’s challenges. How they do it is a mystery. You propose a 3.8-billion-year-old “blueprint” for every undabbled solution and new development throughout life’s history, though you have not yet explained how every single blueprint could have been passed on by bacteria who only had access to their own. Well, maybe...just maybe...the magic stems from a possibly God-designed mechanism known as cellular intelligence.

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DAVID: Bacteria don't do anything with future use of the genome. They only have access to what they are programmed to use. Whenever advances in speciation occur, it is due to activation of a portion of the genome for that advance.

dhw: You still haven’t told us how bacteria could have passed on billions of programmes for evolution if they only had access to their own.

If there was pre-programming in DNA, bacteria carried all the DNA for the future, but only used chapter one. With each future speciation, the next chapter appeared either spontaneously activated or thru God stepping in.

DAVID: Yes, God designs parts, but then H. habilis jumps to H. erectus with all those parts which have now been designed for change in place. You have tried to introduce itty-bitty where it does not exist. You know full well all major speciation introduces gaps!

dhw: Of course there are gaps. But if your always-in-control God’s one and only purpose was to design the brain of Homo sapiens, and he designed a succession of mini and less mini brains before designing the maxi brain, that is itty-bitty design. Ditto all the other bits and pieces passed on from hominins to humans to H. sapiens.

Neat try to minimize gaps. Totally false. The jumps from Lucy phenotype to habilis phenotype were huge. And then there is the Cambrian gap, totally unexplained.

dhw: So when you told me I was quoting a “tiny list” of scientists, you actually meant the majority of scientists, and it is your scientists who constitute the tiny list. But I’m happy with your odds of 50/50. I’m just unhappy with your claim that science supports you.

I am allowed to interpret the scientific findings as I see them and the support my views.

DAVID (under “Biological complexity”): There is lots of cross talk and communication between all parts of the cells:

https://www.nature.com/articles/d41586-019-00792-9?utm_source=Nature+Briefing&utm_c...

DAVID: All of this is automatic activity as the cell produces its products. A complex going factory. Huge article, hard to compress.

dhw: […] I keep pointing out that most cellular activity has to be automatic if a particular system is to survive intact, and intelligence will only be applied (a) when the system first comes into existence, and (b) when there are new conditions, e.g. new problems to be solved or new opportunities to be exploited. In my hypothesis, that is when cross talk and communication – essential elements of intelligent cooperation – precede intelligent decision-making, which in turn produces more automatic activity as new instructions are implemented. [David’s bold]

DAVID: […] And what I can see is that you are describing the exact need for design and a designer. Our only experiences always show is that such complex systems require design and a designer.

dhw: And my proposal is that cell communities are the designers who design the design. But the cell communities themselves may have been designed by your God.

And I maintain automatic cells don't have the ability to design. There are only unproven theories about speciation. I accept God in control.

Under “Magic embryology”
QUOTES: That mounting evidence is leading some biologists to a bold hypothesis: that where information is concerned, cells might often find solutions to life’s challenges that are not just good but optimal — that cells extract as much useful information from their complex surroundings as is theoretically possible.

"How the cells do it remains a mystery. Right now, “the whole thing is kind of wonderful and magical…”

DAVID: Note the important use of information which is guiding the making of an embryo. A blueprint exists in an orchestrated mass of stimuli. As in a symphony, it has to written by a composer.

dhw: As you rightly say, it is USE of information that guides the process. Cells extract information and then USE it to find solutions to life’s challenges. How they do it is a mystery. You propose a 3.8-billion-year-old “blueprint” for every undabbled solution and new development throughout life’s history, though you have not yet explained how every single blueprint could have been passed on by bacteria who only had access to their own. Well, maybe...just maybe...the magic stems from a possibly God-designed mechanism known as cellular intelligence.

Explained above. God opens each new chapter in the use of DNA or it is programmed to open itself. Bacteria have no builtin responsibility to advance into the future. They are still bacteria.

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dhw: You still haven’t told us how bacteria could have passed on billions of programmes for evolution if they only had access to their own.

DAVID: If there was pre-programming in DNA, bacteria carried all the DNA for the future, but only used chapter one. With each future speciation, the next chapter appeared either spontaneously activated or thru God stepping in.

So although bacteria remained bacteria, and only used their own programme for future adaptation and problem solving, they contained and passed on programmes for every single life form, econiche, lifestyle and natural wonder in the history of life. And subsequent cell communities carried all these programmes, spontaneously switched on their own special programme, and then passed the other millions of programmes on to another cell community which spontaneously switched on its own special programme and so on. Or God stepped in and switched on the programme for whale flippers, cuttlefish camouflage, monarch migration, weaverbird’s nest etc., because they had to provide food until he could switch on the programme for the brain of H. sapiens. Don’t you find this just a little far-fetched?

dhw: Of course there are gaps. But if your always-in-control God’s one and only purpose was to design the brain of Homo sapiens, and he designed a succession of mini and less mini brains before designing the maxi brain, that is itty-bitty design. Ditto all the other bits and pieces passed on from hominins to humans to H. sapiens.

DAVID: Neat try to minimize gaps. Totally false. The jumps from Lucy phenotype to habilis phenotype were huge. And then there is the Cambrian gap, totally unexplained.

Your focus on gaps is a neat try to sidestep the issue of why a God in total control would specially design a succession of jumping brains in itty-bitty steps instead of specially designing the only brain he wanted to design. We have dealt with gaps and the Cambrian over and over again. Nobody knows the answer: you suggest divine preprogramming or dabbling; I suggest intelligent cells responding to the demands and opportunities arising from new conditions.

dhw: So when you told me I was quoting a “tiny list” of scientists, you actually meant the majority of scientists, and it is your scientists who constitute the tiny list. But I’m happy with your odds of 50/50. I’m just unhappy with your claim that science supports you.

DAVID: I am allowed to interpret the scientific findings as I see them and the support my views.

Of course. But the majority of scientists apparently disagree with you, so please don’t make out that “my” supporters only constitute a “tiny list”.

https://www.nature.com/articles/d41586-019-00792-9?utm_source=Nature+Briefing&utm_c...

DAVID: All of this is automatic activity as the cell produces its products. A complex going factory. Huge article, hard to compress.

DAVID: […] And what I can see is that you are describing the exact need for design and a designer. Our only experiences always show is that such complex systems require design and a designer.

dhw: And my proposal is that cell communities are the designers who design the design. But the cell communities themselves may have been designed by your God.

DAVID: And I maintain automatic cells don't have the ability to design. There are only unproven theories about speciation. I accept God in control.

As we keep agreeing, all theories about speciation are unproven. Both your theory and my proposal require design, and my proposal does not exclude the participation of your God. Meanwhile, I stand by the statements you bolded. Focusing on automatic behaviour is no response to the question of how that behaviour was first generated and of how cells solve problems and exploit new conditions.

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8871 views

DAVID: If there was pre-programming in DNA, bacteria carried all the DNA for the future, but only used chapter one. With each future speciation, the next chapter appeared either spontaneously activated or thru God stepping in.

dhw: So although bacteria remained bacteria, and only used their own programme for future adaptation and problem solving, they contained and passed on programmes for every single life form, econiche, lifestyle and natural wonder in the history of life. And subsequent cell communities carried all these programmes, spontaneously switched on their own special programme, and then passed the other millions of programmes on to another cell community which spontaneously switched on its own special programme and so on. Or God stepped in and switched on the programme for whale flippers, cuttlefish camouflage, monarch migration, weaverbird’s nest etc., because they had to provide food until he could switch on the programme for the brain of H. sapiens. Don’t you find this just a little far-fetched?

Not at all. Preprogramming has to work in just that way. Or there are also dabbling switches for God to activate.

dhw: Of course there are gaps. But if your always-in-control God’s one and only purpose was to design the brain of Homo sapiens, and he designed a succession of mini and less mini brains before designing the maxi brain, that is itty-bitty design. Ditto all the other bits and pieces passed on from hominins to humans to H. sapiens.

DAVID: Neat try to minimize gaps. Totally false. The jumps from Lucy phenotype to habilis phenotype were huge. And then there is the Cambrian gap, totally unexplained.

dhw: Your focus on gaps is a neat try to sidestep the issue of why a God in total control would specially design a succession of jumping brains in itty-bitty steps instead of specially designing the only brain he wanted to design. ... you suggest divine preprogramming or dabbling; I suggest intelligent cells responding to the demands and opportunities arising from new conditions.

I don't understand your definition of itty-bitty except it doesn't fit the 200 cc jumps in size of the hominin stages of brain development. My comment discussed whole phenotype changes, not just brains. You neatly ignored that.

DAVID: I am allowed to interpret the scientific findings as I see them and the support my views.

Of course. But the majority of scientists apparently disagree with you, so please don’t make out that “my” supporters only constitute a “tiny list”.

https://www.nature.com/articles/d41586-019-00792-9?utm_source=Nature+Briefing&utm_c...

DAVID: […] And what I can see is that you are describing the exact need for design and a designer. Our only experiences always show is that such complex systems require design and a designer.

dhw: And my proposal is that cell communities are the designers who design the design. But the cell communities themselves may have been designed by your God.

DAVID: And I maintain automatic cells don't have the ability to design. There are only unproven theories about speciation. I accept God in control.

dhw: As we keep agreeing, all theories about speciation are unproven. Both your theory and my proposal require design, and my proposal does not exclude the participation of your God. Meanwhile, I stand by the statements you bolded. Focusing on automatic behaviour is no response to the question of how that behaviour was first generated and of how cells solve problems and exploit new conditions.

Exactly. We both see that chance mutations cannot design anything worthwhile. "First generation" given by design is the only reasonable answer.

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dhw: So although bacteria remained bacteria, and only used their own programme for future adaptation and problem solving, they contained and passed on programmes for every single life form, econiche, lifestyle and natural wonder in the history of life. And subsequent cell communities carried all these programmes, spontaneously switched on their own special programme, and then passed the other millions of programmes on to another cell community which spontaneously switched on its own special programme and so on. Or God stepped in and switched on the programme for whale flippers, cuttlefish camouflage, monarch migration, weaverbird’s nest etc., because they had to provide food until he could switch on the programme for the brain of H. sapiens. Don’t you find this just a little far-fetched?

DAVID: Not at all. Preprogramming has to work in just that way. Or there are also dabbling switches for God to activate.

I’m glad that my description of your hypothesis is accurate. I look forward to the day when your scientists discover the programmes for whale flippers, cuttlefish camouflage, monarch migration and weaverbirds’ nests hidden away in the bacterial genome. I rather suspect, though, that it’s more likely they will discover that single cells are intelligent, and are capable of combining their intelligences (much as ants do) in order to innovate as well as to adapt. Just an unproven hypothesis, of course, though apparently the majority of scientists now seem to support the concept of cellular intelligence.

dhw: Your focus on gaps is a neat try to sidestep the issue of why a God in total control would specially design a succession of jumping brains in itty-bitty steps instead of specially designing the only brain he wanted to design. ... you suggest divine preprogramming or dabbling; I suggest intelligent cells responding to the demands and opportunities arising from new conditions.

DAVID: I don't understand your definition of itty-bitty except it doesn't fit the 200 cc jumps in size of the hominin stages of brain development. My comment discussed whole phenotype changes, not just brains. You neatly ignored that.

I did not ignore it. The bit you left out was “We have dealt with gaps and the Cambrian over and over again. Nobody knows the answer...” This and what followed was a reference to speciation (phenotype changes). Our discussion here, however, is specifically on the evolution of H. sapiens. By “itty bitty” I mean one bit at a time. All dealt with under “Big brain evolution”: if your God’s one and only purpose was to produce H. sapiens, and he was in full control, why did he take millions of years fiddling with the big toe, the pelvis, different sizes of brain, different types of hominin, different types of human? No need to repeat the arguments under “Big brain evolution” – I am simply explaining that by “itty bitty” I mean the gradual bit by bit evolution (in my hypothesis) or bit by bit creation (in your hypothesis) of H. sapiens.

dhw: As we keep agreeing, all theories about speciation are unproven. Both your theory and my proposal require design, and my proposal does not exclude the participation of your God. Meanwhile, I stand by the statements you bolded. Focusing on automatic behaviour is no response to the question of how that behaviour was first generated and of how cells solve problems and exploit new conditions.

DAVID: Exactly. We both see that chance mutations cannot design anything worthwhile. "First generation" given by design is the only reasonable answer.

And that first generation design may have been carried out by intelligent cell communities, and their intelligence may have been given to them by your God. And focusing on automatic cellular behaviour does not tell us how that behaviour was first generated. Nor does it tell us how cells solve problems and exploit new conditions, these being the factors involved in the demonstration of what is now widely recognized in the scientific world as cellular intelligence.

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DAVID: Not at all. Preprogramming has to work in just that way. Or there are also dabbling switches for God to activate.

dhw: I’m glad that my description of your hypothesis is accurate. I look forward to the day when your scientists discover the programmes for whale flippers, cuttlefish camouflage, monarch migration and weaverbirds’ nests hidden away in the bacterial genome. I rather suspect, though, that it’s more likely they will discover that single cells are intelligent, and are capable of combining their intelligences (much as ants do) in order to innovate as well as to adapt. Just an unproven hypothesis, of course, though apparently the majority of scientists now seem to support the concept of cellular intelligence.

Still the same problem. All of us are looking in from the outside. NO ONE knows the truth. It is all still opinion. Intelligent cell reactions are still 5/50: some degree of intelligence choice decisions or following intelligent instructions. Scientific conclusions are not by democratic vote, but by paradigm shifts (Kuhn).

dhw: Your focus on gaps is a neat try to sidestep the issue of why a God in total control would specially design a succession of jumping brains in itty-bitty steps instead of specially designing the only brain he wanted to design. ... you suggest divine preprogramming or dabbling; I suggest intelligent cells responding to the demands and opportunities arising from new conditions.

DAVID: I don't understand your definition of itty-bitty except it doesn't fit the 200 cc jumps in size of the hominin stages of brain development. My comment discussed whole phenotype changes, not just brains. You neatly ignored that.

dhw: I did not ignore it. The bit you left out was “We have dealt with gaps and the Cambrian over and over again. Nobody knows the answer...” This and what followed was a reference to speciation (phenotype changes). Our discussion here, however, is specifically on the evolution of H. sapiens. By “itty bitty” I mean one bit at a time. All dealt with under “Big brain evolution”: if your God’s one and only purpose was to produce H. sapiens, and he was in full control, why did he take millions of years fiddling with the big toe, the pelvis, different sizes of brain, different types of hominin, different types of human? No need to repeat the arguments under “Big brain evolution” – I am simply explaining that by “itty bitty” I mean the gradual bit by bit evolution (in my hypothesis) or bit by bit creation (in your hypothesis) of H. sapiens.

Gaps are still huge gaps. Poor Gould fought for years to explain them, and came up with punc inc, which still remains as a weird proposition. Species arrive de novo and no one knows why, based on natural events. There Are no intermediate forms, since the ones we find have huge gaps on either side.

dhw: As we keep agreeing, all theories about speciation are unproven. Both your theory and my proposal require design, and my proposal does not exclude the participation of your God. Meanwhile, I stand by the statements you bolded. Focusing on automatic behaviour is no response to the question of how that behaviour was first generated and of how cells solve problems and exploit new conditions.

DAVID: Exactly. We both see that chance mutations cannot design anything worthwhile. "First generation" given by design is the only reasonable answer.

dhw: And that first generation design may have been carried out by intelligent cell communities, and their intelligence may have been given to them by your God. And focusing on automatic cellular behaviour does not tell us how that behaviour was first generated. Nor does it tell us how cells solve problems and exploit new conditions, these being the factors involved in the demonstration of what is now widely recognized in the scientific world as cellular intelligence.

Still 50/50 chance, and I'll stick to my side of the interpretations.

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8871 views

DAVID: Preprogramming has to work in just that way. Or there are also dabbling switches for God to activate.

dhw: I’m glad that my description of your hypothesis is accurate. […] apparently the majority of scientists now seem to support the concept of cellular intelligence.

DAVID: Still the same problem. All of us are looking in from the outside. NO ONE knows the truth. It is all still opinion. Intelligent cell reactions are still 50/50: some degree of intelligence choice decisions or following intelligent instructions. Scientific conclusions are not by democratic vote, but by paradigm shifts (Kuhn).

Agreed. Let us then eagerly await the shift of paradigm through the discovery of programmes for whale flippers, cuttlefish camouflage, monarch migration and weaverbirds’ nests (multiply examples by a few billion) hidden inside the bacterial genome. Or possibly a shift of paradigm towards cellular intelligence.

DAVID: I don't understand your definition of itty-bitty except it doesn't fit the 200 cc jumps in size of the hominin stages of brain development. […]

dhw: By “itty bitty” I mean one bit at a time. All dealt with under “Big brain evolution”: if your God’s one and only purpose was to produce H. sapiens, and he was in full control, why did he take millions of years fiddling with the big toe, the pelvis, different sizes of brain, different types of hominin, different types of human? […]

DAVID: Gaps are still huge gaps. Poor Gould fought for years to explain them, and came up with punc inc, which still remains as a weird proposition. Species arrive de novo and no one knows why, based on natural events. There Are no intermediate forms, since the ones we find have huge gaps on either side.

Yes, we’ve been over this a hundred times. You suggest divine preprogramming or dabbling, and I suggest cellular intelligence. I trust you now agree that your God’s design of H. sapiens proceeded itty bitty by my definition.

Under "Horizontal gene transfer"
DAVID: It can be physically obtained by needling another bacterium and seizing DNA:
https://www.nature.com/articles/s41564-018-0174-y

QUOTE: "Natural transformation is a broadly conserved mechanism of horizontal gene transfer in bacterial species that can shape evolution and foster the spread of antibiotic resistance determinants, promote antigenic variation and lead to the acquisition of novel virulence factors.” (dhw’s bold)

DAVID: Bacteria can alter their responses with this mechanism, but, for example, E. coli will stay E. coli. Doesn't solve speciation.

Nobody has yet solved speciation, but if you believe that all species descended from other species, that does not mean that all their antecedents have to die out! Of course E.coli are still E.coli, just as apes are still apes. The proposal is that SOME single cells formed multicellular communities, and over billions of years SOME multicellular communities changed themselves into different multicellular communities. And since we now know that bacteria can change their responses, MAYBE that same mechanism is capable of producing “novel factors” which have “shaped evolution” (See the Behe thread)

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8869 views

DAVID: Still the same problem. All of us are looking in from the outside. NO ONE knows the truth. It is all still opinion. Intelligent cell reactions are still 50/50: some degree of intelligence choice decisions or following intelligent instructions. Scientific conclusions are not by democratic vote, but by paradigm shifts (Kuhn).

dhw: Agreed. Let us then eagerly await the shift of paradigm through the discovery of programmes for whale flippers, cuttlefish camouflage, monarch migration and weaverbirds’ nests (multiply examples by a few billion) hidden inside the bacterial genome. Or possibly a shift of paradigm towards cellular intelligence.

I still view cells as incapable of designing their future, well beyond their capacities

DAVID: Gaps are still huge gaps. Poor Gould fought for years to explain them, and came up with punc inc, which still remains as a weird proposition. Species arrive de novo and no one knows why, based on natural events. There Are no intermediate forms, since the ones we find have huge gaps on either side.

d hw; Yes, we’ve been over this a hundred times. You suggest divine preprogramming or dabbling, and I suggest cellular intelligence. I trust you now agree that your God’s design of H. sapiens proceeded itty bitty by my definition.

Not at all. You are ignoring the facts. The gaps are huge and require design.

Under "Horizontal gene transfer"
DAVID: It can be physically obtained by needling another bacterium and seizing DNA:
https://www.nature.com/articles/s41564-018-0174-y

QUOTE: "Natural transformation is a broadly conserved mechanism of horizontal gene transfer in bacterial species that can shape evolution and foster the spread of antibiotic resistance determinants, promote antigenic variation and lead to the acquisition of novel virulence factors.” (dhw’s bold)

DAVID: Bacteria can alter their responses with this mechanism, but, for example, E. coli will stay E. coli. Doesn't solve speciation.

dhw: Nobody has yet solved speciation, but if you believe that all species descended from other species, that does not mean that all their antecedents have to die out! Of course E.coli are still E.coli, just as apes are still apes. The proposal is that SOME single cells formed multicellular communities, and over billions of years SOME multicellular communities changed themselves into different multicellular communities. And since we now know that bacteria can change their responses, MAYBE that same mechanism is capable of producing “novel factors” which have “shaped evolution” (See the Behe thread)

As far as I am concerned speciation requires design. 99% of all species have disappeared, but bacteria are still here. Why? Current microbiome research shows those happy bugs are absolutely necessary for our life and health, which they seriously influence. Talk about an obvious purpose as to why they persisted. Paying attention to 'purpose' is always necessary in these discussions.

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8830 views

DAVID: Scientific conclusions are not by democratic vote, but by paradigm shifts (Kuhn).

dhw: Agreed. Let us then eagerly await the shift of paradigm through the discovery of programmes for whale flippers, cuttlefish camouflage, monarch migration and weaverbirds’ nests (multiply examples by a few billion) hidden inside the bacterial genome. Or possibly a shift of paradigm towards cellular intelligence.

DAVID: I still view cells as incapable of designing their future, well beyond their capacities.

Fair enough. It is a hypothesis. And I still view your own hypothesis (above) as beyond belief.

DAVID: […] Species arrive de novo and no one knows why, based on natural events. There Are no intermediate forms, since the ones we find have huge gaps on either side.

dhw: Yes, we’ve been over this a hundred times. You suggest divine preprogramming or dabbling, and I suggest cellular intelligence. I trust you now agree that your God’s design of H. sapiens proceeded itty bitty by my definition.

DAVID: Not at all. You are ignoring the facts. The gaps are huge and require design.

I agree that they require design, and I propose that cellular intelligence (perhaps God-given) might be the designer. Meanwhile, I trust you now agree that your God’s design of H. sapiens proceeded itty-bitty by my definition.

https://www.nature.com/articles/s41564-018-0174-y
QUOTE: "Natural transformation is a broadly conserved mechanism of horizontal gene transfer in bacterial species that can shape evolution and foster the spread of antibiotic resistance determinants, promote antigenic variation and lead to the acquisition of novel virulence factors.” (dhw’s bold)

DAVID: Bacteria can alter their responses with this mechanism, but, for example, E. coli will stay E. coli. Doesn't solve speciation.

dhw: Nobody has yet solved speciation, but if you believe that all species descended from other species, that does not mean that all their antecedents have to die out! Of course E.coli are still E.coli, just as apes are still apes. The proposal is that SOME single cells formed multicellular communities, and over billions of years SOME multicellular communities changed themselves into different multicellular communities. And since we now know that bacteria can change their responses, MAYBE that same mechanism is capable of producing “novel factors” which have “shaped evolution” (See the Behe thread)

DAVID: As far as I am concerned speciation requires design. 99% of all species have disappeared, but bacteria are still here. Why? Current microbiome research shows those happy bugs are absolutely necessary for our life and health, which they seriously influence. Talk about an obvious purpose as to why they persisted. Paying attention to 'purpose' is always necessary in these discussions.

We were talking about the cause of speciation, and in order to discredit the theory of cellular intelligence as the designer you pointed out that bacteria are still bacteria. I pointed out that if you believe in common descent, SOME organisms change while others remain the same. How does that prove they are not intelligent? And if your God exists, I have no doubt that he would have created them with a purpose. Same question: How does that prove they are not intelligent?

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8828 views

dhw: Yes, we’ve been over this a hundred times. You suggest divine preprogramming or dabbling, and I suggest cellular intelligence. I trust you now agree that your God’s design of H. sapiens proceeded itty bitty by my definition.

DAVID: Not at all. You are ignoring the facts. The gaps are huge and require design.

dhw: I agree that they require design, and I propose that cellular intelligence (perhaps God-given) might be the designer. Meanwhile, I trust you now agree that your God’s design of H. sapiens proceeded itty-bitty by my definition.

Your definition has no basis in fact. Compare Lucy, habilis, and erectus with sapiens. Back further in evolution, leg to flipper is a huge gap as shown by the fossil record.

https://www.nature.com/articles/s41564-018-0174-y
QUOTE: "Natural transformation is a broadly conserved mechanism of horizontal gene transfer in bacterial species that can shape evolution and foster the spread of antibiotic resistance determinants, promote antigenic variation and lead to the acquisition of novel virulence factors.” (dhw’s bold)

DAVID: Bacteria can alter their responses with this mechanism, but, for example, E. coli will stay E. coli. Doesn't solve speciation.

dhw: Nobody has yet solved speciation, but if you believe that all species descended from other species, that does not mean that all their antecedents have to die out! Of course E.coli are still E.coli, just as apes are still apes. The proposal is that SOME single cells formed multicellular communities, and over billions of years SOME multicellular communities changed themselves into different multicellular communities. And since we now know that bacteria can change their responses, MAYBE that same mechanism is capable of producing “novel factors” which have “shaped evolution” (See the Behe thread)

DAVID: As far as I am concerned speciation requires design. 99% of all species have disappeared, but bacteria are still here. Why? Current microbiome research shows those happy bugs are absolutely necessary for our life and health, which they seriously influence. Talk about an obvious purpose as to why they persisted. Paying attention to 'purpose' is always necessary in these discussions.

dhw: We were talking about the cause of speciation, and in order to discredit the theory of cellular intelligence as the designer you pointed out that bacteria are still bacteria. I pointed out that if you believe in common descent, SOME organisms change while others remain the same. How does that prove they are not intelligent? And if your God exists, I have no doubt that he would have created them with a purpose. Same question: How does that prove they are not intelligent?

Same issue: we seem them respond intelligently. No proof of why: just 50/50 possibility. You have't answered the major point, which is bacteria were preserved, and therefore they did not evolve into multicellularity by any mechanism they might have had. As God speciated, they purposely were kept for future functions and God produced something entirely new while using some of what bacteria had: DNA.

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8829 views

dhw: By “itty bitty” I mean one bit at a time […] why did he take millions of years fiddling with the big toe, the pelvis, different sizes of brain, different types of hominin, different types of human? [...]

dhw: I trust you now agree that your God’s design of H. sapiens proceeded itty-bitty by my definition.

DAVID: Your definition has no basis in fact. Compare Lucy, habilis, and erectus with sapiens. […]

I have done exactly that. If your God’s one purpose was to design H. sapiens, it would seem that he did the designing one bit at a time, as described above, which is what I mean by “itty bitty”.

dhw: We were talking about the cause of speciation, and in order to discredit the theory of cellular intelligence as the designer you pointed out that bacteria are still bacteria. I pointed out that if you believe in common descent, SOME organisms change while others remain the same. How does that prove they are not intelligent? And if your God exists, I have no doubt that he would have created them with a purpose. Same question: How does that prove they are not intelligent?

DAVID: Same issue: we see them respond intelligently. No proof of why: just 50/50 possibility.

Already agreed. But you tried somehow to use the non-evolution of bacteria as evidence that they were not intelligent.

DAVID: You haven’t answered the major point, which is bacteria were preserved, and therefore they did not evolve into multicellularity by any mechanism they might have had. As God speciated, they purposely were kept for future functions and God produced something entirely new while using some of what bacteria had: DNA.

I have now answered it twice, but I’ll try again. Evolution does not mean that EVERY existing organism turns into another organism. SOME bacteria would have joined forces to create multicellularity, and others would have remained the same. SOME ape ancestors would have turned into pre-humans, but others would have remained the same. As bacteria have always been able to survive changes to their environment, they did not need to “evolve” into anything but bacteria. But SOME of them decided (“intelligence” theory) or were divinely preprogrammed/dabbled (your theory), or simply happened (chance theory) to form ever evolving communities.

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8809 views

dhw: By “itty bitty” I mean one bit at a time […] why did he take millions of years fiddling with the big toe, the pelvis, different sizes of brain, different types of hominin, different types of human? [...]

dhw: I trust you now agree that your God’s design of H. sapiens proceeded itty-bitty by my definition.

DAVID: Your definition has no basis in fact. Compare Lucy, habilis, and erectus with sapiens. […]

dhw: I have done exactly that. If your God’s one purpose was to design H. sapiens, it would seem that he did the designing one bit at a time, as described above, which is what I mean by “itty bitty”.

That is not my definition. Itty-bitty is Darwin's tiny adaptations until something big happens. Our hominin gaps are huge

dhw: We were talking about the cause of speciation, and in order to discredit the theory of cellular intelligence as the designer you pointed out that bacteria are still bacteria. I pointed out that if you believe in common descent, SOME organisms change while others remain the same. How does that prove they are not intelligent? And if your God exists, I have no doubt that he would have created them with a purpose. Same question: How does that prove they are not intelligent?

DAVID: Same issue: we see them respond intelligently. No proof of why: just 50/50 possibility.

dhw: Already agreed. But you tried somehow to use the non-evolution of bacteria as evidence that they were not intelligent.

We don't know if bacteria are intelligent. It is a 50/50 possibility from our observations.

DAVID: You haven’t answered the major point, which is bacteria were preserved, and therefore they did not evolve into multicellularity by any mechanism they might have had. As God speciated, they purposely were kept for future functions and God produced something entirely new while using some of what bacteria had: DNA.

dhw: I have now answered it twice, but I’ll try again. Evolution does not mean that EVERY existing organism turns into another organism. SOME bacteria would have joined forces to create multicellularity, and others would have remained the same. SOME ape ancestors would have turned into pre-humans, but others would have remained the same. As bacteria have always been able to survive changes to their environment, they did not need to “evolve” into anything but bacteria. But SOME of them decided (“intelligence” theory) or were divinely preprogrammed/dabbled (your theory), or simply happened (chance theory) to form ever evolving communities.

You are right in that 99% of species die out. And since we do not know how things speciate, you have listed possibilities.

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8855 views

DAVID: Your definition has no basis in fact. Compare Lucy, habilis, and erectus with sapiens. […]

dhw: I have done exactly that. If your God’s one purpose was to design H. sapiens, it would seem that he did the designing one bit at a time, as described above, which is what I mean by “itty bitty”.

DAVID: That is not my definition. Itty-bitty is Darwin's tiny adaptations until something big happens. Our hominin gaps are huge.

Ah well, since according to you these huge gaps can only be bridged by your God’s special design, let’s drop the expression “itty bitty” and simply ask ourselves why your God, whose sole purpose was apparently to specially design H. sapiens, spent millions of years specially designing bit by bit of him: big toes, then pelvises, then different sized brains, then different types of hominin, then different types of human. You admit that have no idea, so maybe something is wrong with your hypothesis. See “Big brain evolution”.

dhw: […] you tried somehow to use the non-evolution of bacteria as evidence that they were not intelligent.

DAVID: We don't know if bacteria are intelligent. It is a 50/50 possibility from our observations.

Agreed, but the non-evolution of some bacteria is irrelevant to the question of whether they are or are not intelligent.

DAVID: You haven’t answered the major point, which is bacteria were preserved, and therefore they did not evolve into multicellularity by any mechanism they might have had. As God speciated, they purposely were kept for future functions and God produced something entirely new while using some of what bacteria had: DNA.

dhw: I have now answered it twice, but I’ll try again. Evolution does not mean that EVERY existing organism turns into another organism. SOME bacteria would have joined forces to create multicellularity, and others would have remained the same. SOME ape ancestors would have turned into pre-humans, but others would have remained the same. As bacteria have always been able to survive changes to their environment, they did not need to “evolve” into anything but bacteria. But SOME of them decided (“intelligence” theory) or were divinely preprogrammed/dabbled (your theory), or simply happened (chance theory) to form ever evolving communities.

DAVID: You are right in that 99% of species die out. And since we do not know how things speciate, you have listed possibilities.

Yes indeed. More to the point, as above, is that the non-evolution of some bacteria is irrelevant to the question of whether they are intelligent or not.

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8803 views

DAVID: That is not my definition. Itty-bitty is Darwin's tiny adaptations until something big happens. Our hominin gaps are huge.

dhw: Ah well, since according to you these huge gaps can only be bridged by your God’s special design, let’s drop the expression “itty bitty” and simply ask ourselves why your God, whose sole purpose was apparently to specially design H. sapiens, spent millions of years specially designing bit by bit of him: big toes, then pelvises, then different sized brains, then different types of hominin, then different types of human. You admit that [you] have no idea, so maybe something is wrong with your hypothesis. See “Big brain evolution”.

Gross distortion of my thoughts. God chose to evolve humans over time. The only thing I do not know is His thought process in making that choice. You have agreed He has the right to choose, and I've agreed He might have limits as a reason. Nothing wrong with my hypothesis under those circumstances.

DAVID: You haven’t answered the major point, which is bacteria were preserved, and therefore they did not evolve into multicellularity by any mechanism they might have had. As God speciated, they purposely were kept for future functions and God produced something entirely new while using some of what bacteria had: DNA.

dhw: I have now answered it twice, but I’ll try again. Evolution does not mean that EVERY existing organism turns into another organism. SOME bacteria would have joined forces to create multicellularity, and others would have remained the same. SOME ape ancestors would have turned into pre-humans, but others would have remained the same. As bacteria have always been able to survive changes to their environment, they did not need to “evolve” into anything but bacteria. But SOME of them decided (“intelligence” theory) or were divinely preprogrammed/dabbled (your theory), or simply happened (chance theory) to form ever evolving communities.

DAVID: You are right in that 99% of species die out. And since we do not know how things speciate, you have listed possibilities.

dhw: Yes indeed. More to the point, as above, is that the non-evolution of some bacteria is irrelevant to the question of whether they are intelligent or not.

Not relevant. My main point still persists: bacteria were purposely preserved to play a role now, innately intelligent or not.

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8857 views

DAVID: You are right in that 99% of species die out. And since we do not know how things speciate, you have listed possibilities.

dhw: Yes indeed. More to the point, as above, is that the non-evolution of some bacteria is irrelevant to the question of whether they are intelligent or not.

DAVID: Not relevant. My main point still persists: bacteria were purposely preserved to play a role now, innately intelligent or not.

You have forgotten the starting point of this particular discussion, which was your entry under “Horizontal gene transfer”:

https://www.nature.com/articles/s41564-018-0174-y

QUOTE: "Natural transformation is a broadly conserved mechanism of horizontal gene transfer in bacterial species that can shape evolution and foster the spread of antibiotic resistance determinants, promote antigenic variation and lead to the acquisition of novel virulence factors.” (dhw’s bold)

DAVID: Bacteria can alter their responses with this mechanism, but, for example, E. coli will stay E. coli. Doesn't solve speciation.

The subject was not the purpose of bacteria but whether they were capable of shaping evolution by producing novel factors (linking up with our heading: what genes do and don’t do). Nobody can possibly dispute the essential roles that bacteria have always played in life.

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8834 views

dhw: Yes indeed. More to the point, as above, is that the non-evolution of some bacteria is irrelevant to the question of whether they are intelligent or not.

DAVID: Not relevant. My main point still persists: bacteria were purposely preserved to play a role now, innately intelligent or not.

dhw: You have forgotten the starting point of this particular discussion, which was your entry under “Horizontal gene transfer”:

https://www.nature.com/articles/s41564-018-0174-y

QUOTE: "Natural transformation is a broadly conserved mechanism of horizontal gene transfer in bacterial species that can shape evolution and foster the spread of antibiotic resistance determinants, promote antigenic variation and lead to the acquisition of novel virulence factors.” (dhw’s bold)

DAVID: Bacteria can alter their responses with this mechanism, but, for example, E. coli will stay E. coli. Doesn't solve speciation.

dhw: Nobody has yet solved speciation, but if you believe that all species descended from other species, that does not mean that all their antecedents have to die out! Of course E.coli are still E.coli, just as apes are still apes. The proposal is that SOME single cells formed multicellular communities, and over billions of years SOME multicellular communities changed themselves into different multicellular communities. And since we now know that bacteria can change their responses, MAYBE that same mechanism is capable of producing “novel factors” which have “shaped evolution”

dhw: The subject was not the purpose of bacteria but whether they were capable of shaping evolution by producing novel factors (linking up with our heading: what genes do and don’t do). Nobody can possibly dispute the essential roles that bacteria have always played in life.

Whatever the original subject was we agree on the observation that bacteria were purposefully preserved for future roles.

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Miscarriages from genetic errors:

https://www.newscientist.com/article/2406464-genetic-errors-are-behind-more-than-two-th...

"More than two-thirds of early miscarriages seem to be due to abnormal chromosomes, the packages of DNA within all our cells, in the embryo or fetus. The remaining third are probably also largely due to genetic factors, which we may not be able to detect yet.

"Previously, it had been thought that about half of miscarriages were due to these chromosomal abnormalities. Now, a new technique has found that, in fact, the majority of early miscarriages are the result of such problems.

***

"Miscarriages – generally defined as a pregnancy that is lost before week 23 – often have no clear cause, although if someone has more than one, the expelled tissue may be analysed to try to understand why.

"This is usually done by multiplying the cells in a dish and then analysing their chromosomes, a process called karyotyping. This may find, for instance, that among the 23 pairs of human chromosomes, one chromosome is missing or duplicated.

***

"Looking at the tissue from 1745 miscarriages, with an average gestation of seven weeks, they first used standard karyotyping. The researchers found that 50 per cent of these cases had chromosomal abnormalities, as expected.

"Next, the team took a random subset of 94 of the tissue samples that had been found to have normal chromosomes and put them through a technique called haplarithmisis.

"This doesn’t require growing the cells in a dish, but instead involves analysing the DNA of many of the cells together before comparing them with the DNA of the parents, using donated blood samples.

"This found that about a third of the cells that were initially classed as having normal chromosomes actually had genetic errors. Put together, this suggests that, in the whole group of miscarriages, 68 per cent would have had such errors. “Chromosomal abnormalities have a much bigger contribution to pregnancy loss [than found in] previous studies that used conventional methods,” says Zamani Esteki.

***

"The cause of the remaining third of miscarriages is probably largely also genetic errors that mean the embryo or fetus couldn’t have survived, albeit ones that are more minor than chromosomal abnormalities."

Comment: I view miscarriages as a method by which God corrects errors in genetics. The process has tight controls, but we see that mistakes happen. The mistakes are not God's fault, and a miscarriage is the proper answer rather than a deformed live baby.

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Tour is a world-famous organic chemist who has stated how hard it is to make functional organic molecules:

David: James Tour: " We synthetic chemists should state the obvious. The appearance of life on earth is a mystery. We are nowhere near solving this problem. The proposals offered thus far to explain life’s origin make no scientific sense.”

dhw: Ditto the mysteries of consciousness and speciation. Great article, which should be compulsory reading for all theists and atheists!

DAVID: Dr. Tour is in Houston at Rice University. He is a Jewish believer.

dhw: No problem, so long as he acknowledges that his own explanation of life’s origin makes no scientific sense either. I don’t object to faith. I object to people who have faith in God or in chance denigrating one another’s faith and pretending they know better.

David: The difficulty in making organic molecules by human effort compared to living processes ease in doing it is his main point.

https://www.chemistryworld.com/news/the-five-reactions-on-every-organic-chemists-wish-l...

This article describes the problem for human chemists who cannot imitate what life easily produces:

" Why do so many drugs have structural similarities? If you look at many of the best-selling and most-prescribed medicines – like hepatitis C treatment sofosbuvir, antihypertensive lisinopril or asthma drug fluticasone – they have a few things in common: they are densely functionalised, have at least one ring and some unprotected amines or alcohols, and often a scattering of fluorine atoms.

"Part of the answer is that drug discovery chemists are limited to a chemical space that can be accessed by known reactions and the available building blocks. They also need to consider biology, so reactions that tolerate basic nitrogen atoms are a must since they feature in almost every single biologically active compound. Reactions using only off-the-shelf reagents that don’t catch fire when they’re exposed to air are also a big plus as there’s often no easy access to specialist equipment like glove boxes.

"A 2014 analysis1 showed that only two reactions make up over half of all those used in synthesis to discover and develop drugs: the amide formation and the Suzuki–Miyaura cross coupling. ‘The reason these have contributed so much to medicinal chemistry is that they are the most robust reactions,’ says György Keserű, who leads a medicinal chemistry group at the Hungarian Academy of Sciences.

***

" every medicinal chemist has a list of reactions they wished existed. Here’s what this list might look like.

"1. Fluorination – Exchanging a specific hydrogen for a fluorine atom in molecules with many functional groups. A reaction that installs a difluoromethyl group would be nice too.

"2. Heteroatom alkylation – A reaction that – selectively – attaches an alkyl group onto one heteroatom in rings that have several, such as pyrazoles, triazoles and pyridones.

"3. Carbon coupling – A reaction as robust and versatile as traditional cross coupling for stitching together aliphatic carbon atoms – ideally with control of chirality, too. Chemists also want more options for the kinds of molecules they can use as coupling precursors.

"4. Making and modifying heterocycles – A reaction to install functional groups – from alkyl to halogen – anywhere on aromatic and aliphatic heterocycles, such as pyridine, piperidine or isoxazole. Reactions that can make completely new heterocycles from scratch would be a bonus.

"5. Atom swapping – A reaction that can exchange individual atoms selectively, like swapping a carbon for a nitrogen atom in a ring. This chemical version of gene editing could revolutionise drug discovery, but is probably furthest from realisation."

Comment: The article discusses each wish describing the complex problems, but the point is made. The organic chemistry of living organisms is far beyond what bright designing humans can achieve. Yet atheists claim nature figured it all out naturally. No chance!

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A study using embryos with artificial substitutions:

https://cosmosmagazine.com/biology/exploring-the-precision-of-embryonic-development

"How does the fruit fly get its stripes? Very specifically.

"At least that’s the conclusion of physicists and biologists from Princeton University in the US, who found that during embryo formation fruit fly cells use “all information available from the genetic code” to position themselves within a single cell’s width of where they are supposed to be.

“'The theoretical idea is very simple, which is that every cell is using all the information that it can squeeze out of the relevant genes," says physicist William Bialek.

"'Something we've known for a while, but never stop being amazed by, is that the whole system is incredibly precise, and this fact is what spurred us to believe that the cells are using all the information that they can."

"In a paper published in the journal Cell, the researchers report that using theoretical principles they were able to predict where cells will end up were accurate to within 1% of the ultimate locations.

"Fruit flies form stripes between their segments during embryonic formation. Previous research shows that the stripes are formed according to the directions from the types of “signalling molecules,” which are passed on from fly mother to egg. The molecules activate special genes, known as gap genes, that create the gaps (and stripes) between fly segments.

"Researchers used measurements of the expression of the gap genes and the molecules produced along the embryonic body to model how the cells find their places.

"'One can imagine cells as GPS devices which, instead of satellite signals, collect molecular ones to figure out their locations. We are able to decode how such molecular signals specify positions along the length of the early fly embryo," says Mariela Petkova, who took the initial measurements.

"Petkova also measured placement of cells in fruit fly larva that was genetically mutated, and it was there that the researchers found the most solid proof of their hypothesis. The mathematical predictions for cell placement work for the mutated genes.

"'We used genetic manipulations to shuffle the gap gene patterns and 'trick' the cells into 'thinking' they were somewhere else along the length of the embryo," Petkova says. "We put these shuffled patterns through our decoder and built decoding maps, which told us where the cells were versus where they thought they were.

“'Using these maps, we predicted where the embryos would make stripes. When we looked at these mutant embryos under a microscope, we actually found the stripes at the predicted locations! It was very satisfying."

***

"'The experiment defines the first truly quantitative measure of how much information cells have available for crucial developmental decisions and how much of that information they actually use," he says.

“'This gives us an amazing tool for understanding how decision-making in biology actually works, one that is useful at levels ranging from the way proteins bind to DNA to how new biological pathways arise and compete during evolution.'”

comment: Note the automaticity of the cells response to changed directions. The scientists could not have gotten these results if the cells did not automatically follow the substituted gene patterns. This still does tell us how genes act to create the final physical results they control. We do see they order the production of certain proteins at certain places b ut we do not know exactly how they exert their controls. we just beginning and end but not much of the middle molecular activity.

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DNA is carefully packed in sperm cells to help control the fertilized egg cell:

https://phys.org/news/2019-02-scientists-reveal-d-dna-perpetuate.html

"Using new technology to reveal the 3-D organization of DNA in maturing male reproductive cells, scientists revealed a crucial period in development that helps explain how fathers pass on genetic information to future generations.

"The period was captured during a stage of male sperm development called meiosis. This is when reproductive cells, called germ cells, are maturing into sperm that can fertilize a female egg, laying the foundation to make all the cells of a child.

***

"reproductive biologists at Cincinnati Children's Hospital Medical Center say nature prepares the 3-D organization of DNA before packing it into sperm.

"By the time the germ cells actually become fertile sperm, the genetic material is tightly arranged. The male germ cell's hereditary material has precise 3-D organization in the cell's genetic control center, the nucleus. Researchers report that this 3-D organization is necessary for a male to help produce the next generation of life.

"'We propose that male sperm is not just a carrier of DNA. Our data suggest that the three-dimensional organization in the cell nucleus helps establish a molecular foundation that can reproduce a complete zygote capable of becoming the next generation," said Satoshi Namekawa Ph.D., a principal investigator on the study and member of the Division of Reproductive Sciences.

***

"Using the maturing germ cells of male mice for their study, the researchers honed in on meiosis, the stage when male germ cells shed half of their chromosomes while shuffling around genetic material.

***

"Using a technology called Hi-C, researchers were able to show the 3-D organization and interactions of chromosomes, as well as the genes in the nucleus of meiotic male germ cells. The authors propose that preparing 3-D organization in meiosis is vital for genes that allow germ cells to regain their ability to produce all the cells of the body after fertilizing a female egg.

"'In meiosis, gene expression is extremely high and diverse," said Kris Alavattam, the study's first author and member of the Namekawa laboratory. "Many of these genes are essential for germ cells to develop, and many are expressed nowhere else but germ cells and at no other time." (my bold)

"During this time, the hereditary material in germ cells is organized in spatially related compartments called genomic compartments. In meiotic male germ cells, the researchers noticed genomic compartments are weaker than those in other cells of the body. This weakness helps facilitate what they call a global reprogramming of 3-D chromatin organization. This organization of chromatin—the packaging of DNA with DNA-binding proteins—promotes essential gene expression and germ cell development. After meiosis, genomic compartments of chromatin become stronger and stronger, packing DNA in a highly organized manner as cells ready for procreation."

Comment: Note my bold. There are specialized genes just for control of growing the embryo. In the new stage of sexual reproduction during evolution, all of these moving parts must have appeared all at once by design. It cannot have appeared stepwise by chance.

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8998 views

Most active biochemical molecules are huge, but there are tiny ones that are functional:

https://www.the-scientist.com/features/the-dark-matter-of-the-human-proteome-65628?utm_...

"Researchers had recently recognized that the genome contained genes that were so small that they had been missed by traditional genome annotation methods, and targeted searching for protein-coding snippets of DNA had suggested there may be many thousands of so-called microproteins hard at work in our cells.

***

"Microproteins are not the cell’s only tiny proteins, but similarly diminutive peptide hormones, such as insulin, only become biologically active after they’re cleaved from larger precursor proteins. Microproteins, on the other hand, start out that way. They are translated from a small open reading frame (smORF) directly into their active form. These smORFs are so tiny, in fact, that researchers overlooked them in the early 2000s as they began predicting all the protein-coding regions in the newly sequenced human genome; they used a minimum length cutoff of 100 codons for gene assignment to decrease the rate of false positives. But over the past 10 years, developments in genomics and proteomics methods have revealed hundreds to thousands of smORFs.

***

"Despite the challenges, researchers are making progress in characterizing the functions of the putative microproteins that have already been found in the genetic code. New techniques for identifying protein-microprotein interactions reveal how the tiny molecules function in the context of larger protein complexes, and where those complexes tend to be found in the cell. In the last five years, our group and others have uncovered plausible roles for microproteins in development, metabolism, muscle function, DNA repair, and mitochondrial activity, and some may even have links to disease. We are only beginning to scratch the surface of this field. Hundreds more microproteins have been detected across human cell lines and tissues, and thousands are predicted to exist across species on the basis of genomic data.

***

"These techniques have identified evidence of smORFs in diverse types of supposedly noncoding RNA, including introns of pre-mRNAs, long noncoding RNAs, and primary transcripts of microRNAs and ribosomal RNAs. The next step is to identify the microproteins they encode and understand their biological importance.

***

"Over the past couple of years, these approaches have revealed that, unlike peptide hormones, which carry signals from one cell to another, microproteins function within the cell by interacting with larger protein complexes.

***

"These findings emphasize the importance of further investigations to discover and characterize novel smORFs and the microproteins they encode. Biochemical studies show that microproteins use short sequences of just two to four amino acids to interact with larger protein complexes to regulate biology. "

Comment: I've always suspected there were many hidden layers of genome activity. More will be found. We can't exist as humans with just 20,000 genes described. This is an important beginning to find more of the guidance of multiple dynamic processes.

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8806 views

Backup mechanisms are necessary in nature:

https://www.sciencedaily.com/releases/2019/04/190415172156.htm

"In flowering plants, stem cells are critical for survival. Influenced by environmental factors, stem cells direct how and when a plant will grow. Whether a plant needs deep-reaching roots, taller stems, or more leaves and flowers, it is the stem cells that produce new cells for the job.

"That's also why having too many or too few stem cells can disrupt a plant's growth.

***

"In a paper published in Nature Genetics, Lippman and CSHL Professor David Jackson describe the genetic mechanisms that ensure "a deeply conserved stem cell circuit" maintains some function, even if defects occur in a signaling protein called CLV3, and the receptor with which it interacts, CLV1.

"Those players are critical for ensuring a plant has the right number of stem cells throughout life, and we discovered there are backup systems that kick in when these players are compromised through chance mutations," explains Lippman.

"The researchers determined that although the stem cell circuits are essential for flowering plants, the genetic backup systems can vary drastically from plant to plant.

"If the gene producing CLV3 is disrupted by a mutation in a tomato, for instance, a related gene will stand in for it. However, Jackson's team discovered that in the case of maize, two genes are working in parallel to produce the essential signaling protein.

***

"'We were surprised to see such big differences," says Jackson, "but in retrospect it reveals the power of evolution in finding novel ways to protect critical developmental circuits.'"

Comment: Not exactly the same type of convergence we usually see, but more evidence of an underlying program for evolution. An other evidence of design in that when the plant appeared in evolution, such protection was required and must have developed contemporaneously.

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8650 views

Found to be in independent blocks:

https://www.sciencedaily.com/releases/2019/05/190502143513.htm

"The analysis of the chromatin profiles allowed the scientists to make a first important discovery. "Regulatory activity appears to be organized in fully independent blocks, with series of regulatory elements on the same genomic region being all high or all low at the same time," describes Alexandre Reymond, professor at the Center for Integrative Genomics, UNIL Faculty of Biology and Medicine, who co-lead this work. "As if regulatory elements were stuck together in genomic Lego blocks!" Other geneticists had already pinpointed rather large structures -- called "topologically associating domain" or TAD -- that play a role in gene regulation. However, the "blocks" here identified -- named CRDs -- are of much smaller size, enabling the definition of a much finer resolution map of gene expression.

'To understand their function, the scientists built specific models allowing to measure how genetic variation impacts on these structures, which in turn increase or decrease gene activity. By encompassing several hundreds of samples, the scientists found genetic variants that not only increase or decrease gene expression, but that have the power to change the very structure of these blocks by, for instance, splitting one block into two fully separated structures. By doing so, they change the landscape of regulation, and therefore gene expression.

***

"our model shows that regulatory elements could very well be on another chromosome. Because of the nuclear 3-D structure that brings regions together, a cross-talk of regions can take place in any of our 23 chromosomes, with "trans-regulatory hubs" affecting genes anywhere."
The geneticists were able to create statistical models showing what genetic variant influences what block of chromatin that, in turn, affects multiple genes across the genome.

"In addition, if the identification of gene mutations are relatively easy to observe, the same for regulatory elements -- located in the non-coding DNA -- is more problematic. "Indeed, as we do not understand their "grammar" it is difficult to identify if mutations will have an influence, positive or negative. By pooling them together, we were able to design a method to search for rare variants in non-coding regions" explains Olivier Delaneau. "For the first time, we provide a framework of the burden of complex diseases in the non-coding DNA."

***

"By incorporating the complexity of the genome into a single model, the scientists provide a tree of correlations of all regulatory elements across the whole genome. "Every node of this tree can then be analysed to summarize the effects of that node as well as the variability of all regulatory elements below that could be relevant to a certain phenotype" indicates Alexandre Reymond. This structure allows reducing the number of hypotheses, and opens up a whole new world in the study of the effect of genetic variation in genome function."

Comment: This article shows an attempt to unravel the 3-D nature of gene controls, which are highly complex, nothing a chance process could ever develop. Pure evidence of design.

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8638 views

DNA is not just a two-chain coil. In chromatic it takes many shapes which dictates how DNA is used by different types of cells:

https://www.nature.com/articles/d41586-019-01426-w?utm_source=Nature+Briefing&utm_c...

"Molecular models suggest that chromosomes assemble in an ordered, hierarchical way: DNA wraps around proteins called histones to form nucleosomes, which fold into 30-nanometre fibres, then 120-nanometre ‘chromonema’, and further into larger chromatin structures until they reach their most tightly coiled form — the characteristic X-shaped bodies.

***

"Zhuang’s team mapped several million bases of human chromosome 21 at 30 kilobase resolution, tracing their shape like a dot-to-dot puzzle. The resulting multicoloured image resembles one of the melting clocks in Dalí’s 1931 The Persistence of Memory.

"But that was in just one cell. In each cell that Zhuang’s team looked at, the chromosome assumed a different shape — each one a different solution to some ineffable cellular calculation. “There is very strong cell-to-cell heterogeneity,” Zhuang says.

***

“'The variability, which people had thought was there, and there are hints of, is truly astounding.” Brian Beliveau, a genomic scientist at the University of Washington, Seattle, and a co-author of the paper, says bluntly: “Chromosomes are almost certainly like snowflakes.”

"In biology, function derives from form. It is shape, as a result of amino-acid sequence, that determines whether a given protein acts as a structural scaffold, signalling molecule or enzyme. The same is probably true of the genome. But until recently, there was no easy way for researchers to determine that structure.

"Using a sequencing-based method called Hi-C, which calculates the frequencies at which different chromosomal segments interact in space, researchers discovered that chromatin organizes into relatively stable structures called topologically associating domains (TADs), and larger domains called compartments.

***

"The method’s sensitivity is such that it picks up both intra- and interchromosomal contacts — about one million per cell — from which the team can infer the organization of the entire nucleus. It looks, in computer-generated renderings, like a multicoloured skein of yarn. “We know how that 6 × 109 bases are located in the nucleus,” Xie says.

"And in olfactory neurons, they found that structure reflects cellular biology. Whereas most cells pack their thousand-odd olfactory-receptor genes at the periphery of the nucleus, olfactory neurons mostly pack them near the nuclear centre, where they are silenced — except, presumably, one that remains free to produce the neuron’s olfactory receptor. “Chromatin structure determines cell function,” Xie says.

***

"And the genome is almost certainly dynamic, Dekker adds. A configuration that exists at one moment might disappear minutes later, as the cell samples the genomic landscape. “What we do think is that most of these structures can happen in all cells, but occur transiently.”

"Other mechanisms are probably also at play, says Misteli. Some loci, for instance, are characteristically spaced so far apart it would be difficult for them to interact through chromosome diffusion alone.

***

"...by studying its shape across size scales from nucleosomes to nuclei, the team discerned that cellular chromatin is much more chaotic than conventional wisdom would suggest. In the paper, the researchers describe “a disordered granular chain with varying diameters between 5 and 24 nm and many different nucleosome particle arrangements, unknown densities, and structural conformations”.

"Still, by comparing chromatin’s properties across different stages of the cell cycle, the team found that chromosomal structure seems to vary strongly with local DNA concentration. Small changes in concentration could push the DNA into a more or less fluid state — a finding that provides a potentially simple explanation for the speed and regulation of chromatin dynamics."

Comment: the 3-D formation of DNA controls how different cells use it in different ways. As commented upon in the article, form determines the functions elicited from the DNA. This indicates another layer of genome controls in the cells themselves, picking and choosing what is needed from the DNA.

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8672 views

A new function for ribosomes which were thought to just make proteins:

https://phys.org/news/2019-05-protein-factory-role-ribosomes-human.html

"'For a long time, many people have viewed ribosomes as a passive player in the cell—a molecular machine that's just producing proteins," says Stowers Assistant Investigator Ariel Bazzini, Ph.D. "Now there's growing evidence that ribosomes regulate gene expression, including in human cells."

"These findings, which were recently published online in eLife, could lead to further understanding mRNA's role and the causes of gene misregulation in human diseases.

"In the process of translation, ribosomes make proteins by serving as the site for the biological synthesis of them. Specifically, a ribosome reads codons—sets of three consecutive nucleotides—in an mRNA message to determine which amino acids to add to the growing protein chain. As part of this process, ribosomes also act as quality control, triggering the destruction of improperly made mRNA.

"A growing body of evidence has shown ribosomes also play a role in affecting the stability (life) of properly processed mRNAs, thereby acting as a key factor in modulating mRNA stability, level of mRNA, and protein production. This had been shown in organisms such as yeast, E. coli, and zebrafish. In this study, researchers showed that ribosomes affect mRNA stability in human cell lines as well.

"'We're seeing that the amount of gene expression is a combination of mRNA production (transcription) and stability," Bazzini says. "Think of a glass of water. To get an idea of how much water the glass holds at any particular time, it's important to know how much water you initially pour into the glass but also important to know how much water you drink. The same is true with mRNAs. You can measure how many mRNAs are properly made, but if you don't know how many of them are being broken down, how do you really know how many there are?"

"These findings open the door to two exciting research avenues, says Bazzini. The first is better understanding how ribosomes trigger mRNA destruction, the molecular mechanism of which is still unknown. Ribosomes may not be the passive player researchers have long thought them to be.

"'Similar to ribosomes, molecules called tRNAs, or transfer RNAs, are also fundamentally involved in protein synthesis," says first author on the report and Stowers Predoctoral Researcher Qiushuang Wu. "We think that tRNAs, which recognize codons in mRNA and provide corresponding amino acids to ribosomes, might have a strong regulatory role in development and in human diseases'."

Comment: The real issue is how does life emerge from this enormous suite of active protein molecules with all the multiple layers of gene controls in action simultaneously under tight controls.

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8551 views

Its physical status is just right:

https://www.sciencedaily.com/releases/2019/06/190624173826.htm

"Inspired by ideas from the physics of phase transitions and polymer physics, researchers in the Divisions of Physical and Biological Sciences at UC San Diego set out specifically to determine the organization of DNA inside the nucleus of a living cell. The findings of their study, recently published in Nature Communications, suggest that the phase state of the genomic DNA is "just right" -- a gel poised at the phase boundary between gel and sol, the solid-liquid phase transition.

"Think of pudding, panna cotta -- or even porridge. The consistency of these delectables must be just right to be ideally enjoyed. Just as the "sol-gel" phase transition, according to the scientists, seems just right for explaining the timing of genomic interactions that dictate gene expression and somatic recombination.

***

"By comparing experimental and simulated data, the scientists concluded that constrained motion is imposed by a network of cross-linked chromatin chains, or a mesh of bridges between the DNA strands that are characteristic of a gel phase. Yet, the amount of these cross-links is "just right" to poise the DNA near the sol phase -- a liquid phase describing a solution of uncross-linked chains.

"This pattern suggested to the scientists that a certain organizational principle of genomic DNA exists -- proximity to the sol-gel phase transition -- which explains how the genome can simultaneously possess stability and responsiveness within the nucleus.

"These results indicate that the packing pattern of DNA within a cell's nucleus has consequences for a cell's fate -- whether it becomes a live or diseased cell.

"'We have rigorous theories from physics -- abstract principles and mathematical equations. We have state-of-the-art experiments on biology -- innovative tracking of gene segments in live mammalian cell nuclei," noted Zhang. "It really amazes and excites me when the two aspects merge coherently into one story, where physics is not just a tool to describe the dynamics of gene segments, but helps to pinpoint the physical state of the genome, and further sheds light on the impact of the physical properties of this state on its biological function.''"

Comment: This precise physical status of DNA is a difficult state to achieve, and strongly suggests that it was designed to allow DNA a wide range of functions.

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8412 views

This is exactly the ID viewpoint:

https://uncommondescent.com/intelligent-design/can-one-apply-the-goldilocks-principle-o...

"From what these researchers report, yes, one can definitely apply the principle. But then one must accept that biology shows evidence of design. “Just right” is rarely an accident."

Comment: ID agrees with me, although they won't use the word 'God'.

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8366 views

A complex addition to our knowledge of how memory is created/controlled:

https://medicalxpress.com/news/2019-07-noncoding-rna-important-role-memory.html

"RNA is the messenger that transmits the code to individual cells in the form of proteins.

" However, there are also non-coding RNAs, which do carry instructions to a cell without coding for proteins and whose role—if any—has been poorly understood. Recently, science has come to understand that non-coding RNA may play a more important role than originally believed.

"'NEAT1 is a tissue-specific, non-coding RNA found in the hippocampus region of the brain. This brain region is most associated with learning and memory," said Farah Lubin, Ph.D.,

***

"Lubin says that, when NEAT1 is on, or active, we do not learn as well. But when presented with an outside learning experience, it turns off, allowing the brain to learn from the outside stimulus. She uses a car analogy. The engine might be running; but when the brakes are on, the car does not move. You have to take off the brakes and hit the gas to get the car to move.

"'NEAT1 is the brake: When it is on, we aren't learning, at least not as much as we might with it off," Lubin said. "In a younger brain, when presented with stimulus that promotes learning, NEAT1 turns off. Since one of the hallmarks of aging is a decline in memory, we wondered if NEAT1 was implicated in that decline."

"Lubin says one of the genes that NEAT1 acts upon is c-FOS, which is necessary for memory formation. In an aging brain, NEAT1 is on more than it is in a younger brain, interfering with the epigenetic regulation of c-FOS, which disrupts its memory functions.

Using siRNA techniques in a mouse model, Lubin's team was able to turn off NEAT1 in older mice. With NEAT1 off, the mice demonstrated normal abilities in learning and memory.

"The next step was to change the level of NEAT1 in younger mice, using CRISPR/dCas9 gene-activation technology. Boosting the presence of NEAT1 in younger mice caused a decline in their ability to learn and remember.

"'Turning NEAT1 off in older animals boosted memory, while increasing NEAT1 in younger animals diminished memory," Lubin said. "This gives us very strong evidence that NEAT1 and its effects on the epigenetic control of c-FOS are one of the keys to memory formation. These are significant findings, for not only did we find a novel epigenetic initiator and regulator, we identified a new role for the NEAT1 non-coding RNA."

Comment: As usual a complex arrangement of this sort cannot arise from change mutations. Developed memories are very important in maintaining an individual life. like here can food be obtained. Memory systems must exist from the start of a new species. Only purposeful design fits.

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8349 views

The genome is various cell types differ in humans and I would guess call animals:

https://www.scientificamerican.com/article/the-human-body-is-a-mosaic-of-different-geno...

"The human body is a complex mosaic made up of clusters of cells with different genomes—and many of these clusters bear mutations that could contribute to cancer, according to a sweeping survey of 29 different types of tissue.

***

"Tissue mosaics arise as cells accumulate mutations—from DNA errors that creep in during cell division, or because of exposure to environmental factors such as ultraviolet light or cigarette smoke. When a skin cell with a given mutation divides, it can create a patch of skin that is genetically different from its neighbors.

"Previous studies have found high levels of mosaicism in the skin, esophagus and blood. Those results were typically gleaned from sequencing specific genes in microscopic tissue samples.

***

"Overall, the study found fewer examples of mosaicism in some types of tissue than would be expected on the basis of previous research. But the key, says Martincorena, is that the latest analysis demonstrated that mosaicism is present across a wide array of tissues.

"Tissues with a high rate of cell division, such as those that make up the skin and esophagus, tended to have more mosaicism than tissues with lower rates of cell division. Mosaicism also increased with age, and was particularly prevalent in the lungs and skin—tissues that are exposed to environmental factors that can damage DNA.

":A gene called TP53—which helps to repair DNA damage and is known as the guardian of the genome—was one of the most common mutation sites. Certain changes in TP53 are associated with cancer, but it might take additional mutations in other genes before cells give rise to tumors.

“'What we’re seeing are some of the earliest precancerous changes that are then going to accumulate more mutations,” says Erin Pleasance, who studies cancer genomics at the British Columbia Cancer Agency in Vancouver, Canada. “Eventually a small proportion of these may become cancer.'”

Comment: Part of the mosaicism is due to very different functions among our many cells. This study does not show that our germ cells show these genetic changes, but certainly our bodies are not t he ones we were born with.

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8220 views

Germ cells are not allowed to work on their own. They are monitored by special cells and damaged cells are removed:

https://phys.org/news/2019-07-genome-body-heritable-genomes.html

"Scientists at the CECAD Cluster of Excellence in Aging Research of the University of Cologne have discovered that body cells which are in direct contact with the germ cells in the nematode Caenorhabditis elegans are responsible for controlling the stability of the genome in primordial germ cells (PGCs). All germ cells, including sperm and eggs, originate from primordial germ cells that form during early embryo development. Professor Dr. Björn Schumacher and his team at the UoC's Institute for Genome Stability in Aging and at CECAD discovered that somatic niche cells that surround the PGCs control their response to DNA damage. The study "Somatic niche cells regulate the CEP-1/p53-mediated DNA damage response in primordial germ cells," has now been published in Developmental Cell.

"For more than a hundred years, inheritance of genetic information was thought to be autonomously controlled by the germ cells, explaining why acquired traits cannot be genetically inherited. Scientists believed that mutations occurring only in germ cells were responsible for any heritable genetic changes—be it during evolution or as cause of genetic disorders. Schumacher and his team now challenge this assertion.

"The DNA of an organism constantly gets damaged. Not only environmental influences, but also by-products of the body's energy metabolism damage the molecular structure of the genome in every cell. The scientists investigated how the genome integrity of PGCs is controlled. PGCs need to survey their genomes particularly rigorously because they give rise to all sperm or eggs of the organism. Damaged PGCs are particularly dangerous because they are hereditary and can lead to serious genetic disorders. PGCs thus need to stop dividing when their genomes are damaged until the DNA is repaired. Special niche cells are responsible for signalling to the PGCs that they need to stop dividing and repair before generating further germ cells. If they fail to do so, the PGCs might pass on dangerous mutations to the next generation.

"To fulfil this important function, the niche cells are in intimate contact with the PGCs and instruct them whether to divide and generate germ cells or whether to stay inactive. "This means that the body is responsible for controlling the integrity of heritable genomes," Schumacher remarked. "The parental body thus has somatic control over the integrity of PGC genomes, controlling the quality of the heritable genetic information." Since studying PGCs in mammals is a complicated endeavour, Schumacher's team used C. elegans as a simple animal model to shed new light on to how PGCs control the integrity of the genomes they will pass on to their offspring."

Comment: For original life to continue, DNA had to be protected from damage. This mechanism had to be present when first life started. Only design fits.

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8152 views

The DNA spirals read in opposite directions which increases the information carried:

https://evolutionnews.org/2019/08/the-genius-of-alternative-reading-frames/

Be sure to look at the illustration

***

"When you talk about the complementary strand you are talking about the same chromosome, but the opposite strand of DNA. DNA is made up of two strands of nucleotides running in opposite directions, and coiled about each other, the so called double helix. One strand has typically been called the coding strand because nearly all genes were thought to be encoded on that strand.

"But as techniques for detecting transcripts have gotten better, and scientists have begun to scan for “alternative reading frames,” they are finding them.

"If you look at the figure at the top of this post,you’ll see the sequence of DNA from a human mitochondrion: AAATGAACGAAA and so on. Above in red you see the nucleotides (ATCG) have been grouped in threes, and a letter assigned to each. Each group of three is a codon, and each unique codon specifics a particular amino acid, indicated by the red letters: K W T K I, etc. That is the protein sequence that the DNA specifies for that particular way of reading the DNA. That way of reading the DNA, with that set of groups of three, is called a reading frame, because it establishes the frame for the way we read the information in the gene. In this case it encodes the protein ATP8.

"If DNA were a human code, then it would be inconceivable to have a code that could be read in more than one frame at a time. By this I mean starting at one nucleotide and getting one sequence and starting at another nucleotide and getting another sequence with a different meaning.

"But that is exactly what happens in this stretch of mitochondrial DNA. Look below the nucleotides to a different set of letters in blue. Notice that they are offset from the first reading frame by two nucleotides. This changes the way the nucleotides are read. The first codon is ATG, the second AAC, and so on. And the resulting protein, ATP6, has a very different sequence from that of the first, ATP8.

"And for toppers it is also possible to start on the complementary strand and get yet another reading in the opposite direction. Theoretically it is possible to have a code that reads in all six frames, three forward and three reverse. We see overlapping genes in everything from viruses to humans, sometimes offset from each other on the same strand, and sometimes from the complementary strand.

"So in answer to your question, yes, it is possible to get some protein from the complementary strand as well as the “coding strand.” You can have more than one protein produced from the same stretch of DNA — and I haven’t even mentioned splicing yet… but I’ll leave that for another time.

"This is amazing! Here we have multiple meanings being read from one stretch of digital code. Here it is A T C G combinations, but on a computer it would be 01001, etc. Can anyone write a string of 0s and 1s that can be read in different frames and have each of those readings make sense?

"Only a design genius could do it."

Comment: Yes, only a designing cause is capable of this magnificent complexity of a code. This is taken from an author's answer to a question.

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8099 views

How the genome prepares for pre-mRNA splicing:

https://phys.org/news/2019-09-key-pre-mrna-splicing.html

"The study focuses on the pre-mRNA (precursor-messenger RNA) splicing process where regions in the pre-mRNA that do not encode proteins (referred to as introns) are removed by the spliceosome, a huge protein-RNA complex. Remaining sections of the RNA transcript, called exons, are then stuck back together. Pre-mRNA splicing is one of several essential steps that convert pre-mRNAs into mature mRNA (messenger RNA) for protein production.

***

"How the pre-mRNA splicing process works is still subject to intense investigation by scientists. Specifically, the mechanisms of how introns and exons are defined in a sea of pre-mRNAs and how circular RNAs are generated by a particular back-splicing process are fundamental unanswered questions in pre-mRNA splicing. Through their experiments, Zhao and her colleagues proposed a unified model explaining all three phenomena (intron definition, exon definition, and back-splicing) without the need of a different spliceosome for each process, that are supported by their extensive biochemical experiments.

"'Splicing of pre-mRNA is essential for gene expression in all eukaryotes," Zhao said. "In higher eukaryotes such as mammals, an average of 95 percent of the nucleotides in the primary transcript of a protein-encoding gene are introns. These introns need to be precisely removed by splicing before the mRNA can be transported out of the nucleus and translated. Even a single nucleotide error can cause catastrophic consequences. It has also become increasingly clear that alternative splicing is a fundamental approach for eukaryotic gene expression regulation.'"

Comment: Chop it up, spit it out and start all over again. The genome are extremely complex and to work properly had to be designed in just the right way. It isn't just simple instructions. Bits and pieces have to be put together in a meaningful way. How do the protein molecules know what they are doing as they slice up DNA? Not by Darwin.

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8019 views

A new study finds this is true across DNA's:

https://phys.org/news/2019-09-manual-genome-groups-genes-convenience.html

"Every living organism's cell has a complete copy of DNA, which is condensed tightly in chromosomes. Every time the cell needs to perform a function, it activates genes that open or close different regions in the DNA. Like following an instruction manual with consecutive pages, it's easier to activate two genes that are closer together to complete a function.

***

"'If genes for a specific biological process are placed near each other in the chromosome, they can co-regulate each other in a more coordinated and effective manner," says Gabaldón.
The scientists developed an algorithm capable of identifying genes near each other in genomes of different species according to their evolutionary history, i.e. looking for whether they were conserved clusters in different species of fungi, independently of the function they had. They predicted more than 11000 families of grouped genes in the genome. Of the 300 genomes analysed, they found that a third were part of a conserved group.

"'Natural selection means some genes are near each other for functional relevance. The way they're organized isn't random chance—they have been selected because it makes regulating genes easier. We've found that it's pretty common, and that it affects an important proportion of the genome," says Gabaldón. "The selective forces favor the conformations of genes that allow a smaller investment in energy and improved regulatory processes," he adds.

"Previous studies of gene groups linked to secondary metabolism observed that they had a switch, a type of transcription factor, to turn them on and off. Other observations also found that these gene groups passed from one species to another in block, known as horizontal transfer, though no one knew why.

"The CRG scientists have now provided evidence that horizontal transfer may be less common than previously thought, and their most recent findings don't represent what the genome does as a whole. They saw that a cluster made up of the same groups of genes appeared independently twice, in parallel distant lineages.

"Surely, the groups of genes carry out a specific function. "When you need something at a precise moment, it's when you most need it to be co-regulated. A general function, which is active most of the time, doesn't need such precise regulation," says Marina Marcet-Houben, first author of the study."

Comment: Ease of function is a purposeful design mechanism, and fits my thought about pre-programming by design.

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7909 views

A protein complex in cells directs gene expression:

https://phys.org/news/2019-09-insight-cells-identity.html

"All of the more than 200 different cell types in our body contain the same DNA. Which of those genes that are expressed determine each cell type. Therefore, it is essential that the activity of the genes is controlled with great precision.

"Thus, a stem cell may develop into anything from a skin to a bone cell, depending on which parts of the genome are expressed.

***

"One of the key protein complexes that regulates whether genes are turned on or off is called PRC2. To ensure that the complex binds to the right places in the genome, a number of other proteins are associated to PRC2.

"In the recently published article, the research group has studied the importance of six different proteins associated with PRC2, and the group has shown that all six proteins help direct PRC2 to the right places in the genome.

"In 15 different combinations, the researchers removed the associated proteins from embryonic stem cells one by one. In this way, the researchers were able to study the contribution of each protein to the activity and binding of the PRC2 complex to specific areas. It was found that the ability to find the way to the right places in the genome remained intact until all six associated proteins were removed from the stem cells.

"That finding surprised the researchers, says the study's lead author, Postdoc Jonas Højfeldt:

"We assumed that each of the associated proteins was responsible for its own area to where the PRC2 complex should be guided. Instead, we saw that they all contributed to the places where the complex binds. As long as just one of the associated proteins were left, the ability remained intact," he says."

comment: The importance of activating the correct genes in each cell is backed up by a complex of six special proteins each of which can do the job. Such a system has to be designed, and cannot develop by chance. How does a mindless mechanism recognize the need for such an important backup system?

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7881 views

It is a highly complex series of different specialized proteins and gene controls. All animals age and have rates of end of life:

https://www.quantamagazine.org/longevity-linked-to-proteins-that-calm-overexcited-neuro...

"...recently in Nature, Bruce Yankner, a professor of genetics and neurology at Harvard Medical School, and his colleagues reported on a previously overlooked controller of life span: the activity level of neurons in the brain. In a series of experiments on roundworms, mice and human brain tissue, they found that a protein called REST, which controls the expression of many genes related to neural firing, also controls life span. They also showed that boosting the levels of the equivalent of REST in worms lengthens their lives by making their neurons fire more quietly and with more control. How exactly overexcitation of neurons might shorten life span remains to be seen, but the effect is real and its discovery suggests new avenues for understanding the aging process.

***

"A key early finding was that the inactivation of a gene called daf-2 was fundamental to extending the life span of the worms. “daf-2 mutants were the most amazing things I had ever seen. They were active and healthy and they lived more than twice as long as normal,”

***

"This gene and a second one called daf-16 are both involved in producing these effects in worms. And as scientists came to understand the genes’ activities, it became increasingly clear that aging is not separate from the processes that control an organism’s development before the age of sexual maturity; it makes use of the same biochemical machinery. These genes are important in early life, helping the worms to resist stressful conditions during their youth. As the worms age, modulation of daf-2 and daf-16 then influences their health and longevity.

***

"...REST, which turns genes off, was mainly known for its role in the development of the fetal brain: It represses neuronal genes until the young brain is ready for them to be expressed.
But that’s not the only time it’s active. “We discovered in 2014 that [the REST gene] is actually reactivated in the aging brain,” Yankner said.

***

"Because REST was plentiful in the brains of long-lived people, the researchers wondered if lab animals without REST would have more neural firing and shorter lives. Sure enough, they found that the brains of elderly mice in which the Rest gene had been knocked out were a mess of overexcited neurons, with a tendency toward bursts of activity resembling seizures. Worms with boosted levels of their version of REST (proteins named SPR-3 and SPR-4) had more controlled neural activity and lived longer. But daf-2 mutant worms deprived of REST were stripped of their longevity.

***

"What’s more, Yankner and his colleagues found that in worms the life extension effect depended on a very familiar bit of DNA: daf-16. This meant that REST’s trail had led the researchers back to that highly important aging pathway, as well as the insulin/IGF-1 system. “That really puts the REST transcription factor somehow squarely into this insulin signaling cascade,” said Thomas Flatt, an evolutionary biologist at the University of Fribourg who studies aging and the immune system. REST appears to be yet another way of feeding the basic molecular activities of the body into the metabolic pathway."

Comment: Obviously all organisms must die, or the Earth becomes overpopulated. Besides the carcasses are good food for survivalThis design to accomplish the end of life illustrates how information is exchanged between cells and genes. The cells are programmed to produce those special proteins which then carry the instructions/information turning gens on and off. Only a designer can create this.

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7434 views

To find all the patterns and layers in DNA it requires massiv e computer analysis:

http://cshl.nautil.us/article/488/making-sense-of-the-genome-at-last?utm_source=Nautilu...

"The presenter of a TED talk—a biologist named Riccardo Sabbatini [went] onto the stage to explain the staggering amount of information in the human genetic code. As people began to applaud, five assistants emerged from the wings, wheeling carts containing 175 encyclopedia-size books onto the stage...inside those books were 262,000 pages containing the 3 billion DNA letters of the eminent man’s genome—“the visual perception of the code of life.” The audience gasped when Sabbatini cracked open one of the books: Even stretched out over 175 volumes, the letters had to be written so small that each page resembled a black square filled with dots.

***

"Now, software-literate computational biologists are harnessing advances in machine learning and data mining to begin to do what the human mind alone could not. They are running comparisons between individuals and between species, seeking out meaningful patterns. They are identifying which portions of the genome, when mutated, are most likely to cause disease. And some have begun applying new analytical tools to saving lives.

***

"...it fell to Siepel to design a program that transformed the cross-species comparison into a searchable database. The goal was to let researchers around the globe type in specific genetic sequences and receive a result predicting how likely that sequence was to have some functional importance. Kent and his team reasoned that if a certain chunk of DNA appears nearly the same across divergent species—if it is “highly conserved,” in genetics terminology—it must crucial for life.

***

"Siepel’s LINSIGHT project will be important in filling in information about the whole of the human genome, not just the 1 percent that has a well-understood biological function. Meanwhile, intolerance scoring will help by identifying the parts of the human genome that are most likely to be associated with disease—based entirely on computer-driven data analysis, without any human assumptions or biases in the mix. Goldstein thinks that scientists will need to compile and compare genes from millions of people before an AI can usefully analyze your whole genetic makeup, identify problems, and point to specific treatments.

“'So for those of us who consider ourselves informed experts in the interpretation of genomic variation, I think we still have jobs for at least five plus years,” he says. After that, though, an even greater revolution awaits."

Comment: No natural process could invent the DNA code, as complex as it is just to designate protein production, but it also has underlying significant patterns as a deeper set of layers. If the clever human mind cannot do it by itself and it requires super computers, the conclusion must be that it required a super mind by as super designer.

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7429 views

DAVID: No natural process could invent the DNA code, as complex as it is just to designate protein production, but it also has underlying significant patterns as a deeper set of layers. If the clever human mind cannot do it by itself and it requires super computers, the conclusion must be that it required a super mind by as super designer.

Impeccable logic, which every atheist should be made to study. It is a major reason why agnostics like myself cannot embrace atheism. However, as you know, the question of how an infinite, eternal, all-powerful, unknown, hidden supermind could come into being is just as great a mystery as how the complexities of the DNA code could assemble themselves. The philosophical cop-out of “first cause” can be equally applied to an infinite and eternal supermind and to an infinite and eternal mass of ever changing materials which would eventually produce the combination necessary for life and evolution.

Post reply

7446 views

DAVID: No natural process could invent the DNA code, as complex as it is just to designate protein production, but it also has underlying significant patterns as a deeper set of layers. If the clever human mind cannot do it by itself and it requires super computers, the conclusion must be that it required a super mind by as super designer.

dhw Impeccable logic, which every atheist should be made to study. It is a major reason why agnostics like myself cannot embrace atheism. However, as you know, the question of how an infinite, eternal, all-powerful, unknown, hidden supermind could come into being is just as great a mystery as how the complexities of the DNA code could assemble themselves. The philosophical cop-out of “first cause” can be equally applied to an infinite and eternal supermind and to an infinite and eternal mass of ever changing materials which would eventually produce the combination necessary for life and evolution.

Since such complexity can only be created by mental planning, the only logical possibility is a planning mind.

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7412 views

In what was so-called junk DNA, it is found transposons, jumping genes, can make functional ribozymes:

https://phys.org/news/2019-12-reveals-role-genes-stress.html

"Only percent of human DNA codes for proteins, and approximately half of the rest of the genome is made up of what used to be called "junk" sequences that can copy themselves into RNA or DNA and jump from one location to another. Previous research led by investigators at Massachusetts General Hospital (MGH) had revealed a critical role for one of these jumping genes during times of stress.

***

"The sequences that jump from place to place in the genome are more formally known as transposable elements, and their role in health and disease is not fully understood. But it has long been suspected that they are more than just parasitic elements without good function. In their original study, Jeannie Lee, MD, Ph.D., an investigator in the Department of Molecular Biology at MGH, and her colleagues found that one of these transposable elements—a very abundant, short interspersed nuclear element (SINE) called B2 in mice (ALU in humans)—makes an RNA that is cut when together with a protein called EZH2. However, at the time, they did not know how the RNA is cut. Researchers now make the striking discovery that B2 and ALU cut themselves.

***

"Today, 15 classes of ribozymes have been described, but they are mostly observed in bacteria and viruses. Very few are known in mammals such as humans, and their functions are mostly unclear.

"Because B2 and ALU are so abundant in our cells, the Lee group's discovery puts a new twist to the ribozyme story. "B2 and ALU are present in hundreds of thousands of copies in our DNA and they become massively expressed during stress. This is a mind-boggling amount of ribozyme activity," said Lee. The team found that B2 and ALU are normally silent, but when subjected to heat or other forms of stress, they become activated. Also, their RNA-cutting activity is enhanced by an interaction with the EZH2 protein.

"Lee noted that cells are continually challenged by stress, and a swift response can mean the difference between life and death. "Hinging the induction of stress-related genes to self-cutting RNAs seems highly adaptive," she said. "No new synthesis of gene products would be required and the critical event would instead be the recruitment of a protein factor, EZH2, that already exists inside cells and stands ready to be mobilized.'"

Comment: The genome is like an onion, layers and layers of control discovered and stil to be discovered. This complexity is not the result of chance evolution.

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7348 views

Coiling DNA around histone spools requires chaperone molecules, one of which uses ATP for energy:

https://www.sciencedaily.com/releases/2020/01/200107104936.htm

"The genetic material of our cells -- DNA -- exists in a high-order structure called "chromatin." Chromatin consists of DNA wrapped around histone proteins and efficiently packs DNA into a small volume. Moreover, using a spool and thread analogy, chromatin allows DNA to be locally wound or unwound, thus enabling genes to be enclosed or exposed.

***

'"In order to carefully control the assembly and disassembly of chromatin units, histone chaperones act as molecular escorts that prevent histone aggregation and undesired interactions,"

***

"Song and his team looked to Abo1, the only known histone chaperone that utilizes cellular energy (ATP). While Abo1 is found in yeast, it has an analogous partner in other organisms, including humans, called ATAD2. Both use ATP, which is produced through a cellular process where enzymes break down a molecule's phosphate bond. ATP energy is typically used to power other cellular processes, but it is a rare partner for histone chaperones.

***

"The researchers found through real-time observation that Abo1 is ring-shaped and changes its structure to accommodate a specific histone and deposit it on DNA. Moreover, they found that the accommodating structural changes are powered by ADP.

"'We discovered a mechanism by which Abo1 accommodates histone substrates, ultimately allowing it to function as a unique energy-dependent histone chaperone," Song said. "We also found that despite looking like a protein disassembly machine, Abo1 actually loads histone substrates onto DNA to facilitate chromatin assembly.'"

Comment: Once again we see a very complex control mechanism using very specific proteins which have a very specific function ability. It cannot be assembled stepwise but all at once, since it is irreducibly complex, and all parts have to be designed and put together at the same time.

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7240 views

A very specialized cellular system to remove damaged RNA due to misfolding and other causes:

https://phys.org/news/2020-02-fundamental-discovery-gene.html

"Researchers at Johns Hopkins Bloomberg School of Public Health have discovered a fundamental mechanism that regulates gene activity in cells. The newly discovered mechanism targets RNA, or ribonucleic acid, a close cousin of DNA that plays an important role in cellular activity.

***

"The newly discovered mechanism effectively silences or dials down certain active genes as a basic cellular regulatory or quality-control system. It may even act as a defense against viruses. When genes are active, they are copied out into strands of RNA. These RNA strands perform cellular functions on their own or are translated into proteins. The new mechanism destroys RNA strands that have excessively folded over and stuck to themselves to form knots, hairpins, and other structures. These highly structured RNAs can occur during normal processing but could possibly also be caused by misfolding.

***

"Most of the regulatory and quality-control mechanisms that modulate the levels of RNAs in cells target RNAs containing specific sequences of nucleotides—the building blocks of RNAs. The newly discovered mechanism is unique in that it recognizes not sequences but a broad variety of structures formed where RNA strands, which are relatively sticky, have folded back onto themselves.

"Leung and his team discovered the new mechanism while investigating a protein called UPF1, which is known to work in other RNA regulation pathways. They found that UPF1 and a partner protein called G3BP1 work together in the new mechanism, targeting only RNAs that contain a high level of structures. When the researchers depleted UPF1 or G3BP1 from cells to shut off the new mechanism, levels of highly structured RNAs rose sharply. The team also confirmed that the new mechanism, which they call structure-mediated RNA decay, is distinct from all other known RNA-removal mechanisms and works across different types of RNA throughout the genome.

"'Based on further analyses, we predict that this structure-mediated RNA decay pathway could regulate at least one-fourth of human protein-coding genes and one-third of a class of non-coding genes called circular RNA," Leung says."

Comment: Cells are constantly reproducing themselves so life has to be designed to correct genome mistakes and this is such a required complex design.

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7204 views

How do 20,000 +/- genes create many billions of human proteins? through alternative splicing of the genes:

https://www.the-scientist.com/features/alternative-splicing-provides-a-broad-menu-of-pr...

"Seventeen years ago, the completion of the Human Genome Project revealed that there are around 20,000 protein-coding genes in the human genome—a puzzling result, given our intricate biology. Thanks to the advancement of large-scale proteomic studies over the decade following that milestone, researchers realized that some human cells contain billions of different polypeptides. Researchers realized that each gene can encode an array of proteins. The process of alternative splicing, which had first been observed 26 years before the Human Genome Project was finished, allows a cell to generate different RNAs, and ultimately different proteins, from the same gene. Since its discovery, it has become clear that alternative splicing is common and that the phenomenon helps explain how limited numbers of genes can encode organisms of staggering complexity. While fewer than 40 percent of the genes in a fruit fly undergo alternative splicing, more than 90 percent of genes are alternatively spliced in humans. (my bold)

"Astoundingly, some genes can be alternatively spliced to generate up to 38,000 different transcript isoforms, and each of the proteins they produce has a unique function. Like the chapters of a book, coding segments of the genome, known as exons, appear in series, and alternative splicing works by including or leaving out some of these genomic passages. Some chapters are required—that is, they are found in every transcript—and some are optional, so-called alternative exons. The differential splicing of these regions from an RNA transcript creates customized and condensed genetic messages. Molecular editors control the complicated flurry of exon selection by recognizing the chapters needed for a given protein and discarding the others. The final arrangement of exons in a spliced RNA molecule shapes the resulting protein’s structure and function.

***

"Still, from an evolutionary perspective, the idea of RNA splicing seemed bizarre to some researchers. In September of 2003, the Encyclopedia of DNA Elements (ENCODE) project was launched to identify the functional elements in the human genome, and the effort ignited controversies as to whether introns were genetic “junk” that the cell invested precious energy and resources to transcribe only to trash prior to translation. Alternative splicing gave these seemingly nonfunctional elements an essential role in gene expression, as evidence emerged over the next few years that there are sequences housed within introns that can help or hinder splicing activity. These enhancer and silencer sequences are recognized by RNA-binding proteins (RBPs) whose presence affects spliceosome docking and assembly. The RBPs allow exons or portions of exons to be combined or skipped in unique patterns, such that a single transcript can be spliced into several possible mature mRNA isoforms, or splice variants, each translated into proteins with potentially diverse functions. (My bold)

***

"While some details of the mechanisms of splicing remain to be worked out, it’s known that mature, edited mRNAs result from an interplay between multiple factors within and outside the transcript itself. Among these is the spliceosome, the machinery that carries out the splicing.

***

"A variety of factors affect how transcripts from a particular gene are spliced. Exon recognition by the spliceosome can be influenced by RNA binding proteins (RBPs), which bind to enhancer and silencer motifs within the mRNA and help or hinder spliceosome recognition of the splice sites. And because pre-mRNAs are frequently spliced as they’re transcribed, the speed of transcription by RNA polymerase II further tunes the window of opportunity for splice site recognition by the spliceosome."

Comment: We all knew there had to be hidden levels of genome functionality. We see a portion of it in this research as more 'junk' DNA disappears. Anyone who denies that this is designed is not thinking logically. Note how prominent this is in humans compared to fruit flies. Another discovery that shows how special we are.

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7216 views

A new layer of genome information controls found at the RNA level. The genome is so precise logically there are many more layers of the onion to be found:

https://sciencenorway.no/cells-dna-rna/rna-scientists-have-discovered-a-new-layer-in-th...

"Although genes themselves don’t change, they can be regulated.

"They are turned on and off as we grow and develop. These changes are influenced by our surroundings, so we actually change over the course of our lives. And some of these changes in regulation are passed on to our children.

"Figuratively speaking, our DNA can be described as the recipe book for who and how we are, while epigenetic regulation can be seen as notes that have been pencilled into the margin.

"Epigenetics thus describes a fascinating layer of information and regulation of our genes that enables us to adapt to new environments much faster than via normal evolution.
But lately, scientists have seen evidence of something more.

***

"Initially, researchers thought that RNA worked like a dutiful but slightly boring cook, one that follows the recipe exactly.

But lately, scientists have begun to rethink this idea. RNA appears to be making its own modifications to the DNA recipes.

***

"...several research groups had devised techniques for mapping and investigating a type of RNA modification, called 6-methyladenine (m6A).

"Three different studies, including one that Klungland was involved in, made it clear that these changes could be turned on and off.

"The m6A tags were attached to specific regions of RNA and appeared to be important. Attaching and removing m6A at the right time seemed to be absolutely necessary in some situations, such as in foetal development.

"Gradually, more and more scientists have begun to believe in the existence of something they call epitranscriptomics — that is, epigenetics for RNA, which in turn affects how the information in our DNA is used in practice.

***

“'Together, these new studies reveal a whole new level of gene expression regulation,” wrote Margarita Angelova and her colleagues in Frontiers in Bioengineering and Biotechnology in 2018.

At the same time, researchers have warned that so far, we know very little about what these modifications are doing.

"In addition to m6A, researchers have found about 150 other alterations to RNA. Klungland agrees that there’s a lot we don’t know, such as what actually controls these alterations.
"Epigenetic changes in DNA are clearly influenced by the environment, but we do not know if this is the case with modifications in RNA," he says. “I wouldn't be surprised if the environment was also controlling RNA modification, but this is difficult to study.”

"Unlike DNA, RNA in a cell is volatile. The RNA molecules are formed and dissolved in one go. This makes it much more difficult to assess them to find out how they behave and what affects them.

“But it’s conceivable that these RNA modifications are a way to make rapid, temporary changes in how genes are expressed,” says Klungland.

***

"Klungland and his colleagues have recently published research showing that modifications to RNA must be correct for DNA to work.

"A special m6A modification is needed when RNA separates the strands in DNA and copies a recipe. But it is equally important that the tag be removed again afterwards. If not, the DNA can be damaged.

Both mice and humans get sick if RNA tags aren’t added and removed at the right time, he said.

“'This can lead to both cancer and neurodegenerative disease,” Klungland says.
When he and his colleagues did an experiment where RNA modifications were not read properly, it turned out that fertilized eggs in live mice were unable to develop.

"This means that changes in RNA are a fundamental function of the body. A fundamental mechanism that was completely unknown just a few years ago."

Comment: Biochemistry in living organisms is precisely controlled. One simple example is the sodium level in blood never changes, despite what you eat or drink. All of the controls in the body are this precise, automatic, no cellular intelligence involved just following instructions from the layers of information in the genome through molecular reactions.

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7141 views

This creates a problem for the theories of common descent in which all DNA must represent the past genomes:

https://www.sciencedaily.com/releases/2020/02/200218104740.htm

"Scientists from Trinity College Dublin and the University of Pittsburgh have discovered that de novo genes -- genes that have evolved from scratch -- are both more common and more important than previously believed.

***

"the scientists devised a way of assessing just how frequently genes seem to evolve from scratch. Their results were surprising.

"Explaining de novo genes, first author on the paper, Nikolaos Vakirlis, Trinity, said: "Most of the genes in a genome have 'cousins' in the genomes of other species; genes made up of similar DNA sequences that, once translated into proteins, perform similar functions. However, some genes are unique and can only be found in a single, or small number of closely related species. We call these 'orphan genes' because they appear to have no relatives and are often responsible for unique characteristics and abilities of organisms.

***

"'To our surprise, at most, around one third of orphan genes result from divergence. So, in turn, this suggests that most unique genes in the species we looked at are the result of other processes, including de novo emergence, which is therefore much more frequent than scientists initially thought."

***

"...how can a gene that was never used before suddenly appear and play a major role?
This paradox can be resolved if emerging genes have high potential to be beneficial for the organism. So, while they are expected to play no particular role in their current form, random changes that affect their sequences or increase the amount of protein they produce when translated should lead to beneficial effects.

"The scientists tested whether this hypothesis may be true by doing a series of biological and computational experiments using baker's yeast as a model organism. And when they artificially allowed emerging sequences to be expressed at higher levels than they are naturally, the cells tended to grow faster.

"Importantly, growth was not enhanced by overexpressing established genes. So, emerging sequences do indeed carry the potential to be important to the cells.

"We found that simple order is rampant everywhere in the genome. The propensity to make simple shapes that are stable is already there, waiting to be exposed. De novo gene birth is thus becoming less and less mysterious as we better understand molecular innovation."

Comment: the bolds just an assumption based on hope and wishful thinking. Of course the useful orphans when useful were quickly expressed, but the study did not show why they should spontaneously appear from no antecedent DNA. True de novo is true de novo.

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7092 views

Just as our cells self-modify DNA to perform specific functions, squid are found to modify DNA in their neurons:

https://academic.oup.com/nar/advance-article/doi/10.1093/nar/gkaa172/5809668

Title of article: "Spatially regulated editing of genetic information within a neuron"

"Abstract
In eukaryotic cells, with the exception of the specialized genomes of mitochondria and plastids, all genetic information is sequestered within the nucleus. This arrangement imposes constraints on how the information can be tailored for different cellular regions, particularly in cells with complex morphologies like neurons. Although messenger RNAs (mRNAs), and the proteins that they encode, can be differentially sorted between cellular regions, the information itself does not change. RNA editing by adenosine deamination can alter the genome’s blueprint by recoding mRNAs; however, this process too is thought to be restricted to the nucleus. In this work, we show that ADAR2 (adenosine deaminase that acts on RNA), an RNA editing enzyme, is expressed outside of the nucleus in squid neurons. Furthermore, purified axoplasm exhibits adenosine-to-inosine activity and can specifically edit adenosines in a known substrate. Finally, a transcriptome-wide analysis of RNA editing reveals that tens of thousands of editing sites (>70% of all sites) are edited more extensively in the squid giant axon than in its cell bodies. These results indicate that within a neuron RNA editing can recode genetic information in a region-specific manner."

In the discussion:

"Data from this paper suggest that region-specific RNA editing occurs in squid axons. We base this claim on the following findings: (i) SqADAR2 protein is present in the cytoplasm of nerve cell bodies in both the SG of the PNS and the OL of the CNS; (ii) axoplasm from the GA can catalyze the hydrolytic deamination of A→I in a perfect RNA duplex; (iii) axoplasm from the GA can catalyze site-specific RNA editing in a squid K+ channel substrate; and (iv) RNA editing at known sites is generally higher in the GA than its cell bodies. Editing almost certainly occurs in the nucleus as well. SqADAR2 is clearly present in many nuclei across the regions of the nervous system that were surveyed in this study. Therefore, based on these data we cannot exclude the possibility that all editing occurs in the nucleus and that edited messages bound to SqADAR2B get preferentially sorted to the axon.

***

"In this study, we examined differential editing between two regions: the GFL somata and the initial segment of the GA. SqADAR2 was seen, however, in the synaptic zone of the OL’s plexiform layer as well. It should be noted that the RNA isolated from the GA could have been in transit to other regions. The extent to which it is edited once reaching its destination, or whether it gets edited further after arriving, is unknown. Thus, it is likely that region-specific editing is more complicated in cephalopods than our data have uncovered. Does extranuclear recoding occur in other organisms? ADAR localization has only been examined in a few cases, under a small number of experimental conditions. Even in mammals, ADAR1 p150 is expressed in the cytoplasm and editable substrates occur within mature mRNAs. How this process is regulated in cephalopods should shed light on how RNA editing can be used to tune cellular physiology"

Comment: The octopus is known to do the same thing:

"The octopus has a very large genome and can edit their own genomes, altering their RNA. They “ do not always follow their genetic instructions to the letter:'”

https://mindmatters.ai/2018/09/is-the-octopus-a-second-genesis-of-intelligence/

So we see Shapiro's bacterial work passed on in evolution, but not speciation so far. The authors are surprised how much is done outside the nucleus itself. Note the title reference to 'genetic information'.

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7085 views

Another editorial review:

https://www.sciencenews.org/article/squid-edit-their-genetic-material-uniquely-weird-place

"Longfin inshore squid (Doryteuthis pealeii) are the first known animals that can tweak strings of RNA outside of a nerve cell’s nucleus. These genetic couriers, called messenger RNA, or mRNA, carry a cell’s blueprints for building proteins.

"The squids’ ability to make genetic edits in cytoplasm, the jellylike material that makes up much of a cell, may let the animals make adjustments to mRNAs on the fly. That skill could help squids produce proteins tailored to meet a cell’s needs and hone crucial cell processes, researchers report March 23 in Nucleic Acids Research.

***

'In the new study, Rosenthal and colleagues first looked at where an mRNA-editing protein is found in squid nerve cells, or neurons. The team discovered that the protein, called ADAR2, is located in both the jellylike cytoplasm and the nucleus of squid neurons, a hint that the protein could edit mRNAs in both areas.

"The team then extracted cytoplasm from squid axons — the slender stalk of a neuron — “kind of like you’re squeezing toothpaste out of the tube,” Rosenthal says. ADAR2 extensively edited an mRNA within the cytoplasm siphoned from the axons, which help send electrical impulses along nerve cells, the researchers found."

Comment: Editing from RNA reactions the cytoplasm instead of direct change in the nucleus is an unusual new finding.

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6963 views

Latest paper finds this phenomenon is everywhere:

https://phys.org/news/2020-03-free-range-mitochondria.html

"Transfer of mitochondria between cells is a ubiquitously occurring and now universally known phenomenon. For years, researchers have been serially demonstrating that one particular new cell type can transfer its mitos to yet another particular cell type to achieve some specific metabolic goal essential to survival of the meta-host organism. But what happens when the mitochondria come from the outside world, from other members of your own species, or from a different species altogether? In addressing this very real situation, we first must look at the particulars of how and why mitos are transmitted across cell boundaries in the first place.

"One of the latest dispatches,... describes a curious situation in which mesenchymal stem cells (MSCs) transfer mitos directly to T cells in order to tamp down an overactive immune system and curb an inflammatory response. More specifically, the Chilean authors report that mito uptake by CD+ T cells induces regulatory T cell differentiation and activation through increased expression of FOXP3, IL2RA, CTLA4, and TGFb mRNAs. Mesenchymal stem cell transfer had been well established in earlier disease models of acute respiratory distress (ARDs), in which transfer to macrophages through tunneling nanotubes upregulates their phagocytic capability.

***

"The key is understanding how the mitos actually travel. In other words, what are the mitochondrial circuits? Many clues have recently emerged, including what mitos are capable of doing when they cycle through the master of all networks—the nervous system. The one-way travel to macrophages described above does not necessarily end there. Macrophages can, in turn, donate their mitos directly to nerve endings in times of need. Once there, they can do some incredible things. For example, in sensory neurons of the DRG (dorsal root ganglion) mitos ultimately derived from M2 macrophages turn off the inflammation response and completely resolve the associated pain messaging. This leg of the circuit requires expression of CD200 Receptor (CD200R) on macrophages and the non canonical CD200R-ligand iSec1 on sensory neurons.

"Perhaps even more intriguingly, these mitos also have a side-hussle—they
briefly sojorn as free range mitochondria in whole blood. During these sabbaticals, they persist entirely cell free, but still respiratory competent mitochondria. What this essentially means is that when we donate and receive blood or bone, we are also exchanging not just mitochondria, but also in a very real genetic sense, our identities—at least as defined within the limits of current forensic testing of this mosaic-chimeric state. No one should be all that surprised, because our species is also on the cusp of being actively engaged in a subtle but perhaps more insidious trans-species mitochondrial migration through organ transplant."

Comment: Mitochondrias are as free-ranging as Margulis might have imagined when she proposed her theory. They must play some sort of a role in speciation. This article is actually about using them in therapy.

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6941 views

It requires a specialized protein:

https://cosmosmagazine.com/biology/how-cells-access-data-from-genetic-cotton-reels?utm_...

"Australian geneticists have unravelled part of the mystery about how nature can usefully access genetic information in cells despite it being so tightly packed away.

"The discovery, they say, helps solve what is effectively an input/output problem caused by the need for cells to pack metres of DNA into a space just millionths of a metre across while at the same time reading, copying and repairing the information held in the DNA.

"It also helps provide pathways to understand how defects in this process contribute to diseases such as schizophrenia and cancer.

"Writing in the journal Nature Communications, a team led by Joel Mackay from the University of Sydney reveals that a particular motor protein, CHD4, is used to access genetic information tightly spooled onto what can be imagined as “genetic cotton reels”.

“'This protein effectively remodels our DNA to allow access to the information that determines the fate of a cell and its ability to respond to signals from the outside,” Mackay says.

“'It is a critical protein for almost all the work that cells do, including cell division and DNA repair.”

"Mackay adds that understanding this process is critical for developing treatments for neurodevelopmental disorders and some cancers.

“These illnesses are in part triggered by defects in the remodelling of the DNA that is driven by this process,” he says.

“'The protein CHD4 and its close partners are emerging as important risk factors in polygenic neurodevelopmental disorders, schizophrenia and bipolar disorder, as well as in rare monogenic disorders, such as GAND, which causes severe mental disability.”

"Mutations in the CHD4 protein that impair its function are also associated with endometrial carcinoma."

From an abstract of the study:

https://www.nature.com/articles/s41467-020-15183-2

"We demonstrate that the binding energy for CHD4-nucleosome complex formation—even in the absence of nucleotide—triggers significant conformational changes in DNA at the entry side, effectively priming the system for remodelling. During remodelling, flanking DNA enters the nucleosome in a continuous, gradual manner but exits in concerted 4–6 base-pair steps. This decoupling of entry- and exit-side translocation suggests that ATP-driven movement of entry-side DNA builds up strain inside the nucleosome that is subsequently released at the exit side by DNA expulsion."

Comment: Another very complex mechanism that is irreducibly complex and could not have been built step-by-step by chance activity. Design reqired.

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6951 views

A high speed method captures how a complex enzyme does its work, and it is ot as previously thought:

https://phys.org/news/2020-03-biochemists-visualize-enzyme.html

"The enzyme, ribonucleotide reductase (RNR), is responsible for converting RNA building blocks into DNA building blocks, in order to build new DNA strands and repair old ones... But for decades, scientists struggled to determine how the enzyme is activated because it happens so quickly. Now, for the first time, researchers have trapped the enzyme in its active state and observed how the enzyme changes shape, bringing its two subunits closer together and transferring the energy needed to produce the building blocks for DNA assembly.

***

"It wasn't until the Drennan lab gained access to a key technological advancement—cryo-electron microscopy—that they could snap high-resolution images of these "trapped" enzymes from the Stubbe lab and get a closer look.

***

"The combination of these techniques allowed the team to visualize the complex molecular dance that allows the enzyme to transport the catalytic "firepower" from one subunit to the next, in order to generate DNA building blocks. This firepower is derived from a highly reactive unpaired electron (a radical), which must be carefully controlled to prevent damage to the enzyme. (my bold)

***

"'Before this study, we knew this molecular dance was happening, but we'd never seen the dance in action," he says. "But now that we have a structure for RNR in its active state, we have a much better idea about how the different components of the enzyme are moving and interacting in order to transfer the radical across long distances."

"Although this molecular dance brings the subunits together, there is still considerable distance between them: The radical must travel 35-40 angstroms from the first subunit to the second. This journey is roughly 10 times farther than the average radical transfer, according to Drennan. The radical must then travel back to its starting place and be stored safely, all within a fraction of a second before the enzyme returns to its normal conformation."

Comment: my bold is the key point: fine-tuned control of a dangerous radical (electron on the loose but really not). Not by chance from hunt and peck. There must be a designer. If Darwin had known these facts, his book would not be written in the same way. Darwinism must be preserved to support atheism.

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6935 views

DAVID: […] fine-tuned control of a dangerous radical (electron on the loose but really not). Not by chance from hunt and peck. There must be a designer. If Darwin had known these facts, his book would not be written in the same way. Darwinism must be preserved to support atheism.

Of course his book would have been different, but I wish you wouldn’t lump all his ideas together, as if they are all invalid. Darwin’s theory deals with Chapter Two of life, not with the origin – and that means not with the origin of the mechanisms that enable life, reproduction and evolution. I suspect that being an agnostic, he would have acknowledged all your arguments for design. None of them contradict the theory of common descent or of natural selection as the process that determines which organs and organisms survive. Darwinism does not support atheism. It is neutral. Not even the theory of random mutations and gradualism, which you and I both reject, supports atheism! That was the astonishing discovery I made when I was a schoolboy, and it still astonishes me that so many highly educated people think of it as atheistic.

Post reply

6923 views

DAVID: […] fine-tuned control of a dangerous radical (electron on the loose but really not). Not by chance from hunt and peck. There must be a designer. If Darwin had known these facts, his book would not be written in the same way. Darwinism must be preserved to support atheism.

dhw: Of course his book would have been different, but I wish you wouldn’t lump all his ideas together, as if they are all invalid. Darwin’s theory deals with Chapter Two of life, not with the origin – and that means not with the origin of the mechanisms that enable life, reproduction and evolution. I suspect that being an agnostic, he would have acknowledged all your arguments for design. None of them contradict the theory of common descent or of natural selection as the process that determines which organs and organisms survive. Darwinism does not support atheism. It is neutral. Not even the theory of random mutations and gradualism, which you and I both reject, supports atheism! That was the astonishing discovery I made when I was a schoolboy, and it still astonishes me that so many highly educated people think of it as atheistic.

I'll accept common descent, but natural selection is a tautology that is not proven within itself nor as a possible cause of speciation.

Post reply

6899 views

Mutations can be good or bad and editing is very important:

https://evolutionnews.org/2020/03/more-hints-of-order-in-the-genome/

"... biochemists are finding that the differences in spelling are not just background noise; they alter the protein’s folding. Is that good or bad?

“'Synonymous mutations were long considered to be genomic background noise, but we found they do indeed lead to altered protein folding, and in turn impair cell function,” said Patricia Clark, the Rev. John Cardinal O’Hara professor of biochemistry. “Our results show that synonymous variations in our DNA sequences — which account for most of our genetic variation — can have a significant impact on shaping the fitness level of cellular proteins.”

"Surely many of these mutations are harmful, as are random mutations in humans that cause genetic disease. But E. coli has been around for a long time. Wouldn’t the species have gone extinct by now with the accumulation of defective spellings if they are always deleterious? Other work has suggested a “secret code” in synonymous variations that fine-tunes expression rates or regulates the supply of a given protein based on environmental conditions:

"Synonymous codon substitutions alter the mRNA coding sequence but preserve the encoded amino acid sequence. For this reason, these substitutions were historically considered to be phenotypically silent and often disregarded; it has become clear that synonymous substitutions can significantly alter protein function in vivo through a wide variety of mechanisms that can change protein level, translational accuracy, secretion efficiency, the final folded structure and posttranslational modifications.

***

"Bulock et al., have found one duplication enzyme that proofreads itself while proofreading its partner! “DNA polymerase δ proofreads errors made by DNA polymerase ε,” the paper is titled.

"Polδ and Polε are the two major replicative polymerases in eukaryotes, but their precise roles at the replication fork remain a subject of debate. A bulk of data supports a model where Polε and Polδ synthesize leading and lagging DNA strands, respectively. However, this model has been difficult to reconcile with the fact that mutations in Polδ have much stronger consequences for genome stability than equivalent mutations in Polε. We provide direct evidence for a long-entertained idea that Polδ can proofread errors made by Polε in addition to its own errors, thus, making a more prominent contribution to mutation avoidance.

"In other words, Polδ is a proofreader of a proofreader.

"Thus, the high efficiency of Polδ at correcting errors made by Polε may result from a combination of two factors: the high proclivity of Polε to yield to another polymerase and the greater flexibility and robustness of Polδ when associating with new primer termini.

***

"Researchers have explored further into the formation of this structure, which involves chromatin wrapping around histone proteins so that long strands of DNA can fit within the compact space of the cell nucleus. As with everything else in genomics, the structure doesn’t just happen. It requires a lot of help.

"Regulation of histone proteins allows the DNA strands become more tightly or loosely coiled during the processes of DNA replication and gene expression. However, problems may arise when histones clump together or when DNA strands intertwine...the misregulation of chromatin structures could result in aberrant gene expression and can ultimately lead to developmental disorders or cancers.

Histone chaperones are those proteins, responsible for adding and removing specific histones [found] at the wrong time and place during the DNA packaging process. Thus, they also play a key role in the assembly and disassembly of chromatin.

***

“'The fundamental unit of chromatin, the nucleosome, is an intricate structure that requires histone chaperones for assembly.” Their cryo-EM images of one particular chaperone named Abo1 reveals a six-fold symmetry with precise locations for docking to histones, its hexameric ring “thus creating a unique pocket where histones could bind” with energy from ATP. “Not only is Abo1 distinct as a histone chaperone,” they write, “but Abo1 is also unique compared to other canonical AAA+ protein structures.” Like Lego blocks, Abo1 features “tight knob-and-hole packing of individual subunits” plus linkers and other binding sites, such as for ATP.

"And unlike static blocks, these blocks undergo conformational changes as they work.

"Such sophistication is far beyond the old picture of DNA as a master molecule directing all the work. It couldn’t work without the help of many precision machines like this.

***

"Proteins must fold properly to perform their functions. Small proteins usually fold successfully on their own, but large ones can fall into several misfolding traps that are equally likely as the canonical fold. It appears that the “sequence of the sequence” in a gene has something to do with this. “Interestingly, many of these proteins’ sequences contain conserved rare codons that may slow down synthesis at this optimal window,” explain Amir Bitran et al. in a January 21 paper in PNAS, discovering that “Cotranslational folding” (i.e., folding that begins as the polypeptide exits the ribosome) “allows misfolding-prone proteins to circumvent deep kinetic traps.'”

Comment: Such complexity requires design. Nothing else can create this.

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7069 views

More useful parts of the genome as junk disappears:

https://phys.org/news/2020-07-encode-consortium-rna-sequences-involved.html

"The human genome contains about 20,000 protein-coding genes, but the coding parts of our genes account for only about 2 percent of the entire genome. For the past two decades, scientists have been trying to find out what the other 98 percent is doing.

"A research consortium known as ENCODE (Encyclopedia of DNA Elements) has made significant progress toward that goal, identifying many genome locations that bind to regulatory proteins, helping to control which genes get turned on or off. In a new study that is also part of ENCODE, researchers have now identified many additional sites that code for RNA molecules that are likely to influence gene expression.

"These RNA sequences do not get translated into proteins, but act in a variety of ways to control how much protein is made from protein-coding genes. The research team, which includes scientists from MIT and several other institutions, made use of RNA-binding proteins to help them locate and assign possible functions to tens of thousands of sequences of the genome.

***

"Much of the ENCODE project has thus far relied on detecting regulatory sequences of DNA using a technique called ChIP-seq. This technique allows researchers to identify DNA sites that are bound to DNA-binding proteins such as transcription factors, helping to determine the functions of those DNA sequences.

***

"...the RNA team relied on a technique known as eCLIP, which uses ultraviolet light to cross-link RNA molecules with RNA-binding proteins (RBPs) inside cells. Researchers then isolate specific RBPs using antibodies and sequence the RNAs they were bound to.

"RBPs have many different functions—some are splicing factors, which help to cut out sections of protein-coding messenger RNA, while others terminate transcription, enhance protein translation, break down RNA after translation, or guide RNA to a specific location in the cell. Determining the RNA sequences that are bound to RBPs can help to reveal information about the function of those RNA molecules.

"'RBP binding sites are candidate functional elements in the transcriptome," Burge says. "'However, not all sites of binding have a function, so then you need to complement that with other types of assays to assess function."

***

"Overall, the researchers were able to study about 350 of the 1,500 known human RBPs, using one or more of these techniques per protein. RNA splicing factors often have different activity depending on where they bind in a transcript, for example activating splicing when they bind at one end of an intron and repressing it when they bind the other end. Combining the data from these techniques allowed the researchers to produce an "atlas" of maps describing how each RBP's activity depends on its binding location.

"'Why they activate in one location and repress when they bind to another location is a longstanding puzzle," Burge says. "But having this set of maps may help researchers to figure out what protein features are associated with each pattern of activity."

Comment: the genome is like a huge onion, and this shows another layer of understanding peeled away. How so few genes make a complex human.

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6184 views

dhw: Of course his book would have been different, but I wish you wouldn’t lump all his ideas together, as if they are all invalid. Darwin’s theory deals with Chapter Two of life, not with the origin – and that means not with the origin of the mechanisms that enable life, reproduction and evolution. I suspect that being an agnostic, he would have acknowledged all your arguments for design. None of them contradict the theory of common descent or of natural selection as the process that determines which organs and organisms survive. Darwinism does not support atheism. It is neutral. Not even the theory of random mutations and gradualism, which you and I both reject, supports atheism! That was the astonishing discovery I made when I was a schoolboy, and it still astonishes me that so many highly educated people think of it as atheistic.

DAVID: I'll accept common descent, but natural selection is a tautology that is not proven within itself nor as a possible cause of speciation.

Of course natural selection is not a possible cause of speciation. It simply means that nature selects from EXISTING organs and organisms those that will survive. I agree that it’s a kind of tautology, but it’s a neat term to cover various aspects of evolution. However, that was not my point, which is that Darwin’s various theories, right or wrong, are not atheistic.

Post reply

6886 views

DAVID: […] fine-tuned control of a dangerous radical (electron on the loose but really not). Not by chance from hunt and peck. There must be a designer. If Darwin had known these facts, his book would not be written in the same way. Darwinism must be preserved to support atheism.

dhw: Of course his book would have been different, but I wish you wouldn’t lump all his ideas together, as if they are all invalid. Darwin’s theory deals with Chapter Two of life, not with the origin – and that means not with the origin of the mechanisms that enable life, reproduction and evolution. I suspect that being an agnostic, he would have acknowledged all your arguments for design. None of them contradict the theory of common descent or of natural selection as the process that determines which organs and organisms survive. Darwinism does not support atheism. It is neutral. Not even the theory of random mutations and gradualism, which you and I both reject, supports atheism! That was the astonishing discovery I made when I was a schoolboy, and it still astonishes me that so many highly educated people think of it as atheistic.

DAVID: I'll accept common descent, but natural selection is a tautology that is not proven within itself nor as a possible cause of speciation.

dhw: Of course natural selection is not a possible cause of speciation. It simply means that nature selects from EXISTING organs and organisms those that will survive. I agree that it’s a kind of tautology, but it’s a neat term to cover various aspects of evolution. However, that was not my point, which is that Darwin’s various theories, right or wrong, are not atheistic.

I know, but if it seems we arrived naturally out of thin air by natural chance, that is what the atheists peddle about Darwin.

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6903 views

DAVID: I'll accept common descent, but natural selection is a tautology that is not proven within itself nor as a possible cause of speciation.

dhw: Of course natural selection is not a possible cause of speciation. It simply means that nature selects from EXISTING organs and organisms those that will survive. I agree that it’s a kind of tautology, but it’s a neat term to cover various aspects of evolution. However, that was not my point, which is that Darwin’s various theories, right or wrong, are not atheistic.

DAVID: I know, but if it seems we arrived naturally out of thin air by natural chance, that is what the atheists peddle about Darwin.

Just for the purpose of information, not debate: Darwin deliberately and explicitly does NOT consider the origin of life in propounding his theory of evolution, and atheists have no right to use the theory to peddle their views. (Nor for that matter should theists, though most of them seem unaware of his references in Origin to a creator!) However, I have found a website devoted to his personal views on the subject gleaned through his letters. The article is very long and detailed, and shows some degree of vacillation (inevitable if one is unsure of something), but the two quotes below, taken from letters written near the end of his life, are typical. (Archebiosis is what we now call abiogenesis.)

Charles Darwin and the Origin of Life - PubMed Central (PMC)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2745620

QUOTE: He was to maintain the same attitude for many years to come, as shown by the letter mailed on March 28, 1882, near the end of his life, to George Charles Wallich (de Beer 1959). In it Darwin wrote that,
«My dear Sir,
You expressed quite correctly my views where you say that I had intentionally left the question of the Origin of Life uncanvassed as being altogether ultra vires in the present state of our knowledge, & that I dealt only with the manner of succession. I have met with no evidence that seems in the least trustworthy, in favour of the so-called Spontaneous generation. I believe that I have somewhere said (but cannot find the passage) that the principle of continuity renders it probable that the principle of life will hereafter be shown to be a part, or consequence of some general law; but this is only conjecture and not science.

«[...] I should like to live to see Archebiosis proved true, for it would be a discovery of transcendent importance; or, if false, I should like to see it disproved, and the facts otherwise explained; but I shall not live to see all this». (Editor's apt comment: Nor will we.)

Post reply

6921 views

DAVID: I'll accept common descent, but natural selection is a tautology that is not proven within itself nor as a possible cause of speciation.

dhw: Of course natural selection is not a possible cause of speciation. It simply means that nature selects from EXISTING organs and organisms those that will survive. I agree that it’s a kind of tautology, but it’s a neat term to cover various aspects of evolution. However, that was not my point, which is that Darwin’s various theories, right or wrong, are not atheistic.

DAVID: I know, but if it seems we arrived naturally out of thin air by natural chance, that is what the atheists peddle about Darwin.

dhw: Just for the purpose of information, not debate: Darwin deliberately and explicitly does NOT consider the origin of life in propounding his theory of evolution, and atheists have no right to use the theory to peddle their views. (Nor for that matter should theists, though most of them seem unaware of his references in Origin to a creator!) However, I have found a website devoted to his personal views on the subject gleaned through his letters. The article is very long and detailed, and shows some degree of vacillation (inevitable if one is unsure of something), but the two quotes below, taken from letters written near the end of his life, are typical. (Archebiosis is what we now call abiogenesis.)

Charles Darwin and the Origin of Life - PubMed Central (PMC)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2745620

QUOTE: He was to maintain the same attitude for many years to come, as shown by the letter mailed on March 28, 1882, near the end of his life, to George Charles Wallich (de Beer 1959). In it Darwin wrote that,
«My dear Sir,
You expressed quite correctly my views where you say that I had intentionally left the question of the Origin of Life uncanvassed as being altogether ultra vires in the present state of our knowledge, & that I dealt only with the manner of succession. I have met with no evidence that seems in the least trustworthy, in favour of the so-called Spontaneous generation. I believe that I have somewhere said (but cannot find the passage) that the principle of continuity renders it probable that the principle of life will hereafter be shown to be a part, or consequence of some general law; but this is only conjecture and not science.

«[...] I should like to live to see Archebiosis proved true, for it would be a discovery of transcendent importance; or, if false, I should like to see it disproved, and the facts otherwise explained; but I shall not live to see all this». (Editor's apt comment: Nor will we.)

Thank you for this expansion of our knowledge. The atheists still use him however, and we theists point to the origin of life as a profound reason to believe in God. And I would state that the origin set the groundwork for the subsequent evolution and therefor the entire process is a continuum and cannot be separated in current discussions

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6934 views

New thoughts on how they arise:

https://www.quantamagazine.org/where-do-new-genes-come-from-20200409/

"De novo genes “represent a really unprecedented or unrivaled kind of genetic novelty,” said Caroline Weisman, a doctoral student in biophysics at Harvard University who is conducting research into the origin of genes. “That’s a really exciting possibility for evolutionary biologists who are thinking about how things like novelty evolve.”

***

"During the past decade, researchers have vigorously argued about the relative importance of de novo gene creation and divergence beyond recognition. But there was still no easy way to look at orphan genes and determine how they arose. “The field was hamstrung by that, in a sense, because if you can’t really know how many are real [de novo genes], and what’s the significance of this phenomenon, then you’re a bit stuck,” McLysaght said.

***

"The researchers made a conservative assumption that if a gene’s neighbors appear in the same order in another species, then the gene is likely to correspond to whatever is sandwiched between them in the other species as well — even if the sequences don’t match.

"Using the synteny method, the researchers estimated that at most a third of orphan genes in flies, yeast and humans could be explained by divergence beyond recognition. “The rest must be explained by other ways, and the de novo origin is the best way to explain those,” McLysaght said.

***

"Weisman estimated that somewhere between 55% and 73% percent of the orphan genes in these yeasts — a majority — were explained by divergence; that figure is higher than McLysaght’s synteny approach suggested.

***
"How Function Emerges:
Long and his colleagues identified about 175 genes that originated de novo within the last 3.4 million years; they could tell that these genes were de novo because corresponding nongenic sequences were still recognizable in closely related species. These de novo genes appeared to be biologically active — that is, they were transcribed into RNA and translated into peptide chains, and most of them showed signs of being shaped by natural selection.

***

"Although their study demonstrated the adaptive potential of emerging de novo genes, the actual contribution of de novo genes to adaptation might always “remain somewhat cloaked in mystery,” McLysaght said. As mutations accumulate in de novo genes, it gets harder to identify the nongenic sequences from which they came. Past some uncertain deadline, it may always be impossible to prove that an old gene arose de novo. Pinning down the true number of de novo genes and their contribution to novel adaptations in most complex organisms may therefore be an intractable problem.

"Still, Long emphasized that orphan genes have biology worth investigating regardless of their origin. Weisman thinks that may be particularly true of genes whose divergence seems to have suddenly accelerated at some recent point in their evolution: They might be able to tell us about how novel biological functions evolve.

"For the creation of orphan genes, “we know there’s a diversity of mechanisms,” Begun said. But “the guiding principles for why certain biological processes might have more de novo gene evolution, while others might have more duplication and divergence — that, we don’t really have a grip on yet.'”

Comment: as we knew its not Darwin's theory as ID has pointed out, and the field has not fully explained it. If it is not within the Darwin theory, where does it comes from? The dsigner?

Post reply

6982 views

QUOTE: De novo genes “represent a really unprecedented or unrivaled kind of genetic novelty,” said Caroline Weisman, a doctoral student in biophysics at Harvard University who is conducting research into the origin of genes. “That’s a really exciting possibility for evolutionary biologists who are thinking about how things like novelty evolve.”

Exciting indeed, to think that cell communities can produce novelties. A theist could easily believe that his God created all this complex machinery to enable cells to work out their individual ways of evolving. A very reasonable alternative to Genesis, wouldn’t you say?

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6871 views

QUOTE: De novo genes “represent a really unprecedented or unrivaled kind of genetic novelty,” said Caroline Weisman, a doctoral student in biophysics at Harvard University who is conducting research into the origin of genes. “That’s a really exciting possibility for evolutionary biologists who are thinking about how things like novelty evolve.”

dhw: Exciting indeed, to think that cell communities can produce novelties. A theist could easily believe that his God created all this complex machinery to enable cells to work out their individual ways of evolving. A very reasonable alternative to Genesis, wouldn’t you say?

It doesn't follow Darwin and cell communities are not mentioned. Since it is not common descent, what is it? And it not creating speciation. It is not an alternative to Genesis.

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6872 views

When cells divide there are tight controls. Another is found:

https://phys.org/news/2020-04-geneticists-regulatory-mechanism-chromosome-inheritance.html

"In the course of every single cell division, the genetic information on the chromosomes must be distributed equally between the newly developing daughter cells. The enzyme separase plays a decisive role in this process. Susanne Hellmuth and Olaf Stemmann from the chair of genetics at the University of Bayreuth have now discovered a previously unknown mechanism that regulates the activity of the separase.

***

"Cell division is essential for human growth and reproduction. Before a cell begins to divide, the genetic information stored on the chromosomes is duplicated. When this process is complete, each chromosome consists of two identical DNA threads, the sister chromatids. Cohesin, a ring consisting of several proteins, encloses each chromosome and holds the pair of chromatids together. Already during preparation for cell division, cohesin is removed from the arms of the chromosomes. However, the complete separation of the sister chromatids can only take place when the cohesin remaining in the middle of the chromosomes is cut by the enzyme separase.

***

"geneticists from the University of Salamanca/Spain, have now discovered that the protein shugoshin (Japanese for "guardian spirit") has exactly this regulating function. Shugoshin causes the separase to remain inactive until the right time for cohesin splitting has come. With this discovery, scientists have succeeded in solving an important puzzle of genetics: Until now, only the protein securin was known to suppress premature activity of the separase. It was therefore believed that the separase was exclusively regulated by securin. However, this view contradicted the observation that separase remains properly regulated even when securin is not present. The study now published in "Nature" provides the explanation: Shugoshin and securin both prevent separase from initiating the process of chromsosome segregation at the wrong time. And if the securin fails, even shugoshin alone is able to regulate the activity of separase in human cells.

"'We are dealing with a type of redundancy that is not at all uncommon in the cell cycle: In order for a vital process to proceed in a well-ordered manner, nature has safeguarded it by controlling it simultaneously in two or more different ways. This makes the process particularly robust,

"Indeed, Hellmuth and Stemmann made a further discovery: It is the spindle assembly checkpoint (SAC) that controls the regulating influence of shugoshin as well as that of securin. This finding confirms the well-established assumption in the research that the SAC has, as it were, sovereignty over all processes involved in chromosome inheritance. It had been known for some time that the SAC first stabilizes the securin and does not allow its degradation until the time has come for cohesin splitting by separase. The "Nature" publication now shows how the checkpoint causes shugoshin to suppress the premature activity of separase: namely by associating shugoshin with the SAC component Mad2."

Comment: This precise mechanism must be carefully designed and controlled as cells constantly reproduce during the life of each organism. Life can not continue without this process and the controls over it. Only design fits. A designer exists.

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6870 views

dhw: Exciting indeed, to think that cell communities can produce novelties. A theist could easily believe that his God created all this complex machinery to enable cells to work out their individual ways of evolving. A very reasonable alternative to Genesis, wouldn’t you say?

DAVID: It doesn't follow Darwin and cell communities are not mentioned. Since it is not common descent, what is it? And it not creating speciation. It is not an alternative to Genesis.

I’m simply examining possible implications. You don’t need me to tell you that genes don’t exist independently of cells, and all multicellular organisms are composed of cells/cell communities! Speciation requires novelty, and since novelty has so far not been explained, it’s hardly surprising that our excited evolutionary biologists think they may be onto something. God is not mentioned either, but you will notice that I have included him in my speculations.

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6829 views

QUOTE: De novo genes “represent a really unprecedented or unrivaled kind of genetic novelty,” said Caroline Weisman, a doctoral student in biophysics at Harvard University who is conducting research into the origin of genes. “That’s a really exciting possibility for evolutionary biologists who are thinking about how things like novelty evolve.”

dhw: Exciting indeed, to think that cell communities can produce novelties. A theist could easily believe that his God created all this complex machinery to enable cells to work out their individual ways of evolving. A very reasonable alternative to Genesis, wouldn’t you say?

DAVID: It doesn't follow Darwin and cell communities are not mentioned. Since it is not common descent, what is it? And it not creating speciation. It is not an alternative to Genesis.

dhw: I’m simply examining possible implications. You don’t need me to tell you that genes don’t exist independently of cells, and all multicellular organisms are composed of cells/cell communities! Speciation requires novelty, and since novelty has so far not been explained, it’s hardly surprising that our excited evolutionary biologists think they may be onto something. God is not mentioned either, but you will notice that I have included him in my speculations.

You never seem to realize how your imagined view of God diminishes Him. I can't think of a true theist who thinks as you imagine: "A theist could easily believe that his God created all this complex machinery to enable cells to work out their individual ways of evolving." God has done that only in a small way, epigenetic alterations for minor adaptions. Major gaps (think whales) are a marvelous way of revealing the intricate design problems solved in the whale series.

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6858 views

A professor who studies epigenetics demands it be more fully integrated with Darwin theory, since he gets resistance from strict Darwinist scientists:

https://aeon.co/essays/on-epigenetics-we-need-both-darwin-s-and-lamarck-s-theories?utm_...

"One problem with Darwin’s theory is that, while species do evolve more adaptive traits (called phenotypes by biologists), the rate of random DNA sequence mutation turns out to be too slow to explain many of the changes observed. Scientists, well-aware of the issue, have proposed a variety of genetic mechanisms to compensate: genetic drift, in which small groups of individuals undergo dramatic genetic change; or epistasis, in which one set of genes suppress another, to name just two.

"Yet even with such mechanisms in play, genetic mutation rates for complex organisms such as humans are dramatically lower than the frequency of change for a host of traits, from adjustments in metabolism to resistance to disease. The rapid emergence of trait variety is difficult to explain just through classic genetics and neo-Darwinian theory.

***

"In evolution and biomedicine, the rates of phenotypic trait divergence is far more rapid than the rate of genetic variation and mutation – but why?

***

"Epigenetics involves a number of molecular processes that can dramatically influence the activity of the genome without altering the sequence of DNA in the genes themselves.
One of the most common such processes is ‘DNA methylation’, in which molecular components called methyl groups (made of methane) attach to DNA, turning genes on or off, and regulating the level of gene expression.

***

"Another major epigenetic process discovered in recent years is ‘histone modification’. Histones are proteins that attach to and alter the structure of DNA, which in turn wraps around the histones like beads on a string.

***

"More recently, researchers have documented ‘RNA methylation’ in which methyl groups attach to the genetic helper molecules, in the process altering gene expression and subsequent protein production for generations down the line. Likewise, the action of so-called ‘non-coding RNA’, small RNA molecules that bind to DNA, RNA and proteins, also alter the expression of genes, independent of DNA sequence.

***

"Epigenetic transgenerational inheritance, by contrast, occurs when the germline (sperm or egg) transmits epigenetic information between generations, even in the absence of continued direct environmental exposures.

***

"Environmentally induced epigenetic transgenerational inheritance has now been observed in plants, insects, fish, birds, rodents, pigs and humans. It is, therefore, a highly conserved phenomenon.

***

"Neo-Darwinian and neo-Lamarckian mechanisms both drive evolution, and they appear to be intertwined.

***

"Despite the pushback, I’m convinced that we have reached the point where a paradigm shift is due. Accepting that epigenetics plays a role in evolution does not topple the science of genetics; embracing neo-Lamarckian ideas does nothing to challenge classic neo-Darwinian theory. The accepted sciences are essential and accurate, but part of a bigger, more nuanced story that expands our understanding and integrates all our observations into a cohesive whole. The unified theory explains how the environment can both act to directly influence phenotypic variation and directly facilitate natural selection."

Comment: Readers of this website are not surprised by the importance of epigenetics. It's been covered well. The rigidity of the Darwinist group is well known. It is what I complain about when discussing Darwin theory. It is not Darwin's fault

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Results are not clear at all:

https://phys.org/news/2020-08-faster-evolution-linked-tiny-genomes.html

scientists have found a link between mutation rate—how quickly the DNA sequence changes—and genome size.

***

"'This was a really surprising result," said Professor Tom Bourguignon, co-first author of the study and head of the Evolutionary Genomics Unit at OIST. "Currently, the most accepted idea is that population size is the main factor that determines genome size in prokaryotes, particularly in endosymbionts, but our research challenges this view."

***

"'At small population sizes, natural selection is much less effective, and evolution is driven more strongly by chance," said Dr. Yukihiro Kinjo, co-first author and a postdoctoral scholar from the Evolutionary Genomics Unit. "Without enough selection pressure to maintain specific genes, mutations can arise that inactive and erode these genes, eventually leading to their total loss from the genome."

"While population size as a driving force for genome reduction may be an attractive idea, many free-living prokaryotes that live in larger populations have also evolved smaller genomes, suggesting that it's only part of the story. Additional explanations have also been proposed but, until now, the mutation rate—or the speed at which evolution occurs—has been overlooked.

"In the study, the scientists collected genome data from a diverse range of prokaryotes, including strains from two endosymbiotic lineages and seven free-living lineages.

***

"Surprisingly, the scientists did not find a clear link between estimated population size and rate of gene loss. Instead, they found a relationship between mutation rate and gene loss for seven out of the nine lineages studied, with higher mutation rates associated with faster rates of gene loss, resulting in smaller genomes.

"'Although we haven't established a cause, there is a theoretical prediction that explains this observation; if the rate of mutation outweighs a selection pressure to maintain a gene, the gene will be lost from the genome," said Dr. Kinjo.

"The scientists also found clues as to how the gene loss occurred, as strains with smaller genomes had lost genes involved in repairing DNA.

"DNA repair genes fix damaged DNA, so when they are lost the mutation rate of a strain can quickly increase. Most mutations are harmful, so this can quickly inactivate other genes and drive their loss from the genome. If some of these inactivated genes are also involved in DNA repair, this can further accelerate mutation rate and gene loss," explained Professor Gaku Tokuda, from the University of the Ryukyus.

"Although the answers to how gene loss occurs are becoming clearer, whether there are evolutionary reasons behind why prokaryotes increase their rate of mutation to shrink their genome, and if so, what these reasons are, remains an open question.

"'Figuring out the evolutionary explanation for what we see is really complicated. It could be that an increased rate of mutation occurs to provide an adaptive advantage, such as the removal of unwanted or unnecessary genes. But we still can't rule out the possibility that the increased rate of mutation is non-adaptive and due to chance," said Dr. Kinjo.

"Overall, their findings shed new light on the evolution of small genomes, prompting a re-think of the current dominant idea of genome reduction being driven by small population sizes."

Comment: I think part of the misunderstood results is from trying to apply Darwin theory. The causer may not be evolutionary selection pressure. Natural selection is a passive event.

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6132 views

DAVID: It doesn't follow Darwin and cell communities are not mentioned. Since it is not common descent, what is it? And it not creating speciation. It is not an alternative to Genesis.

dhw: I’m simply examining possible implications. You don’t need me to tell you that genes don’t exist independently of cells, and all multicellular organisms are composed of cells/cell communities! Speciation requires novelty, and since novelty has so far not been explained, it’s hardly surprising that our excited evolutionary biologists think they may be onto something. God is not mentioned either, but you will notice that I have included him in my speculations.

DAVID: You never seem to realize how your imagined view of God diminishes Him. I can't think of a true theist who thinks as you imagine: "A theist could easily believe that his God created all this complex machinery to enable cells to work out their individual ways of evolving." God has done that only in a small way, epigenetic alterations for minor adaptions. Major gaps (think whales) are a marvelous way of revealing the intricate design problems solved in the whale series.

In what way does my theory “diminish” God? The mechanism I propose involves the same astonishing powers of design as having your God popping down to earth every time he wants to add bits and pieces to his whale. Not to mention the other few billion life forms, lifestyles, strategies and natural wonders he has apparently specially designed. See also the post on your theory of evolution for “theism lite”!

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6860 views

QUOTE: De novo genes “represent a really unprecedented or unrivaled kind of genetic novelty,” said Caroline Weisman, a doctoral student in biophysics at Harvard University who is conducting research into the origin of genes. “That’s a really exciting possibility for evolutionary biologists who are thinking about how things like novelty evolve.”

dhw: Exciting indeed, to think that cell communities can produce novelties. A theist could easily believe that his God created all this complex machinery to enable cells to work out their individual ways of evolving. A very reasonable alternative to Genesis, wouldn’t you say?

DAVID: It doesn't follow Darwin and cell communities are not mentioned. Since it is not common descent, what is it? And it not creating speciation. It is not an alternative to Genesis.

dhw: I’m simply examining possible implications. You don’t need me to tell you that genes don’t exist independently of cells, and all multicellular organisms are composed of cells/cell communities! Speciation requires novelty, and since novelty has so far not been explained, it’s hardly surprising that our excited evolutionary biologists think they may be onto something. God is not mentioned either, but you will notice that I have included him in my speculations.

DAVID: You never seem to realize how your imagined view of God diminishes Him. I can't think of a true theist who thinks as you imagine: "A theist could easily believe that his God created all this complex machinery to enable cells to work out their individual ways of evolving." God has done that only in a small way, epigenetic alterations for minor adaptions. Major gaps (think whales) are a marvelous way of revealing the intricate design problems solved in the whale series.

dhw: In what way does my theory “diminish” God? The mechanism I propose involves the same astonishing powers of design as having your God popping down to earth every time he wants to add bits and pieces to his whale. Not to mention the other few billion life forms, lifestyles, strategies and natural wonders he has apparently specially designed. See also the post on your theory of evolution for “theism lite”!

The bold shows your incomplete understanding of true theism. God doesn't pop down from His heavenly throne !!! He is all around us all the time. And your idea of design by organisms using a mechanism on their own without guidelines means God gives up total control of His works is obviously diminishing, as I've told you many times.

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6820 views

Finally able to see exact structural shape:

https://cosmosmagazine.com/biology/taking-a-look-at-rna-s-structure?utm_source=Cosmos+-...

"RNA molecules have a two-dimensional structure that influences how the genetic information contained within them can be accessed.

“'The big question in RNA biology has been whether RNA molecules have a single, constant structure, or whether they can shift between different structures – and what this means for the function of a particular RNA molecule,” says WEHI’s Vincent Corbin.

***

"Some viruses use RNA for their genome, including HIV and SARS-CoV2 (the coronavirus that causes COVID-19). In the case of HIV, RNA splicing influences which protein the virus produces – which changes at different stages of the virus’s lifecycle.

“'Using the HIV genome as a model system, we looked at whether RNA structure influences how HIV’s RNA is spliced,” says Corbin. “We discovered that RNA structure was a critical determinant of RNA splicing in HIV and influenced which viral proteins were produced.

“'This is the first clear evidence of how RNA structure can control RNA function. The techniques we have developed have opened up a new field of research into the role of RNA structure in regulating the function of cells.'”

Comment: Another layer of information is coded into the structural shape.

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6759 views

The series of reactions is actually discontinuous as explained:

https://uncommondescent.com/intelligent-design/for-those-keeping-count-colorado-had-neg...

"I told you the critical physical condition of the system (described as such in the literature) that allows the system to function as it does, in a material universe determined by inexorable physical law. The gene system must have the physical freedom to specify itself, as well as any variation of itself. In case it has not occurred to you, there is no ”capacity to specify” recorded among the physical properties of matter listed on the periodic table, and binding those atoms together does not suddenly create that capacity. It is only established by a particular type of arrangement of matter; one that, as Michael Polanyi noted, “harnesses the laws of inanimate nature” but in an arrangement that is ”irreducible to those laws”. That is exactly what a physical analysis of the system has demonstrated, and is exactly what has been recorded in the literature. (my bold) (Polanyi is a highly regarded philosopher of science: "Polanyi argues that the information contained in the DNA molecule is not reducible to the laws of physics and chemistry.

https://en.wikipedia.org/wiki/Michael_Polanyi

My entry continues: "Although a DNA molecule cannot exist without physical properties, these properties are constrained by higher-level ordering principles".

"Take out a piece of paper and write the words “DNA codon” at the top of the page. Drop down a few inches below and write the words “mRNA codon”. Drop down further still and write the words “charged tRNA anti-codon”, and below that write the phrase “amino acid presented for binding”. You can now draw a straight line from the top of the page to the bottom, indicating the chain of chemical interactions that begins with a codon of DNA and results in an amino acid being presented for binding during protein synthesis. This would include the processes of transcription, translation and polymerization. But as you will quickly notice, there is no chemical reaction in that chain of events that actually specifies which particular amino acid is being presented for binding. (my bold)

"You can now draw another line (joining your original line, but perpendicular to it) directly underneath the words “charged tRNA anti-codon”. At the end of this new perpendicular line, you can now write the word “aaRS”. The set of aaRS are the molecules in biology that specify which particular amino acids will be associated with each tRNA anticodon. And as I told you before, the work of the aaRS is both temporally and spatially independent of the chain of events represented by the first line you drew down the page. This independence, introduced only by the organization of the system, is what allows the system to function as it does – to specify itself among alternatives. Hence, the word “discontinuous” … as in the discontinuous association between a codon of DNA and the resulting amino acid being presented for biding. It is discontinuous because it has to be in order to function as it does. Check your Periodic Table for that. (aaRS refers to very specialized enzymes which specify specific amino acids to tRNA controls)

"What is also worth noting that not a single one of these interactions is even the least bit controversial."

Comment: This means the molecular reactions go on under precise coordination but each stepwise molecule does not know the end point to which it is directing a process. This demands design, because the chemicals do not get arranged this way on their own, with purposeful results all the time. Note Polanyi uses the concept of guidance by information.

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Still not fully understood but it represents left-handed DNA coils appearing in the normally right-handed turns with va special relationship to coding RNA:

https://www.omagdigital.com/publication/?m=21896&i=661897&p=46

Comment: Unfortunately I cannot copy the article but it indicates that some process flips DNA back and forth extremely quickly and this modifies the way RNA is edited and instructed in expressing genes. it also can be modified by methyl groups to give epigenetic changes. Another layer of complexity is uncovered, and I assume more to come. Only design fits.

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6557 views

David: Still not fully understood but it represents left-handed DNA coils appearing in the normally right-handed turns with va special relationship to coding RNA:

https://www.omagdigital.com/publication/?m=21896&i=661897&p=46

Comment: Unfortunately I cannot copy the article but it indicates that some process flips DNA back and forth extremely quickly and this modifies the way RNA is edited and instructed in expressing genes. it also can be modified by methyl groups to give epigenetic changes. Another layer of complexity is uncovered, and I assume more to come. Only design fits.

Article found that I can copy from:

https://www.the-scientist.com/features/left-handed-dna-has-a-biological-role-within-a-d...

:For Herbert, the biological relevance of Z-DNA is massive, as he suspects that flips in DNA chirality influence how RNA molecules are processed across the genome. He suggests that the formation of Z-DNA and the localization of Z-binding proteins during transcription could quickly turn on and off the editing of RNA products at many active genes.

"Because Z-DNA is so unstable, Herbert named DNA sequences that can flip into the left-handed conformation “flipons.” He hypothesizes that the final readout of genetic information from the genome depends on the activity of these flipons at the time of transcription. “It’s not an on-and-off switch for the gene, but it does play a role in regulating how the initial transcript is compiled into different RNAs,” he explains.

"Herbert suggests flipons take on the Z conformation only once transcription is underway, because the DNA supercoiling that accompanies active transcription is thought to promote the conformational change. But a 2012 study provided some evidence that Z-DNA may help open up the DNA that is normally tightly wound around histone proteins in nucleosomes, in preparation for transcription to begin. Keji Zhao of the National Heart, Lung, and Blood Institute found that a protein complex called SWI/SNF (SWItch/Sucrose Non-Fermentable), which is involved in loosening DNA-histone interactions, caused DNA near the promoter region of a gene to flip into the Z conformation.

"Zhao speculates that Z-DNA modulates the placement of nucleosomes on the genome. “Formation of Z-DNA by the activity of SWI/SNF complexes may first generate an unstable nucleosome, which can slide to a nearby B-DNA region or eject the core histones to form a nucleosome-free region,” thus allowing transcription to start, he explains. The idea that Z-DNA could be present on DNA molecules wound around histones is somewhat surprising, notes Ho. “Most of the data that we’ve seen from other laboratories have shown that Z-DNA doesn’t actually sit on nucleosomes, primarily because [Z-DNA] is a very stiff structure,” he says. “It’s very rod-like, whereas nucleosomes require a very large amount of flexibility in the DNA in order to make essentially 200 base pairs wrap around the small complex.”

"Zhao’s work also supports the idea that Z-DNA formation may be influenced by DNA methylation. He and his colleagues created DNA templates assembled into nucleosomes that contained known Z-forming regions, including DNA with methylated and non-methylated guanine bases. The researchers could detect Z-DNA using a restriction enzyme modified with two copies of the Zα binding domain that would cleave the DNA if the Z configuration was present. The team found that Z-DNA was only present when the DNA fragments were made with methylated guanines.

***

"It has taken decades to understand that Z-DNA has significance in biology. Although there is still much to discover, it’s becoming apparent that Z-DNA provides another mechanism to influence the decoding of genomic information, says Herbert. “It’s pretty exciting. . . . It’s a different way of thinking about the biology.'”

Comment: It'd been around awhile, but very hard to work with, but this layer of controls is opening up. I'm not surprised I hadn't heard of it before. I still think we are just at the beginning of understanding the full powers of the whole genome. Designer required.

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How methylation is managed to control gene modifications on Histones:

https://phys.org/news/2020-06-team-decodes-piece-histone-code.html

"Inside our cells, DNA is tightly packed and spooled around proteins called histones. Packaging DNA in this way allows large amounts of genetic material to exist inside the cell in a final form called chromatin. Tiny enzymes modify the histones to make sure the genes that are part of the DNA can be accessed and precisely regulated. The result of this is proper gene expression and the production of proteins important for cell function and human health.

***

"The Histone Code is important for genome function, yet the rules that govern the code are not fully deciphered. One of the early findings in the field of epigenetics was that a class of enzymes called histone methyltransferases can add a chemical modification multiple times on a single amino acid residue of a histone.

"The process by which a histone methyltransferase adds this chemical modification is called methylation. The methyltransferase adds one carbon atom and three hydrogen atoms—a so-called 'methyl group' to a specific amino acid reside of a histone. This process can occur once, twice, or three times on a single amino acid residue, creating different "flavors" of methylation.

"A major question in the field had been: do different "flavors" of methylation have the same or distinct biological functions on, say, gene expression important for the maintenance of healthy cells? While other studies had explored this idea for some histone sites that are methylated, many locations of histone methylation had not been investigated.

"To answer this question, first author Julia DiFiore, Ph.D., a graduate student in the Strahl lab at the time of this research, genetically engineered one such methyltransferase called Set2 so it could perform only select flavors of methylation on its amino acid within histones. By achieving this high degree of specificity, the researchers could finally test if the different degrees of methylation at this site have the same or distinct functions.

***

"In addition to understanding fundamental cellular processes, "This work could also explain how dysregulation of enzymes such as Set2 might lead to incorrect 'flavors' of methylation to cause human disease," said Strahl, an Oliver Smithies Investigator at the UNC School of Medicine and member of the UNC Lineberger Cancer Center.

"One process they examined was how stress conditions—specifically nutrient stress—affects gene expression. Strahl's group observed that when no methylation on the histone H3K36 was present, gene expression was very different than when normal amounts of methylation were present during nutrient stress. Interestingly, they observed that having only two or only three methyl groups (also called di- and trimethylation) had exactly the same effect as having all three types of methylation that are normally present.

"DiFiore explained, "During nutrient stress, the overlapping roles of di- and trimethylation help provide flexibility to dynamic processes and better allow the cell to respond to stress." Being able to quickly respond to stress allows the cells to grow and function properly even under less than ideal conditions."

Comment: This is a highly designed intricately system to allow quick adaptability. Not by chance.

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6660 views

Modeling of the 'bubbles' around the DNA:

https://phys.org/news/2020-06-burping-droplets-dna.html

"Liquid droplets formed from DNA display a peculiar response to enzymes. An international collaboration between LMU and UCSB has now been able to explain the mechanisms behind bubble formation.

***

"Recent advances in cellular biology have found that the molecular components of living cells (such as DNA and proteins) can bind to each other and form liquid droplets that appear similar to oil droplets in shaken salad dressing. These cellular droplets interact with other components to carry out basic processes critical to life, yet little is known about how those interactions function.

***

"To get to the bottom of this mystery, the team carried out a rigorous set of precision experiments quantifying the shrinking and bubbling behaviors. They found that there were two types of shrinking behavior, the first cause by enzymes cutting the DNA only on the droplet surface, and the second caused by enzymes penetrating inside the droplet. "This observation was critical to unraveling the behavior, as it put it into our heads that the enzyme could start nibbling away at the droplets from the inside," notes co-leader Tim Liedl, Professor at the LMU, where the experiments were conducted.

"By comparing the droplet response to the DNA particle design, the team cracked the case: they found that bubbling and penetration-based shrinking occurred together, and only happened when the DNA particles were only lightly bound together, whereas strongly-bound DNA particles would keep the enzyme on the outside.

***

"The bubbles, then, happen only in the lightly-bound systems, when the enzyme can get through the crowded DNA particles to the interior of the droplet, and begin to eat away at the droplet from the inside. The chemical fragments created by the enzyme lead to an osmotic effect, where water is drawn in from the outside, causing a swelling phenomenon that produces the bubbles. The bubbles grow, reach the droplet surface, then release the fragments in a burp-like gaseous outburst. "It is quite striking to watch, as the bubbles swell and pop over and over," says Liedl.

"The work demonstrates a complex relationship between the basic material properties of a biomolecular liquid, and its interactions with external components. The team believes the insight gained from studying the bubbling process will lead to both better models of living processes, and enhanced abilities to engineer liquid droplets for use as synthetic bioreactors."

Comment: The complexity of life includes physio-chemical reactions as well as molecular reactions. We haven't reached the end of unearthing the degree of complexity. It must be designed.

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6364 views

A mechanism in plants is described:

https://phys.org/news/2020-06-histone-epigenetic.html

"Epigenetic regulation of gene expression is associated with switching between chromatin states characterized by distinct histone modifications.

"...researchers characterized a gene from an early flowering Arabidopsis mutant and showed that the mutated gene encodes a protein that modifies chromatin—that is it affects the chemical modifications of the histone proteins that surround the DNA in our cells. This class of modifier had not been well characterized in plants before.

"Further, they find that the modifier protein physically associates with a well-known class of chromatin modifiers—called Polycomb proteins.

"Polycomb proteins add an epigenetic mark (methylation) at a specific point (lysine residue at position 27) in the amino acid sequence of a histone protein that packages the DNA and this leads to silent chromatin.

"The addition of this epigenetic mark can only happen when another nearby site (lysine residue at position 36) in the amino acid sequence is not modified. They are mutually exclusive- that is only one of these specific sites can be modified with the epigenetic mark at any one time.

"Interestingly, the newly discovered modifier protein facilitates removal of the epigenetic mark at lysine 36, thus allows Polycomb to add the epigenetic mark at lysine 27. The physical association of the two activities helps generate a switch of active chromatin to silent chromatin."

Comment: this shows how specific histone proteins add and remove methylation markers while DNA is wound around histones. This complexity requires a designer.

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6353 views

There is a special process:

https://phys.org/news/2017-08-marriage-microscopy-techniques-reveals-d.html

"Researchers at the Stowers Institute for Medical Research have solved the three-dimensional structure of a complex that is essential for the correct sorting of chromosomes into eggs and sperm during reproductive cell division or meiosis.

"When this structure, called the synaptonemal complex, doesn't assemble properly in the cell, it can lead to chromosomal abnormalities, miscarriages, and birth defects.

"Since the synaptonemal complex was first discovered in 1956, researchers have been trying to identify its many moving parts and how they fit together.

***

"'The structure was so much more complicated and beautiful than we ever imagined," says R. Scott Hawley, Ph.D., an investigator at the Stowers Institute and senior author of the study. "We thought it just looked like a railroad track, but we discovered that it is actually more like two railroad tracks, one stacked on top of the other. That changes the way we think about this structure and what it does."

"In meiosis, the cell copies all its chromosomes, pairs them up, and then divides them into eggs or sperm. This carefully choreographed process is helped along by the synaptonemal complex, an assembly of proteins that forms between the paired homologous chromosomes and keeps them properly aligned and in position. Errors during meiosis are a leading cause of miscarriages in humans.

***

"What they found was startling: the structure was divided into two identical layers, which had been indistinguishable at lower resolution. Basically, the synaptonemal complex connects two homologous chromosomes, each with two sister chromatids stacked on one another. The researchers showed that this complex uses a two-tiered approach to connect the two upper chromatids and the two lower chromatids separately. They created a computer model of the structure showing coils of DNA connected by two sets of railroad tracks, which are made up of the four known proteins that are part of the synaptonemal complex. Although in this study the researchers looked at only four proteins, many more unknown proteins likely reside in the structure as well, so there are still more details to fill in.

"'This was a really incredible insight, a technical leap using this new methodology of expansion microscopy and merging it with structured illumination to create a way to look at a structure that hasn't been resolved before," says Hawley. "There is a lot more we can learn. The deeper we dive into structure, the more complexity we see, the more amazing the structure becomes. Structure provides so much insight into function.'"

Comment: Look at the picture. It has to be designed.

https://scx2.b-cdn.net/gfx/news/hires/2017/marriageofmi.png

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6309 views

Jellyfish evolved with lots of complexity, but where are the new genes?:

http://oceans.nautil.us/feature/582/jellyfish-genome-hints-that-complexity-isnt-genetic...

"But a January 2019 study appearing in Nature Ecology & Evolution shows that not to be the case—at least for jellyfish, humble organisms that evolved at a crucial juncture in animal history. They did not need more genes—or even notably different ones—to power their giant leap in complexity. This study adds to a growing body of work that casts doubt on finding straightforward genomic signatures of the evolution of complexity.

***

"Jellyfish begin their lives much like their cousins, as sessile polyps anchored to the seafloor, scrounging for food in the passing currents. Unlike their cousins, they eventually break free and transform into a free-swimming form known as a medusa, “what we normally think of when we think of jellyfish,” said David Gold, a biologist.

"Gold explained that the medusa stage represents a quantum leap in complexity. Medusas actively hunt plankton and navigate the water column with neural sensory structures that detect light and orientation. To go from being a stationary polyp to a floating medusa is almost akin to humans evolving the ability to swim through the air and capture birds with springy, netlike appendages.

***

“'We just had no idea of what sort of genetic changes were needed to go from this more simple lifestyle to this more complex lifestyle,” said Gold. To find out, the researchers decided to sequence the genome of Aurelia, the moon jellyfish, and then compare it to those of cnidarians without medusas.

***

"When it comes to building a body, it’s not just what genes exist that matters but also when they’re used. If you’re looking for genes that build complexity in jellyfish, then it makes sense to look for them when that complexity is manifesting, during medusa development. Gold thought that genes unique to jellyfish would be active during the transformation from polyp to medusa.

***

"She [ Srivastava] was intrigued by the finding that novel genes weren’t overrepresented in the medusa stage because it suggests that “very different body plans can arise by connecting the same genes in different ways.”

"Gold’s results broadly align with those from another jellyfish genome, Clytia. That research, too, found no large role for novel genes. To add to the mystery, there were even hints that in Clytia, more ancient and conserved pathways played a larger role in medusa development.
In any case, for now, the genetic changes that orchestrate this metamorphosis in jellyfish remain unknown. The transformation may depend on regions of the genome that don’t encode proteins, but instead regulate when genes are turned on and off. Perhaps it’s easier for life to innovate by rearranging its existing gene networks instead of evolving scores of new genes.

***

"When Srivastava and colleagues sequenced the first sponge genome in 2010, they were stunned to find genes that built the brains and muscles of other animals already present in this brainless, muscleless sponge. “The genes are the same, but clearly they aren’t working together to do the same things,” she said."

Comment: Not surprising. Certainly there is a strong drive in evolution to become more complex. It is obvious that simple looks at DNA will not give us answers. There are gene relationships we do not understand and layers of control that are still being discovered. we still do not know how cells produce the results they control. God is a clever designer. It ius too complex for production by a chance mechanism.

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6317 views

Under “energy requirements”:

DAVID: It can be assumed each expansion of the brain was accompanied by a proportionate increase in caloric requirement. This means not only had there to be several simultaneous bony changes but also an adjustment in the division of caloric energy usage and an increase in calorie intake. I doubt this all could be naturally coordinated by chance evolution and had to be designed.

dhw: I would suggest that since cells are living organisms that require sustenance, the larger the community, the more sustenance would be required. I really don’t know why this should be regarded as a special problem or how chance versus design enters the argument, but I agree that the complexities of the cell provide the best possible evidence for design.

DAVID: Again skipped over all the triple bony change requirements that dictate the need for design and note the human digestive tract made new adaptations for the energy need as compared to apes:

I was merely pointing out that there was nothing special about the brain’s need for enough sustenance – that applies to all cell communities – and I didn’t know why you brought chance into it. Adaptations generally require the cooperation of all the cell communities in all areas of evolution.

Under “Genome complexity”

QUOTE: Perhaps it’s easier for life to innovate by rearranging its existing gene networks instead of evolving scores of new genes.

DAVID: Not surprising. Certainly there is a strong drive in evolution to become more complex. It is obvious that simple looks at DNA will not give us answers. There are gene relationships we do not understand and layers of control that are still being discovered. we still do not know how cells produce the results they control. God is a clever designer. It ius too complex for production by a chance mechanism.

As regards the quote, life doesn’t innovate. Innovations take place in living organisms, which means there must be some kind of mechanism within the organisms. This means organisms “rearrange their existing gene networks” – or for David, God preprogrammed all the rearrangements 3.8 billion years ago or he steps in to dabble with every existing network. David is quite right: “we do not know how cells produce the results they control”. But the very statement that they control the results might suggest that cellular intelligence (possibly designed by a God) is a very plausible alternative to chance, divine preprogramming and divine dabbling.

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6273 views

Under “energy requirements”:

DAVID: It can be assumed each expansion of the brain was accompanied by a proportionate increase in caloric requirement. This means not only had there to be several simultaneous bony changes but also an adjustment in the division of caloric energy usage and an increase in calorie intake. I doubt this all could be naturally coordinated by chance evolution and had to be designed.

dhw: I would suggest that since cells are living organisms that require sustenance, the larger the community, the more sustenance would be required. I really don’t know why this should be regarded as a special problem or how chance versus design enters the argument, but I agree that the complexities of the cell provide the best possible evidence for design.

DAVID: Again skipped over all the triple bony change requirements that dictate the need for design and note the human digestive tract made new adaptations for the energy need as compared to apes:

dhw: I was merely pointing out that there was nothing special about the brain’s need for enough sustenance – that applies to all cell communities – and I didn’t know why you brought chance into it. Adaptations generally require the cooperation of all the cell communities in all areas of evolution.

The need for accommodation for an enlarged brain required all the changes I noted, including changes in or by three individuals, father, Mother, and new-sized baby. Cell committees must be clairvoyant to cooperate as dhw describes.

Under “Genome complexity”

QUOTE: Perhaps it’s easier for life to innovate by rearranging its existing gene networks instead of evolving scores of new genes.

DAVID: Not surprising. Certainly there is a strong drive in evolution to become more complex. It is obvious that simple looks at DNA will not give us answers. There are gene relationships we do not understand and layers of control that are still being discovered. we still do not know how cells produce the results they control. God is a clever designer. It ius too complex for production by a chance mechanism.

dhw: As regards the quote, life doesn’t innovate. Innovations take place in living organisms, which means there must be some kind of mechanism within the organisms. This means organisms “rearrange their existing gene networks” – or for David, God preprogrammed all the rearrangements 3.8 billion years ago or he steps in to dabble with every existing network. David is quite right: “we do not know how cells produce the results they control”. But the very statement that they control the results might suggest that cellular intelligence (possibly designed by a God) is a very plausible alternative to chance, divine preprogramming and divine dabbling.

Again glossing over 'cell intelligence'. It had a definite cause, but dhw's wishy-washy discussion leaves the source hanging. Chance or God the designer?

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dhw: I was merely pointing out that there was nothing special about the brain’s need for enough sustenance – that applies to all cell communities – and I didn’t know why you brought chance into it. Adaptations generally require the cooperation of all the cell communities in all areas of evolution.

DAVID: The need for accommodation for an enlarged brain required all the changes I noted, including changes in or by three individuals, father, Mother, and new-sized baby. Cell committees must be clairvoyant to cooperate as dhw describes.

We are talking about the brain’s need for sustenance, so why do you go back to an issue already discussed and dealt with? The expansion of the brain will require the expansion of the skull, with the cells of the skull responding to the cells of the brain. These changes will require changes to the mother’s pelvis, the cells of which will respond to the requirements of the foetus. No doubt there would have been many deaths before the adaptation was complete, but in all cases, the cell communities respond to changes – they do not anticipate them. I find this more plausible than your God stepping in and fiddling with a group of homos who wake up next morning with bigger brains, skulls and pelvises.

Under “the obstetric dilemma”: The maternal pelvis is frequently considered to be subject to two counteracting evolutionary forces: decreased height and increased mediolateral breadth in order to optimize the biomechanics of locomotion, and increased anteroposterior dimensions in order to enable birth of the unusually encephalized human infant. The compromise imposed by these antagonistic demands manifests as a difficult passage of the fetal head through the birth canal, resulting in the birth process being a more complex and lengthy procedure in humans than in closely related species of ape. The antagonistic interaction of bipedalism and encephalization has been assumed to have followed the emergence of the large Homo brain within the last 2 million years. (David’s bold)

DAVID: This obstetric dilemma is a major evolutionary issue as this review makes quite clear, and even has major obstetric importance today. I don't believe dhw's 'smart cooperating' cells could solve the problems by themselves, but God could easily.

The above puts paid to your God’s overnight expansion of brain, skull and pelvis, and clearly shows that the whole process of maternal pelvis adaptation was not only long but also difficult, and is still difficult today. Why did your God, who could do it “easily”, make it so lengthy and so difficult? I see nothing in this whole article to contradict the proposal I have put forward. The only new factor is the requirements of “locomotion” (itself a possible cause of brain expansion).

DAVID: There are gene relationships we do not understand and layers of control that are still being discovered. we still do not know how cells produce the results they control.

dhw: David is quite right: “we do not know how cells produce the results they control”. But the very statement that they control the results might suggest that cellular intelligence (possibly designed by a God) is a very plausible alternative to chance, divine preprogramming and divine dabbling.

DAVID: Again glossing over 'cell intelligence'. It had a definite cause, but dhw's wishy-washy discussion leaves the source hanging. Chance or God the designer?

I am delighted that your comment offers no opposition to the theory of cellular intelligence. I don’t “gloss over” the cause – I openly admit that I don’t know whether it’s chance, God, or some form of panpsychism.

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DAVID: The need for accommodation for an enlarged brain required all the changes I noted, including changes in or by three individuals, father, Mother, and new-sized baby. Cell committees must be clairvoyant to cooperate as dhw describes.

dhw: No doubt there would have been many deaths before the adaptation was complete, but in all cases, the cell communities respond to changes – they do not anticipate them. I find this more plausible than your God stepping in and fiddling with a group of homos who wake up next morning with bigger brains, skulls and pelvises.

And I do not believe cell committees can create new species, which is your claim.

Under “the obstetric dilemma”: The maternal pelvis is frequently considered to be subject to two counteracting evolutionary forces: decreased height and increased mediolateral breadth in order to optimize the biomechanics of locomotion, and increased anteroposterior dimensions in order to enable birth of the unusually encephalized human infant. The compromise imposed by these antagonistic demands manifests as a difficult passage of the fetal head through the birth canal, resulting in the birth process being a more complex and lengthy procedure in humans than in closely related species of ape. The antagonistic interaction of bipedalism and encephalization has been assumed to have followed the emergence of the large Homo brain within the last 2 million years. (David’s bold)

DAVID: This obstetric dilemma is a major evolutionary issue as this review makes quite clear, and even has major obstetric importance today. I don't believe dhw's 'smart cooperating' cells could solve the problems by themselves, but God could easily.

dhw: The above puts paid to your God’s overnight expansion of brain, skull and pelvis, and clearly shows that the whole process of maternal pelvis adaptation was not only long but also difficult, and is still difficult today. Why did your God, who could do it “easily”, make it so lengthy and so difficult? I see nothing in this whole article to contradict the proposal I have put forward. The only new factor is the requirements of “locomotion” (itself a possible cause of brain expansion).

Nothing 'put paid'. The new pelvis for upright posture and birthing large baby brain was a complicated redesign of the pelvis. Please remember Lucy had a tiny brain but her pelvis had adapted for mainly upright locomotion. Real brain expansion followed this in newer species. But the resultant very new pelvic shape still requires our difficult births. It is a trade off: we have full use of arms and hands and apes do not. As for why God took time, please remember my observation that God likes to evolve: the universe, the giant Milky Way which gobbled/es up satellite galaxies, the Earth, and then life. You never deny this, just ignore it.

DAVID: There are gene relationships we do not understand and layers of control that are still being discovered. we still do not know how cells produce the results they control.

dhw: David is quite right: “we do not know how cells produce the results they control”. But the very statement that they control the results might suggest that cellular intelligence (possibly designed by a God) is a very plausible alternative to chance, divine preprogramming and divine dabbling.

DAVID: Again glossing over 'cell intelligence'. It had a definite cause, but dhw's wishy-washy discussion leaves the source hanging. Chance or God the designer?

dhw: I am delighted that your comment offers no opposition to the theory of cellular intelligence. I don’t “gloss over” the cause – I openly admit that I don’t know whether it’s chance, God, or some form of panpsychism.

The 'glossing over' refers to a source of the appearance of 'cellular intelligence', which you have just enumerated, adding panpsychism, a nebulous invention that simply pushed further away the issue of where did panpsychism come from, if it even exists? I remind cells follow intelligent instructions implanted by God so they will function properly.

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From previous discussion:

David: As for why God took time, please remember my observation that God likes to evolve: the universe, the giant Milky Way which gobbled/es up satellite galaxies, the Earth, and then life. You never deny this, just ignore it.

This is an important point in understanding God: teh prime use of evolving his creations:

https://phys.org/news/2020-07-stars-born-galaxy-milky.html

"Writing in Nature Astronomy this week, Necib and her collaborators describe Nyx, a vast new stellar stream in the vicinity of the Sun, that may provide the first indication that a dwarf galaxy had merged with the Milky Way disk. These stellar streams are thought to be globular clusters or dwarf galaxies that have been stretched out along its orbit by tidal forces before being completely disrupted.

***

"How did the Milky Way become what it is today?

"'Galaxies form by swallowing other galaxies," Necib said. "We've assumed that the Milky Way had a quiet merger history, and for a while it was concerning how quiet it was because our simulations show a lot of mergers. Now, with access to a lot of smaller structures, we understand it wasn't as quiet as it seemed. It's very powerful to have all these tools, data and simulations. All of them have to be used at once to disentangle this problem. We're at the beginning stages of being able to really understand the formation of the Milky way.'"

Comment: It appears the Milky Way is one of the biggest giant spiral galaxies, which was created by an evolutionary process which used a system of simply gobbling up smaller satellite galaxies. This put the Earth two-thirds of the way out the second spiral arm, as very safe spot from all the life-destroying violent activity at the center. God obviously knows what He is doing, protecting the living planet He created.

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More of the mystery solved:

https://phys.org/news/2020-07-rna-key-stem-cells.html

"How does a stem cell—the raw material with which our organ and tissue cells are made—know what to become?

"In a study published July 8, University of Colorado Boulder researchers come one step closer to answering that fundamental question, concluding that the molecular messenger RNA (ribonucleic acid) plays an indispensable role in cell differentiation, serving as a bridge between our genes and the so-called "epigenetic" machinery that turns them on and off.

***

"'All genes are not expressed all the time in all cells. Instead, each tissue type has its own epigenetic program that determines which genes get turned on or off at any moment," said co-senior author Thomas Cech, a Nobel laureate and distinguished professor of biochemistry. "We determined in great detail that RNA is a master regulator of this epigenetic silencing and that in the absence of RNA, this system cannot work. It is critical for life."

***

"In a landmark paper in Cell, Rinn showed that inside the nucleus, RNA attaches itself to a folded cluster of proteins called polycomb repressive complex (PRC2), which is believed to regulate gene expression. Numerous other studies have since found the same and added that different RNAs also bind to different protein complexes.

***

"'RNA seemed to be playing the role of air traffic controller, guiding the plane—or protein complex—to the right spot on the DNA to land and silence genes," said Long.

"For a third step, they used the gene-editing technology known as CRISPR to develop a line of stem cells destined to become human heart muscle cells but in which the protein complex, PRC2, was incapable of binding to RNA. In essence, the plane couldn't connect with air-traffic control and lost its way, and the process fell apart.

"By day 7, the normal stem cells had begun to look and act like heart cells. But the mutant cells didn't beat. Notably, when normal PRC2 was restored, they began to behave more normally."

Comment: Obviously a carefully designed system which had to overcome the problem in sexual reproduction resulting in one cell with all the instructions. Thousands of different cells have to be produced and isolated and organized into their proper organs by a process called embryology we are barely beginning to understand. Designer absolutely required

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dhw: […] No doubt there would have been many deaths before the adaptation was complete, but in all cases, the cell communities respond to changes – they do not anticipate them. I find this more plausible than your God stepping in and fiddling with a group of homos who wake up next morning with bigger brains, skulls and pelvises.

DAVID: And I do not believe cell committees can create new species, which is your claim.

I gave you a full response to your claim that in the context of brain/skull/pelvis, my theory required clairvoyance. It doesn’t. Skull responds to requirements of brain, pelvis responds to requirements of foetus. No simultaneity, no clairvoyance. Your belief concerning speciation is irrelevant and does not provide an answer to my proposal.

dhw: The above puts paid to your God’s overnight expansion of brain, skull and pelvis, and clearly shows that the whole process of maternal pelvis adaptation was not only long but also difficult, and is still difficult today. Why did your God, who could do it “easily”, make it so lengthy and so difficult? I see nothing in this whole article to contradict the proposal I have put forward. The only new factor is the requirements of “locomotion” (itself a possible cause of brain expansion).

DAVID: Nothing 'put paid'. The new pelvis for upright posture and birthing large baby brain was a complicated redesign of the pelvis. Please remember Lucy had a tiny brain but her pelvis had adapted for mainly upright locomotion. Real brain expansion followed this in newer species. But the resultant very new pelvic shape still requires our difficult births. It is a trade off: we have full use of arms and hands and apes do not.

I am not disputing any of this! Your theory is that your God kept on simultaneously enlarging brains, skulls and pelvises overnight. I suggest that the enlargements would have been sequent and would have required time.

DAVID: As for why God took time, please remember my observation that God likes to evolve: the universe, the giant Milky Way which gobbled/es up satellite galaxies, the Earth, and then life. You never deny this, just ignore it.

There is no point in denying the blindingly obvious fact that evolution took time! But according to you, each enlargement was abrupt – it did not take time, because your God dabbled each one. And to make matters worse, you say he could easily solve what is still a problem that causes difficulty. So why didn’t he?

DAVID: Again glossing over 'cell intelligence'. It had a definite cause, but dhw's wishy-washy discussion leaves the source hanging. Chance or God the designer?

dhw: I am delighted that your comment offers no opposition to the theory of cellular intelligence. I don’t “gloss over” the cause – I openly admit that I don’t know whether it’s chance, God, or some form of panpsychism.

DAVID: The 'glossing over' refers to a source of the appearance of 'cellular intelligence', which you have just enumerated, adding panpsychism, a nebulous invention that simply pushed further away the issue of where did panpsychism come from, if it even exists? I remind cells follow intelligent instructions implanted by God so they will function properly.

“Just enumerated, adding panpsychism…”? I have ALWAYS allowed for God as the inventor of cellular intelligence, and for years I have included a form of panpsychism in my list of possible “first causes”. The issue of where panpsychism came from, if it even exists, applies equally to your God. I don’t know why you are “reminding” me of your theory that 3.8 billion years ago your God programmed the first cells to pass on instructions for every single undabbled development in evolution, including life forms, econiches, strategies, lifestyles, natural wonders, responses to diseases etc. I remain stubbornly convinced that this is just a little far-fetched, and perhaps one might just consider the possibility that your God provided cells with the intelligence to design all of these themselves.

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6324 views

DAVID: And I do not believe cell committees can create new species, which is your claim.

dhw: I gave you a full response to your claim that in the context of brain/skull/pelvis, my theory required clairvoyance. It doesn’t. Skull responds to requirements of brain, pelvis responds to requirements of foetus. No simultaneity, no clairvoyance.

This response is an exact description of simultaneity. One change cannot follow another!

DAVID: Nothing 'put paid'. The new pelvis for upright posture and birthing large baby brain was a complicated redesign of the pelvis. Please remember Lucy had a tiny brain but her pelvis had adapted for mainly upright locomotion. Real brain expansion followed this in newer species. But the resultant very new pelvic shape still requires our difficult births. It is a trade off: we have full use of arms and hands and apes do not.

dhw: I am not disputing any of this! Your theory is that your God kept on simultaneously enlarging brains, skulls and pelvises overnight. I suggest that the enlargements would have been sequent and would have required time.

Same mess. All changes must occur at the same time for survival of baby and/or mother.

DAVID: As for why God took time, please remember my observation that God likes to evolve: the universe, the giant Milky Way which gobbled/es up satellite galaxies, the Earth, and then life. You never deny this, just ignore it.

dhw: There is no point in denying the blindingly obvious fact that evolution took time! But according to you, each enlargement was abrupt – it did not take time, because your God dabbled each one. And to make matters worse, you say he could easily solve what is still a problem that causes difficulty. So why didn’t he?

Never said it. Human pelvis has required shape for upright posture, results in hard births.

DAVID: Again glossing over 'cell intelligence'. It had a definite cause, but dhw's wishy-washy discussion leaves the source hanging. Chance or God the designer?

dhw: I am delighted that your comment offers no opposition to the theory of cellular intelligence. I don’t “gloss over” the cause – I openly admit that I don’t know whether it’s chance, God, or some form of panpsychism.

DAVID: The 'glossing over' refers to a source of the appearance of 'cellular intelligence', which you have just enumerated, adding panpsychism, a nebulous invention that simply pushed further away the issue of where did panpsychism come from, if it even exists? I remind cells follow intelligent instructions implanted by God so they will function properly.

dhw: “Just enumerated, adding panpsychism…”? I have ALWAYS allowed for God as the inventor of cellular intelligence, and for years I have included a form of panpsychism in my list of possible “first causes”. The issue of where panpsychism came from, if it even exists, applies equally to your God. I don’t know why you are “reminding” me of your theory that 3.8 billion years ago your God programmed the first cells to pass on instructions for every single undabbled development in evolution, including life forms, econiches, strategies, lifestyles, natural wonders, responses to diseases etc. I remain stubbornly convinced that this is just a little far-fetched, and perhaps one might just consider the possibility that your God provided cells with the intelligence to design all of these themselves.

To repeat from above, cells follow intelligent instructions given to them by God. Of course, you have forgotten Behe's very strong exposition which shows DNA devolves to advance evolution, strongly suggesting the instructions were there from the beginning.

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6282 views

DAVID: And I do not believe cell committees can create new species, which is your claim.

dhw: I gave you a full response to your claim that in the context of brain/skull/pelvis, my theory required clairvoyance. It doesn’t. Skull responds to requirements of brain, pelvis responds to requirements of foetus. No simultaneity, no clairvoyance.

DAVID: This response is an exact description of simultaneity. One change cannot follow another!

My response is an exact description of how one change follows another. Every change is a response. Why would the pelvis change if the foetus did not require change? Why would the skull expand if the brain didn’t expand? Still you cling to the vision of your God stepping in one evening and next morning our group of homos wake up with bigger brains, skulls and pelvises!

dhw: I am not disputing any of this! Your theory is that your God kept on simultaneously enlarging brains, skulls and pelvises overnight. I suggest that the enlargements would have been sequent and would have required time.

DAVID: Same mess. All changes must occur at the same time for survival of baby and/or mother.

And I have suggested to you that there may well have been many that did not survive until the changes had been finalized. Even now, the article emphasizes that human childbirth is a comparatively difficult process, as you say below.

DAVID: As for why God took time, please remember my observation that God likes to evolve: the universe, the giant Milky Way which gobbled/es up satellite galaxies, the Earth, and then life. You never deny this, just ignore it.

dhw: There is no point in denying the blindingly obvious fact that evolution took time! But according to you, each enlargement was abrupt – it did not take time, because your God dabbled each one. And to make matters worse, you say he could easily solve what is still a problem that causes difficulty. So why didn’t he?

DAVID: Never said it. Human pelvis has required shape for upright posture, results in hard births.

Yes, birth is hard. And no doubt it was even harder when the changes began to take place, and no doubt there were plenty of babies and mothers who did not survive. Concerning the “obstetric dilemma”, you wrote: “I don’t believe dhw’s ‘smart cooperating cells could solve the problems by themselves, but God could easily.” So God’s easy solution resulted in hard births. Why didn’t it result in easy births?

DAVID: I remind cells follow intelligent instructions implanted by God so they will function properly.

dhw: I don’t know why you are “reminding” me of your theory that 3.8 billion years ago your God programmed the first cells to pass on instructions for every single undabbled development in evolution, including life forms, econiches, strategies, lifestyles, natural wonders, responses to diseases etc. I remain stubbornly convinced that this is just a little far-fetched, and perhaps one might just consider the possibility that your God provided cells with the intelligence to design all of these themselves.

DAVID: To repeat from above, cells follow intelligent instructions given to them by God. Of course, you have forgotten Behe's very strong exposition which shows DNA devolves to advance evolution, strongly suggesting the instructions were there from the beginning.

Does Behe support your theory, as summarized above, with instructions for every new life form etc.? Please tell me how his theory (a theory, not a fact) disproves the theory that cellular intelligence was there from the beginning, and the cells themselves worked out how to use their DNA in order to advance evolution. And please remember that this theory allows for God as the creator of the original cells, their DNA and their intelligence.

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6294 views

DAVID: This response is an exact description of simultaneity. One change cannot follow another!

dhw: My response is an exact description of how one change follows another. Every change is a response. Why would the pelvis change if the foetus did not require change? Why would the skull expand if the brain didn’t expand? Still you cling to the vision of your God stepping in one evening and next morning our group of homos wake up with bigger brains, skulls and pelvises!

My point is all the changes have to occur at once, spontaneously

dhw: I am not disputing any of this! Your theory is that your God kept on simultaneously enlarging brains, skulls and pelvises overnight. I suggest that the enlargements would have been sequent and would have required time.

DAVID: Same mess. All changes must occur at the same time for survival of baby and/or mother.

dhw: And I have suggested to you that there may well have been many that did not survive until the changes had been finalized. Even now, the article emphasizes that human childbirth is a comparatively difficult process, as you say below.

DAVID: . Human pelvis has required shape for upright posture, results in hard births.

dhw: Yes, birth is hard. And no doubt it was even harder when the changes began to take place, and no doubt there were plenty of babies and mothers who did not survive. Concerning the “obstetric dilemma”, you wrote: “I don’t believe dhw’s ‘smart cooperating cells could solve the problems by themselves, but God could easily.” So God’s easy solution resulted in hard births. Why didn’t it result in easy births?

Silly question. Pelvis architecture is whet it has to be for upright posture

DAVID: To repeat from above, cells follow intelligent instructions given to them by God. Of course, you have forgotten Behe's very strong exposition which shows DNA devolves to advance evolution, strongly suggesting the instructions were there from the beginning.

dhw: Does Behe support your theory, as summarized above, with instructions for every new life form etc.? Please tell me how his theory (a theory, not a fact) disproves the theory that cellular intelligence was there from the beginning, and the cells themselves worked out how to use their DNA in order to advance evolution. And please remember that this theory allows for God as the creator of the original cells, their DNA and their intelligence.

Behe is a design theorist. I've personally talked with him. He and I think alike.

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6297 views

DAVID: This response is an exact description of simultaneity. One change cannot follow another!

dhw: My response is an exact description of how one change follows another. Every change is a response. Why would the pelvis change if the foetus did not require change? Why would the skull expand if the brain didn’t expand? Still you cling to the vision of your God stepping in one evening and next morning our group of homos wake up with bigger brains, skulls and pelvises!

DAVID: My point is all the changes have to occur at once, spontaneously

And my point is that each change was a response: skull responds to brain, pelvis (female) responds to foetus – though later you sudden jettison the importance of the foetus by focusing solely on the upright position. Spontaneously? Well, there’s a turn-up for the books. You mean your God didn’t dabble? The cell communities did it all by themselves?

DAVID: All changes must occur at the same time for survival of baby and/or mother.

dhw: And I have suggested to you that there may well have been many that did not survive until the changes had been finalized. Even now, the article emphasizes that human childbirth is a comparatively difficult process, as you say below.

DAVID: Human pelvis has required shape for upright posture, results in hard births.

dhw: Yes, birth is hard. And no doubt it was even harder when the changes began to take place, and no doubt there were plenty of babies and mothers who did not survive. Concerning the “obstetric dilemma”, you wrote: “I don’t believe dhw’s ‘smart cooperating cells could solve the problems by themselves, but God could easily.” So God’s easy solution resulted in hard births. Why didn’t it result in easy births?

DAVID: Silly question. Pelvis architecture is whet it has to be for upright posture.

You have forgotten the “dilemma” – female pelvis architecture had to be what it had to be to give birth to the larger brained foetus. And your sudden switch does not explain why God could easily find a solution and the easy solution was a hard birth.

dhw: Does Behe support your theory, as summarized above, with instructions for every new life form etc.? Please tell me how his theory (a theory, not a fact) disproves the theory that cellular intelligence was there from the beginning, and the cells themselves worked out how to use their DNA in order to advance evolution. And please remember that this theory allows for God as the creator of the original cells, their DNA and their intelligence.

DAVID: Behe is a design theorist. I've personally talked with him. He and I think alike.

I know he is a design theorist, as you are. Please tell us where he supports your theory that an all-powerful God’s one and only purpose was to specially design H. sapiens, but first he specially designed 3.X billion years’ worth of extinct, non-human life forms, natural wonders etc. And please explain how his theory disproves the theory summarized above.

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6248 views

dhw: My response is an exact description of how one change follows another. Every change is a response. Why would the pelvis change if the foetus did not require change? Why would the skull expand if the brain didn’t expand? Still you cling to the vision of your God stepping in one evening and next morning our group of homos wake up with bigger brains, skulls and pelvises!

DAVID: My point is all the changes have to occur at once, spontaneously

dhw: And my point is that each change was a response: skull responds to brain, pelvis (female) responds to foetus – though later you sudden jettison the importance of the foetus by focusing solely on the upright position. Spontaneously? Well, there’s a turn-up for the books. You mean your God didn’t dabble? The cell communities did it all by themselves?

No. God did it by programming and/or dabble. Mother, Father, and new-sized baby head all happened spontaneously as God designed them.

DAVID: Human pelvis has required shape for upright posture, results in hard births.

dhw: Yes, birth is hard. And no doubt it was even harder when the changes began to take place, and no doubt there were plenty of babies and mothers who did not survive. Concerning the “obstetric dilemma”, you wrote: “I don’t believe dhw’s ‘smart cooperating cells could solve the problems by themselves, but God could easily.” So God’s easy solution resulted in hard births. Why didn’t it result in easy births?

DAVID: Silly question. Pelvis architecture is what it has to be for upright posture.

dhw: You have forgotten the “dilemma” – female pelvis architecture had to be what it had to be to give birth to the larger brained foetus. And your sudden switch does not explain why God could easily find a solution and the easy solution was a hard birth.

It was a solution which resulted in hard births. I conducted about 90 births in my training, so I don't forget the dilemma.

dhw: Does Behe support your theory, as summarized above, with instructions for every new life form etc.? Please tell me how his theory (a theory, not a fact) disproves the theory that cellular intelligence was there from the beginning, and the cells themselves worked out how to use their DNA in order to advance evolution. And please remember that this theory allows for God as the creator of the original cells, their DNA and their intelligence.

DAVID: Behe is a design theorist. I've personally talked with him. He and I think alike.

dhw: I know he is a design theorist, as you are. Please tell us where he supports your theory that an all-powerful God’s one and only purpose was to specially design H. sapiens, but first he specially designed 3.X billion years’ worth of extinct, non-human life forms, natural wonders etc. And please explain how his theory disproves the theory summarized above.

His 'Darwin Devolves' book shows his scholarship in evolutionary theory. He looks to the genome for all sources of the information that runs living biology (cell intelligent processes). I discussed this with him personally. He does not accept your theory of intelligent cells. Since he thinks degrading DNA advances evolution, he obviously thinks that pre-programming happened. I presented this thought in the past.

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6268 views

dhw: And my point is that each change was a response: skull responds to brain, pelvis (female) responds to foetus – though later you sudden jettison the importance of the foetus by focusing solely on the upright position. Spontaneously? Well, there’s a turn-up for the books. You mean your God didn’t dabble? The cell communities did it all by themselves?

DAVID: No. God did it by programming and/or dabble. Mother, Father, and new-sized baby head all happened spontaneously as God designed them.

Programming/dabbling are a strange form of spontaneity, which I understand as meaning without planning or organization. I wouldn’t accept the word anyway, as I propose that the cell communities all adjusted to the new requirements with an organized sequence of responses (not a simultaneous, programmed/dabbled expansion in advance of new requirements).

dhw:… you wrote: “I don’t believe dhw’s ‘smart cooperating cells could solve the problems by themselves, but God could easily.” So God’s easy solution resulted in hard births. Why didn’t it result in easy births?

DAVID: Silly question. Pelvis architecture is what it has to be for upright posture.

dhw: You have forgotten the “dilemma” – female pelvis architecture had to be what it had to be to give birth to the larger brained foetus. And your sudden switch does not explain why God could easily find a solution and the easy solution was a hard birth.

DAVID: It was a solution which resulted in hard births. I conducted about 90 births in my training, so I don't forget the dilemma.

You said the architecture was for upright posture, whereas you began the discussion with the problem of accommodating the foetus’s larger brain. And you still haven’t explained why your God could easily find the solution if the solution he came up with was hard. I suppose you mean he found it easy to come up with a solution that made birth hard.

DAVID: Behe is a design theorist. I've personally talked with him. He and I think alike.

dhw: I know he is a design theorist, as you are. Please tell us where he supports your theory that an all-powerful God’s one and only purpose was to specially design H. sapiens, but first he specially designed 3.X billion years’ worth of extinct, non-human life forms, natural wonders etc. And please explain how his theory disproves the theory summarized above.

DAVID: His 'Darwin Devolves' book shows his scholarship in evolutionary theory. He looks to the genome for all sources of the information that runs living biology (cell intelligent processes). I discussed this with him personally. He does not accept your theory of intelligent cells. Since he thinks degrading DNA advances evolution, he obviously thinks that pre-programming happened. I presented this thought in the past.

I’m quite happy with the idea that cellular intelligence lies within the genome, but thank you for discussing my idea with him. As regards degrading and preprogramming, please see the entry under “brain expansion”.

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6273 views

Two helices found in human cells:

https://www.newscientist.com/article/2249390-quadruple-stranded-dna-seen-in-healthy-hum...

"The world’s most famous molecule – the DNA double helix – sometimes doubles up again. Researchers have now found this quadruple-stranded form in healthy human cells for the first time.

"Four-stranded DNA has been seen before in some cancer cells and in lab-based chemistry experiments, but this is the first time the molecule has been visualised in healthy, living human cells, as a stable structure created by normal cellular processes.

“'We’ve undoubtedly demonstrated that the quadruple-strand DNA forms in living cells,” says Marco Di Antonio at Imperial College London. “This forces us to rethink the biology of DNA.”

"The DNA molecule is made up of four nucleobases – adenine, cytosine, guanine and thymine – and can configure itself in a number of ways. It creates a four-stranded structure when four guanine bases form a square – guanine is the only base able to bond with itself.

***

“'We know exactly what DNA does,” says Di Antonio, “but how does the cell know where to express genes and how much protein to make?” The researchers speculate that the quadruplex structure forms to hold the molecule open and facilitate the reading of the genetic code and thus the production of proteins. It may also influence the amount of each protein that is made.

"Usually, this function is performed by epigenetic markers – chemical tags on DNA that increase or decrease the activity of genes – and it seems that the quadruplex form of DNA has a similar role. “There is a sort of crosstalk between the formation of quadruplex DNA and epigenetic markers,” says Di Antonio. “The quadruplex form is an epigenetic mark in its own right.”

"Zoë Waller at the University of East Anglia, UK, says the work adds to the evidence that the quadruplex structures form part of normal DNA regulation and function, and that our view of the DNA double helix may be out of date. “We presume that this is the normal, native state of DNA, but this work is another exceptional example of mounting evidence that DNA is not a fixed structure or shape,” she says."

Comment: The DNA molecule has much more complex activity demonstrated. We keep learning how DNA imparts information in very many different ways so that our small number of genes creates our complexity

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6251 views

RNA can stop expression of genes:

https://phys.org/news/2020-07-amazing-small-rnas.html

"In most organisms, small bits of RNA play a key role in gene regulation by silencing gene expression. They do this by targeting and docking onto complementary sequences of gene transcripts (also RNA molecules), which stop the cell machinery from using them to make proteins. This mechanism is called RNA interference (RNAi), and it is critically important in biology.

"Remarkably, the RNAi phenomenon is not necessarily confined to single cells; it can also manifest in other tissues and organs far away from the cell of origin. Researchers have been able to observe it mostly in plants, but also in 'lower' animals such as the nematode worm C. elegans.

***

"They are the first to demonstrate unequivocally that these distant messengers in plants are short double-stranded RNA molecules. These consist of pairs (or double-strands) of just 21 to 24 nucleotides (the building blocks of RNA) called small interfering RNAs, or siRNAs for short. The team's paper was recently published in the journal Nature Plants.

"siRNAs usually emerge as large and complex populations from the genomes of viruses that have infected a cell. But a cell's own genes can also serve as blueprints for these molecules. As a result, cells can use RNAi to silence not only invading viruses but also their own genes.

***

"Not only did the ETH researchers identify the elusive long-distance messengers, they also show, in their study, how siRNAs move and carry out their function. They found that, as long as an siRNA molecule exists as a free double-strand, it is mobile because it cannot bind to a matching RNA transcript. To bind, it first has to be "uploaded" to a specific Argonaute (AGO) effector protein. Only once bound to the correct AGO protein can the siRNA silence the target transcript; the process eventually destroys the fragment itself. The model plant used for the study has ten different AGO proteins, several of which recognize matching siRNA fragments with specific signatures; these signatures are not homogeneous among the large cohorts of mobile siRNAs produced from viruses or the plant's own genes.

***

"'The amount and diversity of AGO proteins in traversed cells coupled to the siRNA-intrinsic signatures function together as a kind of molecular sieve, the form of which may differ from cell type to cell type along the siRNA path. Depending on the spatial configuration of this sieve, a wide variety of siRNA movement patterns can be produced," Voinnet explains. He adds, "Even more interestingly, some AGOs can be induced by stress or developmental signals such that the spatial shape of the sieve can change and evolve at any given time".

"The countless movement patterns thus lend the mobile RNAi system almost boundless flexibility and versatility in shaping gene expression across distances. Now that they have understood the process, the team of researchers is trying to engineer artificial sieves in plants as a way to control, with high precision, when and where specific siRNAs can move, a method which could have applications in agriculture."

Comment: Certainly another layer of genetic controls. Perhaps it is the same in humans, where so few genes produce so complex an organism.

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6176 views

It is a very complex process of dividing chromosome which uses supposed junk DNA to guide it:

https://evolutionnews.org/2020/07/dna-may-be-junk-at-one-level-but-of-utmost-significan...

I mentioned that chromosomes can and do have roles that go far beyond the so-called “Central Dogma.” Nowhere is this point better demonstrated, it would seem, than in the phenomenon of meiosis or “reductional division,” which generates a haploid gamete from a diploid germ cell by means of an intricate series of developmental events. Indeed, it is during the latter stages of the production of an animal oocyte that many functionalities of what some disparage as “junk DNA” take center stage.

***

Chromosomes that are about to undergo meiosis (or mitosis) have a distinct ensemble of functions that are grouped and harnessed ever so intricately into kinetochores, which are the “levers” of their maneuverings. These are “over and above” (indeed, epi– to) nucleotides have long been observed to be peculiar in their qualities. For one thing, they are dynamic platforms that have roles that are phase- or stage-specific. In the case of metaphase I, for example, those of one set of sister chromatids have to be in cohesion (or be paired) and jointly linked to one pole, while those of the other set of sister chromatids have to likewise be in cohesion (or be paired) but jointly linked to the opposite pole.

***

What these two pieces of evidence suggest, then, is that what may be “junk” at one level may be of the utmost significance at another level. (my bold) This happens I think by way of a top-down causal process that Paul Davies (2012) has alluded to, explainable in part by the augmentation of:

the normal terms referring to local forces contained in the Hamiltonian for chromatin with additional (presumably small) non-local terms representing functional (i.e. semantic or contextual) information. By coupling the mechanical and informational dynamics in this manner, the dynamical laws describing chromatin behaviour would become time-dependent and change according to the informational state of the system. Information would then possess direct, albeit subtle, traction over matter and permit epigenetic control to be exercised directly on the chromatin itself. (my bold)

Such would involve an “explicit coupling between dynamical laws and information-rich states, thus endowing higher level entities, such as contextual information, with direct causal efficacy on matter alongside intermolecular forces.”

If we take such “contextual information” to be resident at all tiers of the meiosis I network, from the spindle as whole to (say) each and every centromeric locus, then “with direct causal efficacy” retroelement and satellite DNAs can be endowed with information-bearing states. Of course, “such a proposal represents a decisive break with the normal formulation of the theory of dynamical systems,” as Davies notes, which means that “theories of this sort remain largely unexplored.” But explore it we should…and especially where cytology meets “junk” DNA.

Comment: I have skipped over a highly complex description of the many protein parts of this mechanism. Note the two bolds. The first tells us, that junk DNA at one level, because it does not code for protein, has active duties elsewhere in the reproductive genome processes. The second bold notes the passage of information to the molecules to control the process. The final paragraph discusses that information and that much more research has to be done to explore how the information is utilized. The information drives the functions. Information implies a designing mind created the process.

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6222 views

Two active x chromosomes in female cells is toxic. Only one can be active:

https://phys.org/news/2020-08-reveals-sex-chromosomes-female-embryo.html

"Researchers at Massachusetts General Hospital (MGH) have solved a mystery that has long puzzled scientists: How do the bodies of female humans and all other mammals decide which of the two X chromosomes it carries in each cell should be active and which one should be silent?

"...the MGH team discovered the role of a critical enzyme in the phenomenon known as X chromosome inactivation (XCI), which is essential for normal female development and also sets the stage for genetic disorders known as X-linked diseases (such as Rett Syndrome) to occur.

"Scientists have known for over a half century that female mammals undergo XCI during embryo formation. Females have two copies of the X chromosome, and each carries many genes. Having genes expressed on both X chromosomes would be toxic to the cell, as would having both X chromosomes inactivated. To avoid these fates, females evolved with a mechanism that inactivates, or silences, one of the chromosomes. (my bold)

***

"It was already known that, prior to pairing, both X chromosomes are identical, or "symmetrical," meaning that they express the same genes.

"Importantly, both express a form of noncoding RNA called Xist, which plays a vital role in inactivating the X chromosome. However, both X chromosomes also express another form of RNA, Tsix, which blocks Xist and prevents XCI.

"In the Nature Cell Biology paper, Lee and her team show that an enzyme called DCP1A randomly chooses one X chromosome to bind to, and in doing so it cuts off, or "decaps," Tsix's protective cover, making the RNA unstable. However, because DCP1A exists in tiny quantities, there is only enough to bind to one X chromosome. "DCP1A flips the switch that starts the entire cascade of X chromosome inactivation," says Lee.

"As a result, a protein called CTCF—the "glue" that holds X chromosomes together during pairing—binds to the unstable Tsix RNA and causes it to shut down permanently. Xist is then able to complete the silencing of that X chromosome.

"DCP1A allows the two X chromosomes to have a fateful 'conversation'," says Lee, noting that there are many other instances where the body must choose which copy of a gene to express in order to maintain a healthy state. "This discovery," says Lee, "will help scientists understand how other molecular conversations take place in the cell."

Comment: Both chromosomes are identical so either will do. When sexual reproduction appeared during the evolutionary process, this mechanism had to be in place for survival after reproduction to occur. My bold points out the Darwinist authors assuming natural evolution created this by chance. I don't believe it. DCP1A is a giant enzyme molecule specific for the process. Unguided nature is extremely unlikely to find it in a necessary form. Only design fits.

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6136 views

Discovering the structure of mRNA initiation shows how it is guided:

https://phys.org/news/2020-09-protein-mrna-complex-insight-cancer.html

"Although nearly all our cells contain our entire genome, cells use different subsets of genes to make the proteins they need to perform their various functions. This requires precise control over the processes by which the DNA is first transcribed to produce mRNA and then mRNA is translated to make protein.

"Translation begins when a ribosome attaches to a piece of mRNA and scans along it until it finds a start codon, three letters of RNA that say "start translating here." There are over a dozen different proteins known as initiation factors involved in this process.

***

"Based on this structure, the researchers proposed a model of how the mRNA slots into a channel in the small ribosomal subunit, and a mechanism for how the mRNA might be pulled through the ribosome for scanning, like a strip of film through an old-style projector.

"They were able to predict that for most mRNAs, the start codon would need to be sufficiently far from the front end of the mRNA for it to be found in the scanning process, which was the confirmed biochemically by Sokabe and Fraser. Further conformation of the model was obtained by mass spectrometry carried out by Mark Skehel of the LMB."

Comment: It is an amazing designed structure, and of course can make mistakes.

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6064 views

It is highly complex:

https://science.sciencemag.org/content/369/6509/1286

"When the human genome was sequenced almost 20 years ago, many researchers were confident they'd be able to quickly home in on the genes responsible for complex diseases such as diabetes or schizophrenia. But they stalled fast, stymied in part by their ignorance of the system of switches that govern where and how genes are expressed in the body. Such gene regulation is what makes a heart cell distinct from a brain cell, for example, and distinguishes tumors from healthy tissue. Now, a massive, decadelong effort has begun to fill in the picture by linking the activity levels of the 20,000 protein-coding human genes, as shown by levels of their RNA, to variations in millions of stretches of regulatory DNA.

***

"But the complex main analysis (p. 1318) drives home just how convoluted the interconnections between genes and their regulatory DNA can be. The papers “are written in bureaucratese,” and the announced results are hard to decipher, says Dan Graur, an evolutionary biologist at the University of Houston and a well-known critic of big science.

***

"GTEx can't yet pin down sequences responsible for illnesses such as heart disease and kidney failure, or trace how the layers of gene regulation work together. “We shouldn't pack up our bags and say gene expression is solved,” says genomicist Ewan Birney, deputy director general of EMBL, who led another big genomics project called ENCODE.

***

"The heart of the GTEx database is a compilation of the complex relationships between stretches of regulatory DNA called expression quantitative trait loci, or eQTLs, and the genes they regulate.

***

"Now, after analyzing almost 20,000 samples, GTEx “has reached a size where we can gain much clearer, crisper insights,” says co-leader Kristin Ardlie, a human geneticist at the Broad Institute. She and her colleagues found that almost every human gene is regulated by at least one eQTL, many of which target multiple genes and presumably affect multiple traits.

***

"Likewise, Broad co-leader François Aguet and colleagues confirmed certain eQTLs extend their reach to distant genes, even those on other chromosomes. GTEx documented 143 such “trans” elements, some of which affect multiple genes across the genome.

***

"GWAS studies had identified more than 500 genetic variations that appeared to affect heart rhythm and electrical conductance. Frazer wanted to know how a heart-specific transcription factor called NKX2-5 influenced those traits. Her team had identified thousands of DNA variations that might affect NKX2-5's activity and so perhaps shift heart rhythm."

Comment: This degree of complexity involving many parts of the genome is not surprising, since we are formed from only 20,000+ genes.

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6038 views

This reveals the complexity:

https://science.sciencemag.org/content/369/6509/1359

Abstract
In bacteria, transcription and translation are coupled processes in which the movement of RNA polymerase (RNAP)–synthesizing messenger RNA (mRNA) is coordinated with the movement of the first ribosome-translating mRNA. Coupling is modulated by the transcription factors NusG (which is thought to bridge RNAP and the ribosome) and NusA. Here, we report cryo–electron microscopy structures of Escherichia coli transcription-translation complexes (TTCs) containing different-length mRNA spacers between RNAP and the ribosome active-center P site. Structures of TTCs containing short spacers show a state incompatible with NusG bridging and NusA binding (TTC-A, previously termed “expressome”). Structures of TTCs containing longer spacers reveal a new state compatible with NusG bridging and NusA binding (TTC-B) and reveal how NusG bridges and NusA binds. We propose that TTC-B mediates NusG- and NusA-dependent transcription-translation coupling.

Bacterial transcription and bacterial translation occur in the same cellular compartment, occur at the same time, and are coordinated processes in which the rate of transcription by the RNA polymerase (RNAP) molecule synthesizing an mRNA is coordinated with the rate of translation by the first ribosome (“lead ribosome”) translating the mRNA. Data indicate that the coordination is mediated by transcription elongation factors of the NusG/RfaH family, which contain an N-terminal domain (N) that interacts with RNAP β′ and β subunits and a flexibly tethered C-terminal domain (C) that interacts with ribosomal protein S10. These factors are thought to bridge, and thereby connect, the RNAP molecule and the lead ribosome. Further data indicate that the coordination is modulated by the transcription elongation factor NusA.

***

The results presented reframe our understanding of the structural and mechanistic basis of transcription-translation coupling. The results provide high-resolution structures of the previously described expressome;TTC-A that demonstrate its incompatibility with general transcription-translation coupling. In addition, the results provide high-resolution structures of a new structural state, TTC-B, with properties assignable to general, NusG-dependent, NusA-dependent transcription-translation coupling. Our results also show that NusG stabilizes TTC-B by bridging RNAP and the ribosome 30S head, that NusA stabilizes TTC-B by bridging RNAP and the ribosome 30S body, and that NusA serves as a coupling pantograph that bridges RNAP and the ribosome 30S body in a flexible manner that allows rotation of RNAP relative to the ribosome 30S body. Finally, the results provide testable new hypotheses regarding the identities of the RNAP and NusA structural modules crucial for transcription-translation coupling (RNAP β′ ZBD and NusA KH1) and the interactions made by those structural modules (interactions with ribosomal protein S3 in the S30 head and interactions wit1h ribosomal proteins S2 and S5 in the S30 body).

Comment: If this looks highly complex, it is. Only design can create this degree of controls resulting in accurate translation and transcription. Miraculous, yet we know mistakes can happen. It depends upon your viewpoint as to how to conceive of this. Paul Davies calls life a miracle in his book about life. But some wail over the mistakes in molecular function as though they are a huge disaster and present an impotent God. It all depends on the real recognition that life functions perfectly well almost all the time. I have presented the problem of errors to demonstrate a more complete picture of the problems attendant with this mechanism of life. If each reaction had a group of mentoring/monitoring molecules to make sure each fold occurred always correctly and on time, it would have been too cumbersome to work at the speed required. Yet many mechanisms like the ones presented here have very precise controls. But keep in mind, even they can allow an error.

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6064 views

A repeat due to the website acting up

The transcription and translation of DNA code is highly complex and tightly controlled:

https://science.sciencemag.org/content/369/6509/1335.2?utm_campaign=twis_sci_2020-09-10...

In bacteria, the rate of transcription of messenger RNA (mRNA) by RNA polymerase (RNAP) is coordinated with the rate of translation by the first ribosome behind RNAP on the mRNA. Two groups now present cryo–electron microscopy structures that show how two transcription elongation factors, NusG and NusA, participate in this coupling. Webster et al. found that NusG forms a bridge between RNAP and the ribosome when they are separated by mRNA. With shortened mRNA, NusG no longer links RNAP and the ribosome, but the two are oriented so that newly transcribed mRNA can enter the ribosome. Wang et al. provide further insight into the effect of mRNA length on the complex structures. They also include NusA and show that the NusG-bridged structure is stabilized by NusA.

Abstract: In bacteria, transcription and translation are coupled processes in which the movement of RNA polymerase (RNAP)–synthesizing messenger RNA (mRNA) is coordinated with the movement of the first ribosome-translating mRNA. Coupling is modulated by the transcription factors NusG (which is thought to bridge RNAP and the ribosome) and NusA. Here, we report cryo–electron microscopy structures of Escherichia coli transcription-translation complexes (TTCs) containing different-length mRNA spacers between RNAP and the ribosome active-center P site. Structures of TTCs containing short spacers show a state incompatible with NusG bridging and NusA binding (TTC-A, previously termed “expressome”). Structures of TTCs containing longer spacers reveal a new state compatible with NusG bridging and NusA binding (TTC-B) and reveal how NusG bridges and NusA binds. We propose that TTC-B mediates NusG- and NusA-dependent transcription-translation coupling.

Bacterial transcription and bacterial translation occur in the same cellular compartment, occur at the same time, and are coordinated processes in which the rate of transcription by the RNA polymerase (RNAP) molecule synthesizing an mRNA is coordinated with the rate of translation by the first ribosome (“lead ribosome”) translating the mRNA . Data indicate that the coordination is mediated by transcription elongation factors of the NusG/RfaH family, which contain an N-terminal domain (N) that interacts with RNAP β′ and β subunits and a flexibly tethered C-terminal domain (C) that interacts with ribosomal protein S10. These factors are thought to bridge, and thereby connect, the RNAP molecule and the lead ribosome. Further data indicate that the coordination is modulated by the transcription elongation factor NusA.

The results presented here define four structural classes of TTCs: TTC-A [the previously reported expressome; TTC-B, TTC-C, and TTC-D, and show that TTC-B has structural properties indicating that it mediates NusG-dependent, NusA-dependent transcription-translation coupling in E. coli.

The results presented reframe our understanding of the structural and mechanistic basis of transcription-translation coupling. The results provide high-resolution structures of the previously described expressome TTC-A that demonstrate its incompatibility with general transcription-translation coupling. In addition, the results provide high-resolution structures of a new structural state, TTC-B, with properties assignable to general, NusG-dependent, NusA-dependent transcription-translation coupling. Our results also show that NusG stabilizes TTC-B by bridging RNAP and the ribosome 30S head, that NusA stabilizes TTC-B by bridging RNAP and the ribosome 30S body, and that NusA serves as a coupling pantograph that bridges RNAP and the ribosome 30S body in a flexible manner that allows rotation of RNAP relative to the ribosome 30S body. Finally, the results provide testable new hypotheses regarding the identities of the RNAP and NusA structural modules crucial for transcription-translation coupling (RNAP β′ ZBD and NusA KH1) and the interactions made by those structural modules (interactions with ribosomal protein S3 in the S30 head and interactions wit1h ribosomal proteins S2 and S5 in the S30 body).

Comment: This is certainly a very highly complex system for decoding the genome with lots of controls. Accurate results are dependent upon no errors occurring and are critical because cells are constantly reproducing themselves all through life. Life is miraculous as Paul Davies calls it in his book. I have brought up the issue of errors to give a more complete view of what God has created. I believe this is the molecular system that has to be designed. I think a more complex system of molecular controls using more chaperoning molecules would have been too cumbersome resulting in reactions that were too slow for the high speed results required in life. Any analysis will show that the error rate is very tiny, indicating to me God did His design very well. Those who magnify the errors thinking that makes God look impotent or incompetent are not taking the view of God I take.

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6030 views

The study defines the proteins and genes involved:

https://phys.org/news/2020-10-dueling-proteins.html

"Wagner and her team have been studying two key groups of proteins that influence plant form and timing of developmental transitions. Terminal Flower 1 (TLF1) proteins promote branch formation. When it is repressed, flowers grow. Flowering Locus T (FT) proteins, on the other hand, promote flowering in response to seasonal cues like day length. Strangely enough, the two proteins are almost identical.

"'These two elements have significance galore," Wagner says. "Besides flowering, they're involved in tuberization in potatoes, bulb formation in onions, tendril formation in grapes, growth cessation in trees, lots of things."

***

"It was known that TFL1 and FT1 acted in opposing directions, each "tuning" the activity of the other, but the mechanism of their antagonism has remained fuzzy. In part this was because studying them has presented a technical challenge: They are only present in low levels in a limited number of cells.

***

"In the current study, to flesh out TFL1 and FT1's molecular mechanism, they first looked to see where TFL1 was found in the nuclei of plant cells, using the model species Arabidopsis thaliana. They found thousands of sites to which it bound, acting through the transcription factor FD, as neither TFL1 nor FT otherwise can bind directly to DNA. The sites to which TFL1 was recruited were consistent with its role in suppressing flowering and in suppressing gene expression.

"The researchers next examined the relationship of both TFL1 and FT with LEAFY, a gene that is known to give rise to flowers. When they mutated the sites where TFL1 regulates the LEAFY gene, LEAFY protein was now found in parts of the plant where TFL1 is present.

"'We also saw something that we didn't expect," Wagner says. "LEAFY was gone from all the regions that should make flowers."

"That suggested to the team that an unknown factor may be activating the LEAFY gene specifically in the flowering portion of plants via the same site through which TFL1 acts. So, they looked to FT, because of its importance in promoting flowering. By experimentally augmenting FT expression, they found that FT, also binding to the FD transcription factor, was required to act upon LEAFY to promote flower formation.

***

"They saw that under conditions that would normally induce the plant to flower, plants that still had normal FT failed to. "It was a strong phenotype and made it very clear to us that FT and TFL1 compete for this FD factor binding site," she says."

Comment: Again a very complex system to control various parts if plant shape and function. It requires design

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5932 views

Unearthing new layers of translation:

https://phys.org/news/2020-11-functions-evolution.html

"A large-scale study conducted by molecular biologists from Heidelberg University has yielded groundbreaking new insights into the evolution and regulation of gene expression in mammalian organs. The scientists investigated RNA synthesis and subsequent protein synthesis in the organs of humans and other representative mammals, and with the aid of sequencing technologies, they analyzed more than 100 billion gene expression fragments from various organs. They were able to demonstrate that the finely tuned interplay of the two synthesis processes during evolution was crucial for shaping organ functions.

"A complex interplay of activity between a large number of genes—known as gene expression—underlies organ functions. "Until now, our understanding of these essential genetic programs in mammals was limited to the first layer of gene expression—the production of messenger RNAs," explains Prof. Dr. Henrik Kaessmann, group leader of the "Functional evolution of mammalian genomes" research team at the Center for Molecular Biology of Heidelberg University (ZMBH). "The next layer—the actual synthesis of proteins at the ribosome through the translation of the messenger RNAs—remained largely unknown."

***

"In their large-scale study, the ZMBH researchers showed that the finely tuned interplay of the two synthesis processes during evolution was critical for shaping organ functions. For the first time, they were able to show that—in addition to regulation of messenger RNA production—other regulatory mechanisms at the layer of translation are crucial for optimizing the amount of protein produced in all organs. This is especially true in the testes, where translational regulation is key for sperm development. Another important finding concerns mutational changes in gene expression regulation that arose during evolution. These changes were often balanced between the two layers. Changes that offset one another were primarily maintained to ensure the production of consistent amounts of protein."

Comment: No surprise. A network of genes must exert control the size of an organ's protein output. Genes do much more than simply identify a protein type to be produced. As we delve into each biological process the layers appear with increased complexity. Not by chance.

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5907 views

Found in plants:

https://phys.org/news/2020-11-rna-genome.html

"RNA is the intermediary nucleic acid that carries these instructions from DNA to ribosomes, where proteins are produced within the cell. But in humans and in plants, only a tiny fraction of DNA produces the RNA that carries out protein-building instructions. In humans, almost 98% of the genome does not encode proteins. However, it often gives rise to RNA that does not produce proteins, called noncoding RNA. So what does this portion of the genome do?

***

"Now, research led by Wierzbicki shows that in plants, a portion of this noncoding RNA may play an essential role in protecting the integrity of the genome. This portion of noncoding RNA is produced from transposons, rogue pieces of genes that jump around within DNA, inserting themselves haphazardly and causing genetic diversity. Sometimes this diversity is beneficial, aiding evolution, says Wierzbicki, but sometimes it can trigger mutations that can lead to disease.

"The noncoding RNA produced from transposons is thought to protect the genome by making sure that transposable elements are permanently turned off. But how are transposons selected for silencing in the first place? In a recent study, the research team found evidence that this noncoding RNA is produced throughout the entire genome, not just at or around transposons.

***

"With the polymerase enzyme mutated, the researchers then compared the mutated plant to a wild-type plant—a plant that had not been altered. If they detected RNA in the wild-type plant but not in the mutant plant, they could confirm that the noncoding RNA was real. And they did.

"Next, the researchers wanted to understand the role of this noncoding RNA. They expected to find that noncoding transcription was taking place on transposons, but nowhere else outside of the transposons. But what they found was that noncoding transcription was happening almost everywhere in the genome.

***

"They found evidence that noncoding RNA is produced across almost 50% of the plant genome, while transposons composed only 10%-20% of the genome. By comparing their data to previously published results they further found evidence that this noncoding RNA is needed for silencing of transposons that became reactivated.

"'So when the transposon is new, or it has been activated in a way that the cell forgot it was previously marked as a foreign object, how can it be recognized as being foreign? Wierzbicki said. "There's one common factor that's always needed, and that's this noncoding RNA that we are studying. No matter where the transposon was inserted in the gene, it could not be turned off if the noncoding RNA was not present."

Comment: An amazing control process found in junk DNA. The exact role of jumping genes (transpons) is not known, but they are obviously active as described.

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5900 views

The finding of genome complexity is a bottomless pit of never ending steps of control:

https://science.sciencemag.org/content/370/6520/1105

"Human mitochondria have their own genome and ribosomes called mitoribosomes that respectively encode and synthesize essential subunits of complexes that use the energy from the oxidation of metabolites to drive the synthesis of adenosine triphosphate (ATP). These complexes are key to the health of the cell. Desai et al. studied a mitoribosome-associated quality control pathway that prevents aberrant translation. They purified mitoribosomes under conditions designed to induce stalling and determined the structures of two intermediates in the rescue pathway. These structures revealed two proteins that eject the unfinished polypeptide chain and peptidyl transfer RNA from the ribosome. Their cryo–electron microscopy dataset also revealed additional states that may correspond to intermediates in the mitochondrial translation elongation cycle. (my bold)

"Abstract
The human mitochondrial ribosome (mitoribosome) and associated proteins regulate the synthesis of 13 essential subunits of the oxidative phosphorylation complexes. We report the discovery of a mitoribosome-associated quality control pathway that responds to interruptions during elongation, and we present structures at 3.1- to 3.3-angstrom resolution of mitoribosomal large subunits trapped during ribosome rescue. Release factor homolog C12orf65 (mtRF-R) and RNA binding protein C6orf203 (MTRES1) eject the nascent chain and peptidyl transfer RNA (tRNA), respectively, from stalled ribosomes. Recruitment of mitoribosome biogenesis factors to these quality control intermediates suggests additional roles for these factors during mitoribosome rescue. We also report related cryo–electron microscopy structures (3.7 to 4.4 angstrom resolution) of elongating mitoribosomes bound to tRNAs, nascent polypeptides, the guanosine triphosphatase elongation factors mtEF-Tu and mtEF-G1, and the Oxa1L translocase.

***

"A paradigm shift occurred in the field of translation when it was discovered that cells use the translation machinery itself to detect errors and activate quality control mechanisms. Although the existence of quality control in mitochondria was predicted on the basis of analogy with bacteria and eukaryotic cytosol, very little was known about the molecular mechanisms. Our discovery of a mitoribosome-associated quality control pathway and structural characterization of elongating mitoribosomes now set the stage to understand the regulation of mitochondrial translation. We also demonstrate that exhaustive in silico classification of large cryo-EM datasets can serve as a viable alternative strategy to uncover processes involved in translation in the absence of suitable in vitro tools."

Comment: This last paragraph discusses the many levels of quality control that exist. My bold in the first paragraph indicates how important this control really is. It indicates the level of concern the designer had.

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5913 views

A new technique:

https://science.sciencemag.org/content/370/6520/1054.3?utm_campaign=ec_sci_2020-11-25&a...

" Unlike DNA, RNA can fold into a staggering number of distinct structures that perform diverse functions. Some structures transfer genetic information, and others regulate their own activities and life spans to act as catalysts for crucial reactions inside the cell. Our ability to visualize or predict the RNA structures that a cell can make is limited, hindering exploitation for RNA therapeutics. Aw et al. improved on a technology that uses nanopore technology to sequence RNA by measuring the changing current as the RNA nucleotides are pulled through the nanopore. This “PORE-cupine” technology incorporates structural probing by chemical modification and machine learning to capture structural information on a genome scale. The technique can detect structural differences between closely related RNAs encoded by the same genes."

Nat. Biotechnol. 10.1038/s41587-020-0712-z (2020).

Comment: A genomic workhorse. What information/instructions controls the RNA is still unknown. Requires intense design.

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5862 views

A new method of study finds out how:

https://www.sciencedaily.com/releases/2020/11/201127085440.htm

"During transcription, an enzyme called RNA polymerase wraps itself around the double helix of DNA, using one strand to match nucleotides to make a copy of genetic material -- resulting in a newly synthesized strand of RNA that breaks off when transcription is complete. That RNA enables production of proteins, which are essential to all life and perform most of the work inside cells.

"Just as with any coherent message, RNA needs to start and stop in the right place to make sense. A bacterial protein called Rho was discovered more than 50 years ago because of its ability to stop, or terminate, transcription. In every textbook, Rho is used as a model terminator that, using its very strong motor force, binds to the RNA and pulls it out of RNA polymerase. But a closer look by these scientists showed that Rho wouldn't be able to find the RNAs it needs to release using the textbook mechanism.

***

"The research, published online by the journal Science today, Nov. 26, 2020, determined that instead of attaching to a specific piece of RNA near the end of transcription and helping it unwind from DNA, Rho actually "hitchhikes" on RNA polymerase for the duration of transcription. Rho cooperates with other proteins to eventually coax the enzyme through a series of structural changes that end with an inactive state enabling release of the RNA.

***

"'It answers a fundamental question -- transcription is fundamental to life, but if it were not controlled, nothing would work. RNA polymerase by itself has to be completely neutral. It has to be able to make any RNA, including those that are damaged or could harm the cell. While traveling with RNA polymerase, Rho can tell if the synthesized RNA is worth making -- and if not, Rho releases it."

***

"'RNA polymerase moves along, matching hundreds of thousands of nucleotides in bacteria. The complex is extremely stable because it has to be -- if the RNA is released, it is lost," Artsimovitch said. "Yet Rho is able to make the complex fall apart in a matter of minutes, if not seconds.

***

"Though the study was conducted in bacteria, Artsimovitch said this termination process is likely to occur in other forms of life.

"'It appears to be common," she said. "In general, cells use similar working mechanisms from a common ancestor. They all learned the same tricks as long as these tricks were useful.'"

Comment: The last comment above makes sense given common descent. The mechanisms that control these molecular dances is not known, but my guess is that there are designed electrical forces that control The electrical parts of the molecules. The decision making must follow instruction al information in the genome.

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5871 views

Found in zebra fish:

https://www.sciencedaily.com/releases/2020/12/201203200557.htm

"Researchers at the Garvan Institute of Medical Research have uncovered a new form of DNA modification in the genome of zebrafish, a vertebrate animal that shares an evolutionary ancestor with humans ~400 million years ago.

"Dr Ozren Bogdanovic and his team discovered that unusually high levels of DNA repeats of the sequence 'TGCT' in the zebrafish genome undergo a modification called methylation, which may change the shape or activity of the surrounding DNA.

"We've revealed a new form of DNA methylation in zebrafish at TGCT repeats, and crucially, the enzyme that makes the modification," says Dr Bogdanovic,

***

"'DNA methylation is vital to cellular function, as it controls which genes are turned on and off," explains first author of the paper, PhD student Sam Ross. "This is why the cells in our body can carry out vastly different functions, despite having almost identical DNA." (my bold)

"There are four 'base' letters that make up DNA -- C, G, T and A. In vertebrates, methylation occurs mostly where the letter G follows a C ('CG'), but there are some exceptions. One example is methylation at non-CG sites in human brain cells, aberrations of which have been linked to Rett Syndrome, a genetic disorder that impairs growth, movement and speech in children.

***

"'We were fascinated to see that methylation levels at TGCT repeats were higher than any non-CG methylation previously observed in the majority of adult vertebrate tissues," says Dr Bogdanovic. "Further, this methylation was present at high levels in the sperm and egg, absent in the fertilised egg, and then appeared again in the growing embryo, reaching its highest levels in adult tissues such as the brain and gonads. While we are yet to reveal how this modification changes gene expression, we believe TGCT methylation to be linked to the 'awakening' of the embryonic genome in zebrafish."

"The researchers further revealed that the enzyme Dnmt3ba was responsible for methylating the TGCT repeats in the zebrafish genome."

Comment: It is not surprising there is more than one methylation mechanism to modify DNA. Note the bold above.

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5822 views

Extreme complexity of specialized molecules:

https://science.sciencemag.org/content/370/6523/eabc3753

"Abstract
Spliceosome activation involves extensive protein and RNA rearrangements that lead to formation of a catalytically active U2/U6 RNA structure. At present, little is known about the assembly pathway of the latter and the mechanism whereby proteins aid its proper folding. Here, we report the cryo–electron microscopy structures of two human, activated spliceosome precursors (that is, pre-Bact complexes) at core resolutions of 3.9 and 4.2 angstroms. These structures elucidate the order of the numerous protein exchanges that occur during activation, the mutually exclusive interactions that ensure the correct order of ribonucleoprotein rearrangements needed to form the U2/U6 catalytic RNA, and the stepwise folding pathway of the latter. Structural comparisons with mature Bact complexes reveal the molecular mechanism whereby a conformational change in the scaffold protein PRP8 facilitates final three-dimensional folding of the U2/U6 catalytic RNA."

***

"Conclusions
The human pre-Bact structures presented here reveal that there is an intricate cascade of highly coordinated structural changes during the activation phase of the human spliceosome, involving mutually exclusive protein-protein and protein-RNA interactions that facilitate the directionality of the activation process. One unexpected finding of our studies was that the conformational change in PRP8 leading to its closed conformation first occurs during the late stages of activation. An open PRP8 conformation would be important to allow space for the initial stepwise rearrangements in the U2 and U6 snRNAs that lead to the U6 ISL and U2/U6 helix Ib and to accommodate KIN17 in pre-Bact-2 and WBP11, which appears to stabilize and/or position the U6 ISL in pre-Bact-1. Our studies show that the folding of the native 3D structure of the U2/U6 active site proceeds as follows. First, key U2/U6 secondary structural elements are sequentially formed and, together with a large number of proteins—including CDC5L, PLRG1, SYF3, SKIP, and CWC15—they are anchored and/or positioned on the central PRP8 scaffold while in its open B complex conformation. Second, during PRP8’s subsequent conformational change, the U2/U6 RNA elements that are docked to the Large domain are moved toward the U6 ISL. Concomitantly, all proteins docked to the PRP8 Large domain are also repositioned, thereby restricting the space in the closed PRP8 cavity. In this manner a proteinaceous folding chamber or mold is generated that aids U2/U6 helix Ia formation and the final tertiary folding of the active site RNA. Thus, the cryo-EM structures of two human pre-Bact complexes presented here allow new insights into the strategy used by the spliceosome to assemble its catalytic RNA network and how a conformational rearrangement in PRP8 facilitates the 3D folding of the catalytically active U2/U6 RNA."

Comment: Look at the models of the machinery. Design cannot be denied. The orchestrated opening and folded of orchestrated molecules in concert reeks of mental design.

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5787 views

Everyone's DNA has a variety of differing enhancers that make each of us different:

https://medicalxpress.com/news/2020-12-vary-biologically.html

"Genetics has made huge strides over the past 20 years, from the sequencing of the human genome to a growing understanding of factors that turn genes on and off, namely transcription factors and the DNA "enhancer" sequences they bind to. New research from Boston Children's Hospital introduces another previously unknown layer of human genetics. It finds genetic variation in a gene's ability to react to chemical signals from the outside.

***

"'We found that human genetics determine, on a gene to gene basis, whether a cell will respond to an outside signal," says Zon, who is also affiliated with Dana-Farber/Boston Children's Cancer and Blood Disorders Center, the Howard Hughes Medical Institute, and the Harvard Stem Cell Institute. "We believe that many genetic conditions are due to a defect in this response—a 'signalopathy.'"

***

"As it turns out, many variants tied to these traits mapped to a small subset of gene enhancers. These enhancers bind to two types of gene regulators: master transcription factors that regulate which type of blood cell is being made, and signaling transcription factors that coordinate responses to signals from outside the cell.

"When Zon and colleagues looked at blood cell progenitors in the lab, they found that many of the variants altered the DNA sequences of enhancers to which signaling transcription factors bind. This, they showed, prevented the factors from binding to the enhancer. That missed signal prevented adjacent genes from turning on—genes that normally would turn on in response to cues driving red blood cell maturation.

***

"GWAS studies have mapped many traits to variations in DNA enhancer sequences. But no one had ever shown that traits can be altered because of a failure of signals to get through.

"'This wasn't known before," says Zon. "If we want to better understand human variation, we have to find those regions in the genome, in every tissue, that are receiving transcriptional signals from outside the cell. People vary in how much signaling can happen in an individual gene.'"

Comment: Most of the DNA active in these processes is not in the coding areas and shows that non-coding areas are vital to functions. 3-D relationships are extremely important.

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5811 views

How does life search for the right folded protein for the right function to result?:

https://evolutionnews.org/2020/12/protein-folding-breakthrough-evolution-or-design/

"DeepMind is a leader in artificial intelligence (AI). Its geniuses managed to beat humans at the popular name Go using its AlphaGo algorithm. Its AI systems have now reached 90 percent success at predicting how a protein will fold.

***

"A major challenge, however, is that the number of ways a protein could theoretically fold before settling into its final 3D structure is astronomical. In 1969 Cyrus Levinthal noted that it would take longer than the age of the known universe to enumerate all possible configurations of a typical protein by brute force calculation — Levinthal estimated 10^300 possible conformations for a typical protein. Yet in nature, proteins fold spontaneously, some within milliseconds — a dichotomy sometimes referred to as Levinthal’s paradox.

***

"But we need to remember that this folding problem that has baffled humans for 50 years is solved rapidly in living cells at every moment. Levinthal noted that proteins routinely “fold spontaneously, some within milliseconds” inside the cell. A few need help from chaperones to find their native fold, but many go directly from 1D amino acid sequence to 3D functional protein.

"That’s not all. The cell has repair enzymes, too, that can dismantle improperly folded proteins and fix them or replace them if they are irreparable.

***

"Returning to the protein folding problem, we have seen that the search space for protein folds is vast beyond comprehension, like an island as big as the universe. Observing cells routinely folding proteins quickly and accurately, one can conclude therefore that a mind was behind the information. That conclusion is certified by watching AI experts using their minds to reverse engineer protein folds. AI is not inventing sequences that will fold; it is trying to figure out how a given sequence will produce an observed functional fold. Inventing a fold de novo is the harder problem.

***

"In short, DeepMind’s achievement is laudable, but the real prize goes to the designer of protein systems: their encoding in DNA, their translation in the ribosome, their spontaneous (sometimes chaperone-assisted) folding, their functions, their interactions, and their repair mechanisms. All those get perfect scores when not harmed by random mutations that degrade information. AI has not even begun to imitate those capabilities. Any higher scores through AI in the future will be attained by intelligent design, not evolution. The news only underscores the superior knowledge built into the molecular basis of life."

Comment: If this doesn't prove a designer did it, nothing will. Life is here because the proteins are expertly folded for coordinated function

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5775 views

Massive numbers of cell divisions make organisms, so no chromosome can be left behind:

https://phys.org/news/2021-01-cell-biologists-decipher-chromosome-left.html

"Starting as a single cell, organisms undergo millions of generations of divisions to ultimately generate the bones, heart, brain and other components that make up a living being. The mainspring within this intricate process is the transfer of DNA through each subsequent cell split within discrete packets called chromosomes.

***

"A new study published in the journal Science by postdoctoral scholar Pablo Lara-Gonzalez, Division of Biological Sciences Professor Arshad Desai and their colleagues addresses the mystery of how chromosomes are inherited correctly every time a cell divides. Using a novel probe that monitors a key aspect of this process, Lara-Gonzalez and Desai have detailed the mechanics behind a "wait" signal that ensures that cell division isn't prematurely set in motion.

"The researchers concentrated their investigations on a pathway in the cell called the "spindle checkpoint," which is a type of quality control mechanism that ensures accurate chromosome inheritance during cell division. The spindle checkpoint pathway is activated at a site on the chromosome called the kinetochore, a mechanical interface where protein fibers are coupled to pull chromosomes apart.

"'When kinetochores are not attached to these protein fibers, they send out a 'wait' signal that halts the cell in mitosis (cell division), thereby giving time for attachments to be formed," said Desai, a professor in the Section of Cell and Developmental Biology (Biological Sciences) and the Department of Cellular and Molecular Medicine (School of Medicine). "In this way, the cell makes sure all chromosomes are attached properly and ready to be pulled apart before the cell divides, thereby leaving no chromosome behind."

"In the Science paper, the researchers describe how the wait checkpoint signal is specifically generated at kinetochores of unattached chromosomes. Serendipitously, they developed a fluorescent probe that enabled them to watch for the first time the key molecular event in wait signal generation at kinetochores in living cells.

"'This work identified a key 'matchmaker' molecule that brings together two constituents of the wait signal that do not like to associate with each other on their own," said Lara-Gonzalez. "These findings help explain why the 'wait' checkpoint signal is selectively generated at kinetochores and not elsewhere in the cell."

Comment: This is another example where all parts must be designed to appear at the same time for life to continue, not step by step. Chance developments cannot do this.

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5783 views

They both will have different mutations that create some difference:

https://www.sciencenews.org/article/some-identical-twins-dont-have-identical-dna-genetics

"On average, identical twins differ by 5.2 genetic changes, researchers report January 7 in Nature Genetics. The finding is important because identical twins — also called monozygotic twins because they come from a single fertilized egg — are often studied to determine whether particular traits, diseases or conditions result from genetics or from environmental influences. Identical twins were thought to be genetically the same, so differences in their health were considered to be the product of their environment. The new finding suggests that some genetic changes could also account for differences between twins.

"Researchers in Iceland deciphered the complete genetic makeup, or genome, of 381 pairs of identical twins. Of those, 38 pairs were genetic duplicates of each other, but most had some differences in DNA that probably arose very early in development, either just before one embryo split to form two or shortly after the split. Some of the twins had many genetic differences, including 39 pairs who had more than 100 changes between the twins."

Comment: Not surprising with the known ability for epigenetic changes. In my experience having lived with identical twins, obvious differences soon become obvious.

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5732 views

Now seen in videos, and it ties itself and then unties:

https://www.sciencedaily.com/releases/2021/01/210115115247.htm

"Using data from RNA-folding experiments, the researchers generated the first-ever data-driven movies of how RNA folds as it is made by cellular machinery. By watching their videos of this folding occur, the researchers discovered that RNA often folds in surprising, perhaps unintuitive ways, such as tying itself into knots.

***

"'Folding takes place in your body more than 10 quadrillion times a second," Lucks said. "It happens every single time a gene is expressed in a cell, yet we know so little about it. Our movies allow us to finally watch folding happen for the first time."

***

"Lucks and his collaborators used this strategy to model the folding of an RNA called SRP, an ancient RNA found in all kingdoms of life. The molecule is well-known for its signature hairpin shape. When watching the videos, the researchers discovered that the molecule ties itself into a knot and unties itself very quickly. Then it suddenly flips into the correct hairpin-like structure using an elegant folding pathway called toehold mediated strand displacement.

"'To the best of our knowledge, this has never been seen in nature," Lucks said. "We think the RNA has evolved to untie itself from knots because if knots persist, it can render the RNA nonfunctional. The structure is so essential to life that it had to evolve to find a way to get out of a knot.'"

Comment: I love the strange Darwinist discussion in bold. Folding and unfolding must have a reason and purpose. Why does it bother to form a knot in the first place, instead of directly forming?

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5770 views

They sneak into tiny pores in cell walls:

https://www.quantamagazine.org/plant-cells-of-different-species-can-swap-organelles-202...

"More than a decade ago, plant geneticists noticed something peculiar when they looked at grafted plants. Where two plants grew together, the cells of each plant showed signs of having picked up substantial amounts of DNA from the other one. In itself, that wasn’t unprecedented, because horizontal transfers of genes are not uncommon in bacteria and even in animals, fungi and plants. But in this case, the transferred DNA seemed to be the entire intact genomes of chloroplasts. This posed a conundrum, because plant cells seal themselves inside a protective cell wall that offers no obvious way for so much DNA to get in.

***

“'The real novelty is that they’ve shown the actual physical organelle is moving, [and] not only from one cell to another,” said Charles Melnyk, a plant biologist who studies grafting at the Swedish University of Agricultural Sciences in Uppsala. “It’s two different plants that are exchanging organelles.”

***

"The mystery persisted until Bock teamed up with his postdoctoral fellow Alexander Hertle, who had expertise in live-cell imaging and microscopy. Hertle was determined to look at what was going on in the callus. Examining thin sections of the graft with electron microscopy, he saw that the cells had openings larger than any previously seen. But even those, which were up to 1.5 microns across, seemed too narrow for the chloroplasts.

"Then, while observing live cells in the callus, Hertle caught images of the chloroplasts in the act of migration. Some of the chloroplasts changed into more primitive, more motile proto-plastids that could get as small as 0.2 microns. As Hertle watched, the proto-plastids crawled along the inside of the cell membrane to positions beneath the newly discovered holes in the cell wall. Budlike protrusions of the cell membranes then bulged into neighboring cells and delivered the organelles. As the tissue organization in the graft reestablished itself, the plastids returned to the normal size for chloroplasts.

“'So there’s definitely holes in the cell wall that would allow the plastids to move through,” Hertle said. The dogma that a plant cell wall is a thick, more or less permanent barrier “basically disappears with this study.”

***

"It’s not clear yet how frequently this kind of horizontal genome transfer through organelle migration occurs in nature. Perhaps plants move chloroplasts between cells routinely in response to injuries or other events; no one knows. Bock, Maliga and other researchers were able to document genome transfers only because the differences in the grafted tissues gave away what was happening. But if plants have evolved a mechanism for organelle transfers, then relatively rare natural grafting events may be only one occasion for them.

"Common or not, the phenomenon might have evolutionary or ecological implications. Hertle points out that once a mosaic cell in a graft callus starts to produce roots, shoots and flowers, it could give rise to a new species or subspecies, especially if cell walls open wide enough to admit nuclear genomes."

Comment: I can easily see this as a God-designed method for plant evolution and new species creation.

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5724 views

Fully understood now:

https://phys.org/news/2021-01-biologists-unravel-full-sequence-dna.html

Break-induced replication (BIR) is a way to solve those problems. In humans, it is employed chiefly to repair breaks in DNA that cannot be fixed otherwise. Yet BIR itself, through its repairs to DNA and how it conducts those repairs, can introduce or cause genomic rearrangements and mutations contributing to cancer development.

"It's kind of a double-edged sword," says Anna Malkova, professor in the Department of Biology at the University of Iowa, who has studied BIR since 1995. "The basic ability to repair is a good thing, and some DNA breaks can't be repaired by other methods. So, the idea is very good. But the outcomes can be bad."

***

"Our study shows that when BIR comes to the rescue at these collisions, its arrival comes at a very high price," says Malkova, the study's corresponding author. "When BIR meets transcription, it can introduce even more instability, which can lead to even higher mutations. As a result, we think that instabilities that mainly were found at collisions between transcription and replication that have been suggested to lead to cancer might be caused by BIR that came to the rescue. It comes, it rescues, but it's kind of questionable how helpful it really is."

Scientists have known how BIR works at some stages. For example, they know the DNA repair apparatus forms a bubble of sorts around the damaged DNA, then moves forward, unzipping the DNA, copying intact segments, and finally transferring those copied segments to a new DNA strand.

But what remained elusive was following BIR throughout its entire repair cycle. Using a technique involving Droplet Digital PCR and a new DNA purification method developed by biology graduate student Liping Liu, the researchers were able to observe BIR from beginning to end.

"If you imagine this as a train, Liping installed a bunch of stations, and she watched how the train proceeded at each station, tracking the increase in DNA at each station, how much increase is occurring at each station, and thus, in aggregate, how the entire process unfolds," Malkova explains.

The team then intentionally introduced obstructions at some stations—transcription and another obstruction called internal telomere sequences—to observe how BIR responded to the obstacles. One finding: when transcription is introduced near the beginning of the BIR process, the repairs fail to commence, as if they're being suppressed. Also, the researchers found the orientation of the transcription with respect to BIR can affect the repair cycle and may be an important factor affecting instability that can promote cancer in humans.

"Scientists already know there's a lot of instability in places where high transcription meets normal replication," Malkova says. "What we did not know until now is where is it coming from and why is it happening."

Comment: We still see that mistakes can happen when molecules are acting and BIR is not a perfect solution. Perhaps perfection is impossible even with God in charge of possible designs.

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5701 views

A special provision when food is scarce:

https://www.sciencedaily.com/releases/2021/01/210123091016.htm

"The enzyme that makes RNA from a DNA template is altered to slow the production of ribosomal RNA (rRNA), the most abundant type of RNA within cells, when resources are scarce and the bacteria Escherichia coli needs to slow its growth.

***

"'RNA polymerase is an enzyme that produces a variety of RNAs using information encoded in DNA," said Katsuhiko Murakami, professor of biochemistry and molecular biology at Penn State and the leader of the research team. "This is one of the key steps in the central dogma of molecular biology: transferring genetic information from DNA to RNA, which in turn often codes for protein. It's required for life and the process is basically shared from bacteria to humans.

***

"'When you talk about RNA, most people think about messenger RNA (mRNA), which is the template for making proteins," said Murakami. "But the most abundant type of RNA in cells doesn't actually code for protein. Ribosomal RNA is the major structural component of the ribosome, which is the cellular machinery that builds proteins using messenger RNAs as templates. Ribosomal RNA synthesis accounts for up to 70 percent of total RNA synthesis in E. coli cells."

***

"'If you do some back-of-the-envelope calculations, an E. coli cell needs to make around 70,000 ribosomes every 20 minutes," said Murakami. "This means RNA polymerase starts ribosomal RNA synthesis every 1.7 seconds from each ribosomal RNA promoter. So, the polymerase has to bind the ribosomal RNA promoter transiently in order to quickly move onto the ribosomal RNA synthesis step. (my bold)

***

"When E. coli needs to slow its growth due to limited resources, two molecules -- a global transcription regulator called DksA and a bacterial signaling molecule called ppGpp, bind directly with the polymerase to reduce production of ribosomal RNA. The research team investigated how the binding of these two factors alters the conformation of the polymerase and affects its activity in a promoter-specific manner.

"'DksA and ppGpp binding to the polymerase alters its conformation, which prevents the opening of a gate and therefor the polymerase has to follow an alternative pathway to form the open complex," said Murakami. "This is not an ideal pathway for the ribosomal RNA promoter and thus slow its activity. It's exciting to see these conformational changes to the polymerase that have direct functional consequences."

Comment: processes need speed controls and this is one of them. It reeks of design. Note my bold. The high speed of these processes is illustrated, from our knowledge that the bacteria replicating every 20 minutes. Occasional molecular mistakes must be expected.

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5714 views

A new studty of these DNA controls in T c ells:

https://phys.org/news/2021-01-behavior-transcription-factors-theories-gene.html

"Now, a new study from the Rothenberg lab examines certain proteins that supervise gene regulation in developing T cells and finds that these proteins behave in a manner quite different from that assumed in previous theory. The work suggests that theories of gene regulation may need to be reevaluated.

***

"There are many different kinds of transcription factors, with each acting upon defined sets of genes, sometimes with multiple transcription factors working together to regulate gene expression. The Rothenberg laboratory focused on two very similar transcription factors, Runx1 and Runx3, to find if they play a role during the cascade of sharp changes in gene expression that cause stem cell–like progenitors to become transformed into future T cells.

***

"The conventional genetics theory is that when a factor regulates a target gene, the activity of the factor is correlated with the level of the target gene. But Rothenberg's study found that this was not the case for Runx factors. Although the Runx factors themselves stay active at steady levels through key developmental events, the great majority of genes that respond to the Runx factors change dramatically in expression during this period. In fact, the Runx factors act upon "incredibly important" genes for T cell development, according to Rothenberg, and regulate them strongly.

"The findings open up new questions, such as how can the Runx factors cause these dramatic changes in gene expression when levels of Runx themselves do not change?

"The team also found that the positions where the Runx factors bind to the genome change markedly over time, bringing Runx to different target DNA sites. At any one time, the study found, the factors are only acting on a fraction of the genes they could regulate; they shift their "attention" from one set to another over time. Interestingly, in many of these shifts, large groups of Runx proteins leave their initial sites and travel to occupy clusters of new sites grouped across large distances of the genome, as they act on different genes at different times.

"'There's no good explanation yet for this group behavior, and we find that Runx are interacting with the physical genomic architecture in a complex way, as they're regulating genes that have totally different expression patterns than the transcription factors themselves," says Shin. "What is controlling the deployment of the transcription factors? We still don't know, and it's far more interesting than what we thought."

"'This work has big implications for researchers trying to model gene networks and shows that transcription factors are more versatile in their actions than people have assumed," Rothenberg says.'

Comment: Same old story. We humans have about 20,000 genes, which is a low number compared to many organisms, but we are highly complex due to transcription controls causing many variations in expression of genes. God's design of te4h genome is highly complex. Never by chance

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5737 views

They can create bad mutations:

https://phys.org/news/2021-02-underestimated-mutation-potential-retrogenes.html

"Genetic information is stored in DNA and transcribed as mRNA. The mRNA is usually translated into proteins. However, it has long been known that mRNA can also be reverse transcribed to DNA and integrated back into the genome. Such cases are referred to as retrogenes. In an article, a team from the Max Planck Institute for Evolutionary Biology in Plön and the Zoological Institute of the Chinese Academy of Sciences in Beijing now reports that this process was previously underestimated by at least a factor of one thousand and that it is an important new mutation mechanism.

"There are two main reasons for this. On one hand, the common search algorithms used in genome sequence analysis do not usually take new insertions of retrogenes into account. These therefore remain hidden in the mass of data. Only with an optimized algorithm like the one developed by the scientists can these insertions be systematically discovered. On the other hand, the authors showed that most of the insertions are relatively short-lived. In previous genome comparisons between species, they appear to be comparatively rare.

"For this most recent study, it was therefore crucial to examine populations that have only recently developed. The authors found that mouse populations that have been separated for only about 3000 years carry different retrogenes (i.e. in each population, retrogenes emerge at a very high rate but are also lost again comparatively quickly). This is because retrogenes can be harmful—even if they are integrated into non-coding DNA. If retrogenes are transcribed back into mRNA (as is the case for most of them), this new mRNA can negatively influence the mRNA of the gene from which they originated. The retrogene thus acts as a regulatory mutation, which is usually harmful.

"The scientists show that the genetic burden of this mechanism is higher than that of the point mutations, which until now have been the primary focus of investigations. They therefore suggest that the search for disease-causing mutations also take the retrogene mechanism into account.

Comment: what is the real purpose of retrogene production is not apparent from this study. But recognizing the issue will bring future research to try to explain it. Perhaps there is a regulatory role that is important.

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5726 views

A new study:

https://phys.org/news/2021-03-reveals-clues-architecture-chromosomes.html

"To prevent both X chromosomes from being active, female mammals have a mechanism that inactivates one of them during development. X chromosome inactivation is orchestrated by a noncoding form of RNA called Xist, which silences genes by spreading across the chromosome, recruiting other proteins (such as Polycomb repressive complexes) to complete the task.

***

"In this study, Lee and Andrea Kriz, a Ph.D. student and first author of the paper, were interested in understanding the role of clusters of proteins called cohesins in X inactivation. Cohesins are known to play a critical role in gene expression. Imagine a chromosome as a long piece of string with genes and their regulatory sequences being far apart, says Lee. For the gene to be turned "on" and do its job, such as producing a specific protein, it has to come in contact with its distant regulator. Chromosomes allow this to happen by forming a small loop that brings together the gene and regulator. Ring-shaped cohesins help these loops form and stabilize. When the gene's work is done and it's time to turn off, a scissor-like protein called WAPL snips it, causing the gene to disconnect from its regulator. An active chromosome has many of these loops, which are continually forming and dissociating (or separating).

"These small loops, which are essential for gene expression, are relatively suppressed on an inactivated X chromosome. One reason, as Lee and her colleagues have already shown, is that Xist "evicts" most cohesins from the inactive X chromosome and that this cohesin depletion may be necessary to reorganize the shape and structure of the chromosome for silencing.

"In the current study, Lee and Kriz used embryonic stem cells from female mice to find out what happens when cohesin or WAPL levels are manipulated during X chromosome inactivation by using protein-degradation technology. "We found that if cohesin levels build up too high, the X chromosome cannot inactivate properly," says Lee. Normally, retaining cohesins (which are normally supposed to be evicted) prevented the X chromosome from folding into an inactive shape and gene silencing was affected. "You need a fine balance between eviction and retention of cohesins during X chromosome inactivation," says Lee.

***

"These findings suggests that shape and structure of the X chromosome play a vital role in allowing Xist to spread from one side to the other and achieve inactivation. "The more we learn about what's important for silencing the X chromosome," says Lee, "the more likely we'll be to find ways to reactivate it and to treat conditions like Rett syndrome.'"

Comment: Probably cohesins are managed by a feedback loop. When sexual reproduction appeared, the necessity of silencing one x chromosome is obvious. It had to be provided at the same time for success, so simultaneous design is a requirement.

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5618 views

A new study on sperm finds methylation changes in histones:

https://phys.org/news/2021-03-discovery-non-dna-mechanism-involved-transmitting.html

"A new study from McGill, published recently in Developmental Cell, has made a significant advance in the field by identifying how environmental information is transmitted by non-DNA molecules in the sperm. It is a discovery that advances scientific understanding of the heredity of paternal life experiences and potentially opens new avenues for studying disease transmission and prevention.

***

"To determine how information that affects development gets passed on to embryos, the researchers manipulated the sperm epigenome by feeding male mice a folate deficient diet and then tracing the effects on particular groups of molecules in proteins associated with DNA.

"They found that diet-induced changes to a certain group of molecules (methyl groups), associated with histone proteins, (which are critical in packing DNA into cells), led to alterations in gene expression in embryos and birth defects of the spine and skull. What was remarkable was that the changes to the methyl groups on the histones in sperm were transmitted at fertilization and remained in the developing embryo."

"'Our next steps will be to determine if these harmful changes induced in the sperm proteins (histones) can be repaired. We have exciting new work that suggest that this is indeed the case," adds Kimmins. "The hope offered by this work is that by expanding our understanding of what is inherited beyond just the DNA, there are now potentially new avenues for disease prevention which will lead to healthier children and adults.'"

Comment: Lamarck is still with us. An interesting result.

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5626 views

More is teased apart as the controls are further studied:

https://phys.org/news/2021-03-dna-replication.html

"DNA replication is fundamental for life—indeed, we copy a light-year's length of DNA over the course of our lifetimes. This copying must be carried out accurately by a molecular machine consisting of protein components, and as such, it is carefully controlled. However, how this control of the protein components is achieved in the watery environment of the cell is by no means clear. (my bold)

***

"...the researchers established for the first time that the protein that sets into motion the building of the replication machinery (the origin recognition complex (ORC) – originally discovered by the winner of the 2020 Dr. H.P. Heineken Prize for Biophysics and Biochemistry, Dr. Bruce Stillman) is a mobile protein that diffuses along the DNA. Importantly, however, its motion is brought to a halt at particular DNA sequences that ORC was previously established to have high affinity for. This reduction of ORC mobility at these sequences then facilitates the assembly of additional components of the replication machinery at these locations on the DNA.

"Using this approach, the researchers also found that the key motor component of the replication machinery (known as MCM) can stably associate with the DNA not only in its canonical double hexameric form, but also in a hitherto unknown single hexameric form uncoupled from ORC that displays significant mobility. This expansion of knowledge about the forms that MCM adopts on DNA may imply that its role inside cells is larger than what textbook knowledge currently indicates.

"With this work, the TU Delft and Francis Crick Institute researchers shed new light on a fundamental biological process that affects our daily lives through its connections to embryo development, tissue regeneration, and cancer progression. Quoting the first author of the work, Dr. Humberto Sánchez, "We are just at the beginning of a molecular journey that will be full of surprises."

***

"Abstract (original article)
DNA replication in eukaryotes initiates at many origins distributed across each chromosome. Origins are bound by the origin recognition complex (ORC), which, with Cdc6 and Cdt1, recruits and loads the Mcm2-7 (MCM) helicase as an inactive double hexamer during G1 phase. The replisome assembles at the activated helicase in S phase. Although the outline of replisome assembly is understood, little is known about the dynamics of individual proteins on DNA and how these contribute to proper complex formation. Here we show, using single-molecule optical trapping and confocal microscopy, that yeast ORC is a mobile protein that diffuses rapidly along DNA. Origin recognition halts this search process. Recruitment of MCM molecules in an ORC- and Cdc6-dependent fashion results in slow-moving ORC-MCM intermediates and MCMs that rapidly scan the DNA. Following ATP hydrolysis, salt-stable loading of MCM single and double hexamers was seen, both of which exhibit salt-dependent mobility. Our results demonstrate that effective helicase loading relies on an interplay between protein diffusion and origin recognition, and suggest that MCM is stably loaded onto DNA in multiple forms."

Comment: Obviously there is much more to be learned, and my bold above again points to the problems that can happen as molecules are free to make mistakes. It is obvious there are various forms of control, but never 100% perfect. Certainly a complexly designed system.

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5645 views

This is a review of the human genome project showing junk DNA has in large part disappeared:

https://www.nature.com/articles/d41586-021-00314-6

"Our analysis shows that, between the start of the HGP in 1990 and its completion in 2003 (after the draft was published in 2001), the number of discovered (or ‘annotated’) human genes grew drastically. It levelled out suddenly in the mid-2000s at about 20,000 protein-coding genes (see ‘Twenty years of junk, stars and drugs: Non-coding elements’), far short of the 100,000-strong estimate previously adopted by many in the scientific community.

***

"A great debate pre-dated the start of the HGP: was it worth mapping the vast non-coding regions of genome that were called junk DNA, or the dark matter of the genome? Thanks in large part to the HGP, it is now appreciated that the majority of functional sequences in the human genome do not encode proteins. Rather, elements such as long non-coding RNAs, promoters, enhancers and countless gene-regulatory motifs work together to bring the genome to life. Variation in these regions does not alter proteins, but it can perturb the networks governing protein expression.

"With the HGP draft in hand, the discovery of non-protein-coding elements exploded. So far, that growth has outstripped the discovery of protein-coding genes by a factor of five, and shows no signs of slowing. Likewise, the number of publications about such elements also grew in the period covered by our data set. For example, there are thousands of papers on non-coding RNAs, which regulate gene expression.

***

"There are now more than 30,000 papers per year linking SNPs and traits. A large fraction of these associations are in the once-dismissed non-coding regions.

My insertion re' SNPs: "In genetics, a single-nucleotide polymorphism (SNP) is a substitution of a single nucleotide at a specific position in the genome that is present in a sufficiently large fraction of the population (e.g. 1% or more). For example, at a specific base position in the human genome, the C nucleotide may appear in most individuals, but in a minority of individuals, the position is occupied by an A."

"Cellular function relies on weak and strong links between genetic material and proteins. Mapping out this network now complements the Mendelian perspective. Today, more than 300,000 regulatory network interactions have been charted — proteins binding with non-coding regions or with other proteins.

***

"In summary, we think that the HGP is more notable for the new era of genomics it ushered in, than for the protein catalogue itself. As the theory of complex systems shows, an accurate survey of components is necessary — but not sufficient — to understand any system. Complexity arises from the diversity of the interactions between components. After 20 years of research building on the HGP, biologists now have a glimpse of the network structure and dynamics that define life."

Comment: The finding that most all of DNA is coordinated into control systems suggests a high degree of thoughtful design created this code. The disappearance of so-called 'junk' DNA re moves the Darwinian tenet that chance mutations made DNA. But Jerry Moran on his blog still fights for 'junk' as a concept and calls the Nature Mag approach as totally misguided. I view it as desperation.

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5581 views

This study describes the assembling structure of a transcription mechanism making RNA:

https://science.sciencemag.org/content/372/6537/52.full?intcmp=trendmd-sci

"Mediating transcription
The Mediator complex is recruited by transcription factors to all protein-coding genes in eukaryotes and helps to assemble the machinery necessary to transcribe the gene. Abdella et al. present the cryo–electron microscopy structure of the human Mediator-bound preinitiation complex (Med-PIC). The structure shows how Mediator positions the long, flexible C-terminal domain of RNA polymerase II to be phosphorylated by the kinase CDK7, a crucial step for further processing of the RNA into a mature RNA. Most sites where transcription factors bind to Mediator are flexibly tethered to the complex, allowing the large Med-PIC to assemble at any gene.

"Abstract
Eukaryotic transcription requires the assembly of a multisubunit preinitiation complex (PIC) composed of RNA polymerase II (Pol II) and the general transcription factors. The coactivator Mediator is recruited by transcription factors, facilitates the assembly of the PIC, and stimulates phosphorylation of the Pol II C-terminal domain (CTD) by the TFIIH subunit CDK7. Here, we present the cryo–electron microscopy structure of the human Mediator-bound PIC at a resolution below 4 angstroms. Transcription factor binding sites within Mediator are primarily flexibly tethered to the tail module. CDK7 is stabilized by multiple contacts with Mediator. Two binding sites exist for the Pol II CTD, one between the head and middle modules of Mediator and the other in the active site of CDK7, providing structural evidence for Pol II CTD phosphorylation within the Mediator-bound PIC.

***

"Here, we present the structure of the human Med-PIC assembled on a closed promoter DNA construct, with the TBP subunit of TFIID replacing the full TFIID complex. Human Mediator is held together by a central scaffold subunit, Med14, which forms two contact sites with MedTail. The precise orientation of the CAK module within Med-PIC is revealed, with clear density for the Pol II CTD in the active site. A second CTD binding site between MedHead and MedMiddle shows how Mediator positions the rest of the CTD for phosphorylation by CDK7. Many regions of Mediator that interact with transcription factors are flexibly tethered, facilitating its assembly. The structure also provides key insights into the conformational landscape of Mediator relative to the PIC."

Comment: I do not expect the reader to be able to fully understand this presentation. It requires deep training in the subject. Viewing the illustrations would help. My real point is these molecules have jobs to do and perform them as if each molecule had a mind and had memorized its function in the production line. Innate Intelligence or intelligent design? Design is obvious.

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5617 views

They came from Archaea in a simpler form and play a major role in decoding DNA in eukaryotes:

https://www.quantamagazine.org/dnas-histone-spools-hint-at-how-complex-cells-evolved-20...

"In the biology of complex cells, or eukaryotes, the ballet of molecules that transcribe and translate genomic DNA into proteins holds centerstage, but that dance would be impossible without the underappreciated work of histone proteins gathering up the DNA into neat bundles and unpacking just enough of it when needed.

"Histones, as linchpins of the apparatus for gene regulation, play a role in almost every function of eukaryotic cells. “In order to get complex, you have to have genome complexity, and evolve new gene families, and you have to have a cell cycle,” explained William Martin, an evolutionary biologist and biochemist at Heinrich Heine University in Germany. “And what’s in the middle of all this? Managing your DNA.”

"New work on the structure and function of histones in ancient, simple cells has now made the longstanding, central importance of these proteins to gene regulation even clearer. Billions of years ago, the cells called archaea were already using histones much like our own to manage their DNA — but they did so with looser rules and much more variety. From those similarities and differences, researchers are gleaning new insights, not only into how the histones helped to shape the origins of complex life, but also into how variants of histones affect our own health today.

"Eukaryotes arose about 2 billion years ago, when a bacterium that could metabolize oxygen for energy took up residence inside an archaeal cell. That symbiotic partnership was revolutionary because energy production from that proto-mitochondrion suddenly made expressing genes much more metabolically affordable, Martin argues. The new eukaryotes suddenly had free rein to expand the size and diversity of their genomes and to conduct myriad evolutionary experiments, laying the foundation for the countless eukaryotic innovations seen in life today. “Eukaryotes are an archaeal genetic apparatus that survives with the help of bacterial energy metabolism,” Martin said.

***

"The four primary histones of eukaryotes — H2A, H2B, H3 and H4 — assemble into octamers with two copies of each. These octamers, called nucleosomes, are the basic units of eukaryotic DNA packaging.

"By curving the DNA around the nucleosome, the histones prevent it from clumping together and keep it functional.

***

"Their observations confirmed that the structures of archaeal nucleosomes are less fixed. Eukaryotic nucleosomes are always stably wrapped by about 147 base pairs of DNA, and always consist of just eight histones. (For eukaryotic nucleosomes, “the buck stops at eight,” Luger said.) Their equivalents in archaea wind up between 60 and 600 base pairs. These “archaeasomes” sometimes hold as few as three histone dimers, but the largest ones consist of as many as 15 dimers.

***

"Kurdistani’s conjecture also suggests an alternative hypothesis for why eukaryotic genomes got so big. The histones’ copper-reducing activity only occurs at the interface of the two H3 histones inside an assembled nucleosome wrapped with DNA. “I think there’s a distinct possibility that the cell wanted more histones. And the only way to do that was to expand this DNA repertoire,” Kurdistani said. With more DNA, cells could wrap more nucleosomes and enable the histones to reduce more copper, which would support more mitochondrial activity. “It wasn’t just that histones allowed for more DNA, but more DNA allowed for more histones,” he said.

***

"Although Warnecke is not convinced that the viral histones tell us much about the origin of eukaryotic histones, he is fascinated by their possible functions. One possibility is that they help to compact the viral DNA; another idea is that they could be disguising the viral DNA from the host’s defenses.

"Histones have had myriad roles since the dawn of time. But it was really in the eukaryotes that they became the linchpins for complex life and countless evolutionary innovations. That’s why Martin calls the histone “a basic building block that never could realize its full potential without the help of mitochondria.'”

Comment: A long paper describing how Archaeal histones might have evolved into eukaryotic forms. This paper exposes how important the histones are to genomic functioning.

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5398 views

Each genome has a system:

https://iai.tv/articles/the-gene-illusion-auid-1813?_auid=2020

"Errors occur during the copying process. The chemical specificity of the bonding of the complementary nucleotides is not perfect. Roughly speaking, an error occurs every 10,000 nucleotide bases. That may not seem very much. If this article, which is around 10,000 letters long, contained just a single typo, you would almost certainly still understand it.

"Now, the genome in your cells is not just 10,000 base pairs, It is around 3,000,000,000 (3 billion!) base pairs. At one error in 10,000, that means 300,000 errors. No organism could survive replication errors of that frequency. The genome would become badly degraded in just a few cell divisions.

"Instead, an even larger system of proteins come along with cut and paste abilities to clean up after the replication process. That system – the cell’s proof-correcting system – systematically looks for any mismatch, cuts the thread when it finds one, and pastes in the correct nucleotide. Amazing, but true. The outcome is that the complete 3 billion long genome gets replicated at each cell division with often no errors, or just one or two.

"That is one reason why DNA cannot function outside a living cell. The replicator, DNA, is therefore not separate from the vehicle, the complete cell because that proof-correcting process only occurs in living cells.

"The distinction between DNA as a replicator and the cell as its vehicle is therefore also an illusion. They necessarily live or die together. That disposes of Selfish Gene theory in evolution since genes are not “sealed off from the outside world”. The same process by which those proof-correcting proteins can cut and paste DNA is precisely what enables genes to be influenced by the organism and its environment. (my bold)

***

"We must therefore move away from the Central Dogma and its one-way causation, what Dawkins refers to as “ancient replicators manipulating it by remote control”.

"Living systems are organised at many nesting levels, from molecules to cells to organs and the whole organism. Each level influences the processes occurring at molecular levels. In my book Dance to the Tune of Life: Biological Relativity I give the full details of this multi-level causation view, which is precisely the concept of Biological Relativity.

"You experience multi-level causation in everyday life. If you train hard as an athlete you will increase the RNAs that enable your muscles to grow more protein and so become stronger. Many other molecular changes will follow in the wake of your lifestyle decision.

"That fact fundamentally changes our view of ourselves and our place in nature since it restores to us and other organisms the sense of control and agency. The levels of causation mesh with each other, so that higher-level processes, such as our mental states and lifestyles, necessarily influence the processes at a molecular level that control our genes."

Comment: The error control system had to be present when DNA appeared or we would not be here. The first paragraphs show this. The last comments were directed at criticisms of Dawkins 'selfish gene' theory I've not quoted.

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5242 views

A molecular machine is picked apart for viewing all the complexity of the arrangement:

https://science.sciencemag.org/content/372/6546/eabg0635

"A complete PIC-Mediator structure
As a critical transcription coactivator, the multisubunit Mediator complex binds RNA polymerase II (Pol II), facilitates preinitiation complex (PIC) assembly, and stimulates transcription and phosphorylation of the Pol II C-terminal domain (CTD). However, how these critical transcriptional events are coordinated by Mediator is not fully understood. Chen et al. determined the structures of human Mediator and Mediator-bound PIC in distinct conformational states, the latter of which represents a complete PIC-Mediator complex assembled on the 14-subunit transcription factor IID (TFIID). The structures show that Mediator undergoes reorganization during PIC-Mediator assembly, sandwiches and facilitates phosphorylation of Pol II CTD, and works with TFIID to organize TFIIH in PIC for transcription initiation.

"Structured Abstract
INTRODUCTION
The multisubunit Mediator binds RNA polymerase II (Pol II), transduces regulatory signals from transcription factors to Pol II, facilitates preinitiation complex (PIC) assembly, and stimulates cyclin-dependent kinase 7 (CDK7)–mediated Pol II C-terminal domain (CTD) phosphorylation. The 14-subunit transcription factor IID (TFIID) is globally required for almost all Pol II–mediated transcription initiation and cannot be replaced by TATA box–binding protein (TBP), a TFIID subunit. Previous structural studies focused on the TBP-based system. However, the mechanism by which Mediator is assembled into TFIID-based PIC and regulates Pol II CTD phosphorylation remains elusive.

"RATIONALE
We reconstituted and determined the cryo–electron microcopy structures of human 26-subunit Mediator and its complex with TFIID-based PIC (76 polypeptides, ~4.1 megadaltons). Structural analyses were performed using the structures of Mediator and PIC-Mediator in distinct conformations, as well as the previously reported TBP-based PIC-Mediator structure.

"RESULTS
Mediator in the Tail-extended (MEDE) and Tail-bent (MEDB) conformations reveals similar separation of the Head and Middle modules. The structure of MEDE at 3.5-Å resolution reveals the mechanism of Mediator assembly. Binding of PIC induces concerted modular reorganization (Head-tilting and Middle-down) of Mediator through two connected molecular levers. The α-helix bundle HB1 of the Head and the Knob of the Middle form a Head-Middle sandwich, which stabilizes two CTD segments with the longer segment extending toward the CDK7 active site. The CTD-Mediator-CDK7 binding pattern suggests a CTD-gating mechanism, by which Mediator binds and brings Pol II CTD to CDK7 for efficient and persistent phosphorylation. Structures of PIC-Mediator in distinct conformations indicate that PIC’s architecture modulates Mediator organization. Mediator and TFIID together position TFIIH, stabilize xeroderma pigmentosum type B (XPB)–promoter–Pol II contacts, and may facilitate XPB-mediated promoter melting and DNA translocation toward Pol II. Structural comparison with TBP-based PIC-Mediator reveals considerable differences in Mediator conformation, CTD-Mediator interaction, and XPB stabilization, underscoring the critical role of TFIID in organizing PIC-Mediator.

"CONCLUSION
Our study provides the structure of the human Mediator at near-atomic resolution as well as the structure of the complete PIC-Mediator holocomplex. These structures provide insights into PIC-Mediator assembly and Mediator-stimulated CTD phosphorylation. TFIID may confer considerable complexity and dynamics of PIC-Mediator organization to accommodate highly dynamic processes of transcription initiation. The structures also provide a framework for further studies of Mediator-stimulated transcription activation by transcription factors."

Comment: Except for the initiated investigators, this is difficult for anyone else to follow and understand. The diagrams are just as complex as the word descriptions. I've shown this to remind everyone of the degrees of underlying complexity that atheists say can appear by natural causes.

The diagrams, which may not open without the proper cookies:

https://www.sciencemagazinedigital.org/sciencemagazine/04_june_2021/MobilePagedArticle....

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5248 views

Shades of Shapiro's work:

https://phys.org/news/2021-06-discovery-human-cells-rna-sequences.html

"Now, Thomas Jefferson University researchers provide the first evidence that RNA segments can be written back into DNA, which potentially challenges the central dogma in biology and could have wide implications affecting many fields of biology.

***

"'The reality that a human polymerase can do this with high efficiency, raises many questions." For example, this finding suggests that RNA messages can be used as templates for repairing or re-writing genomic DNA.

***

"Of the 14 DNA polymerases in mammalian cells, only three do the bulk of the work of duplicating the entire genome to prepare for cell division. The remaining 11 are mostly involved in detecting and making repairs when there's a break or error in the DNA strands. Polymerase theta repairs DNA, but is very error-prone and makes many errors or mutations. The researchers therefore noticed that some of polymerase theta's "bad" qualities were ones it shared with another cellular machine, albeit one more common in viruses—the reverse transcriptase. Like Pol theta, HIV reverse transcriptase acts as a DNA polymerase, but can also bind RNA and read RNA back into a DNA strand.

"In a series of elegant experiments, the researchers tested polymerase theta against the reverse transcriptase from HIV, which is one of the best studied of its kind. They showed that polymerase theta was capable of converting RNA messages into DNA, which it did as well as HIV reverse transcriptase, and that it actually did a better job than when duplicating DNA to DNA. Polymerase theta was more efficient and introduced fewer errors when using an RNA template to write new DNA messages, than when duplicating DNA into DNA, suggesting that this function could be its primary purpose in the cell.

***

"'Our research suggests that polymerase theta's main function is to act as a reverse transcriptase," says Dr. Pomerantz. "In healthy cells, the purpose of this molecule may be toward RNA-mediated DNA repair. In unhealthy cells, such as cancer cells, polymerase theta is highly expressed and promotes cancer cell growth and drug resistance. It will be exciting to further understand how polymerase theta's activity on RNA contributes to DNA repair and cancer-cell proliferation.'"

Comment: Just now far this process is naturally used is not yet known. But re-writing DNA is shown to be possible. James Shapiro is applauding.

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5203 views

Many species have two different ways of doing it:

https://www.sciencenews.org/article/cells-nucleus-dna-chromosomes-genome-organization

"There appear to be two methods to stuff all of that DNA in, researchers report in the May 28 Science. Cells can even flip-flop which arrangement they have by inactivating a molecule called condensin II, the team found.

"If chromosomes were pieces of paper, some, like those of humans, would look like a crumpled ball inside the nucleus, says Claire Hoencamp, a molecular biologist at the Netherlands Cancer Institute in Amsterdam (SN: 10/8/09). Others, like those of fruit flies (Drosophila melanogaster), resemble flat sheets of stacked paper.

"Throughout evolutionary history, organisms across the tree of life have switched among different packing methods, the researchers found. “We worked with a zoo of species, and [at first] it looked like a zoo of patterns of genome folding,” Dudchenko says. “Some maps would look like a checkerboard pattern. Other ones would look like a mattress with weird x’s.” Over time, it became clear that many of the same chromosome folding features were popping up again and again in different species.

"Three types of interactions result in stacked sheets of chromosomes, giving the heat maps that checkerboard or mattress look. In one interaction, seen in the ground peanut (Arachis hypogaea) for example, the ends of different chromosomes tend to touch. In another, chromosomes from organisms like fruit flies touch in the middle. And in an interaction seen in bread wheat (Triticum aestivum), the arms of different chromosomes fold on top of one another.

***

"Breaking parts of condensin II — a complex of proteins that helps assemble chromosomes as cells divide — can switch which organization a nucleus has. Tweaks to condensin II can make a crumpled human nucleus look like a folded fly’s nucleus, the team found. But some organisms have stacked sheets despite having intact condensin II. That means there may be other factors researchers haven’t yet found that push cells to cram chromosomes into the nucleus in a specific way, Hoencamp says."

Comment: This is just a new fact with more needed to come. It is not clear why DNA has to be packed in two different way. What is clear is that cells can still split no matter how the DNA is arranged.

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5183 views

Found in mice:

https://phys.org/news/2021-06-genes-dna-mum-dad-extra.html

"Biologists at the Universities of Bath and Vienna have discovered 71 new 'imprinted' genes in the mouse genome, a finding that takes them a step closer to unraveling some of the mysteries of epigenetics—an area of science that describes how genes are switched on (and off) in different cells, at different stages in development and adulthood.

"To understand the importance of imprinted genes to inheritance, we need to step back and ask how inheritance works in general. Most of the thirty trillion cells in a person's body contain genes that come from both their mother and father, with each parent contributing one version of each gene. The unique combination of genes goes part of the way to making an individual unique. Usually, each gene in a pair is equally active or inactive in a given cell. This is not the case for imprinted genes. These genes—which make up less than one percent of the total of 20,000+ genes—tend to be more active (sometimes much more active) in one parental version than the other.

***

"Close examination of the newly identified genes has allowed Professor Perry and his colleagues to make a second important discovery: the switching on and off of imprinted genes is not always related to DNA methylation, where methyl groups are added to genomic DNA- a process that is known to repress gene activity, switching them off). DNA methylation was the first known type of imprint, and was discovered around thirty years ago. From the results of the new work, it seems that a greater contribution to imprinting is made by histones—structures that are wrapped up with genomic DNA in chromosomes.

"Although scientists have known for some time that histones act as 'dimmer' switches for genes, fading them off (or back on), until now it was thought that DNA methylation provided the major switch for imprinted gene activity. The findings from the new study cast doubt on this assumption: many of the newly identified genes were found to be associated with changes to the histone 3 lysine 27 (H3K27me3), and only a minority with DNA methylation.

***

"Although it only involves a small proportion of genes, imprinting is important in later life. If it goes wrong, and the imprinted gene copy from one parent is switched on when it should be off (or vice versa), disease or death occur. Faulty imprinted genes are associated with many diseases, including neurological and metabolic disorders, and cancer."

Comment: It is not surprising to find another mechanism than methylation. It doesn't tell us how speciation works.

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5239 views

Very complex, highly controlled system:

https://www.sciencedaily.com/releases/2021/06/210622142832.htm

"Almost all cells in our body contain a nucleus: a somewhat spherical structure that is separated from the rest of the cell by a membrane. Each nucleus contains all the genetic information of the human being. So it serves as a kind of library -- but one with strict requirements: If the cell needs the building instructions for a protein, it won't simply borrow the original information. Instead, a transcript of it is made in the nucleus.

"The machinery required for this is very complex, not least because the transcripts are not simple copies. In addition to essential information, genes also contain numerous passages of meaningless "garbage." They are removed when the transcript is made. Biologists call this editorial revision "splicing."

"'An important role in splicing is played by the SMN complex, a 'molecular machine' consisting of nine different proteins," explains Prof. Dr. Oliver Gruss from the Institute of Genetics at the University of Bonn, who is also a member of the university's transdisciplinary research area "Life and Health." "Interestingly, these machines are not evenly distributed in the nucleus. Instead, they accumulate at specific sites called Cajal bodies." However, there are no transport mechanisms in the cell nucleus that bring the SMN complexes to Cajal bodies. Instead, the SMN proteins themselves have certain properties that are responsible for their aggregation.

"SMN complexes have a prominent feature: They carry an unusually large number of phosphate groups, which are small molecular residues with a phosphorus atom in the center. "We suspected that this phosphorylation promotes their mass clustering into Cajal bodies," explains Dr. Maximilian Schilling from the research group around Oliver Gruss.

"Phosphate groups are not part of the actual blueprint of a protein -- they are added later and can also be removed again. This is often how the cell regulates the activity of the respective protein. The phosphate group is attached in this process by certain enzymes, the kinases.

***

"In this way, they encountered a network of kinases, which, when inhibited, caused the Cajal bodies to largely disappear. Further analyses showed that in the absence of these kinases, phosphorylation of SMN complexes at specific sites decreased sharply. This then causes the flash mobs in the nucleus to cease -- the Cajal bodies disintegrate. The finding is particularly interesting because the kinases identified not only regulate splicing, but also the translation of the gene transcripts edited in this way into proteins. These are therefore enzymes that are crucial for various steps in this vital process."

Comment: Mind-bending complexity, not designed by chance. All done by free-floating molecules which are free to make mistakes. The article shows one that might be helped in new therapy approaches. Our brains help undo some of the biological mistakes that occur, that God cannot prevent in the present system of life.

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5175 views

Controls over methylation expression is complex:

https://science.sciencemag.org/content/372/6549/1434

Abstract:
"DNA methylation is associated with transcriptional repression of eukaryotic genes and transposons, but the downstream mechanism of gene silencing is largely unknown. Here, we describe two Arabidopsis thaliana methyl-CpG–binding domain proteins, MBD5 and MBD6, that are recruited to chromatin by recognition of CG methylation, and redundantly repress a subset of genes and transposons without affecting DNA methylation levels. These methyl readers recruit a J-domain protein, SILENZIO, that acts as a transcriptional repressor in loss-of-function and gain-of-function experiments. J-domain proteins often serve as co-chaperones with HSP70s. Indeed, we found that SILENZIO’s conserved J-domain motif was required for its interaction with HSP70s and for its silencing function. These results uncover an unprecedented role of a molecular chaperone J-domain protein in gene silencing downstream of DNA methylation."

From the discussion:

"In conclusion, this work identifies a pathway that links DNA methylation to silencing of sites marked by CG methylation. The characterization of the methyl-binding proteins MBD5 and MBD6 shows that they likely act through a mechanism distinct from that of known MBD proteins in animals. The identification of the J-domain protein SILENZIO as a silencing effector further suggests that gene repression downstream of methylation is linked to chaperone activity, and this new pathway is likely to be conserved among divergent plant lineages.

Comment: so complex, it had to be designed. The molecular chaperones act like feedback loops.

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5189 views

Transcription factors control gene expression:

https://phys.org/news/2021-07-essential-genes.html

"Proteins known as transcription factors act as switches that regulate the expression of nearby genes, but the identity of some of these genetic levers has so far remained mysterious. Now, researchers from the Schübeler group have pinpointed a new switch that regulates essential genes in the mouse and the human genome. Identifying missing gene switches and their function is critical to fully understand the molecular basis of health and disease.

"If the human genome were a company, transcription factors would be the top-level managers, controlling when and how much genes are turned on in specific cells. These proteins typically bind short strings of DNA called 'motifs'. Scientists estimate that there are up to 2,800 transcription factors, but binding motifs have been identified for only about 800 of them.

"One DNA motif that is bound by no known transcription factor is called the CGCG element, as it contains two cytosine nucleotides sitting next to guanine nucleotides. This motif is associated with highly expressed genes across human tissues and is commonly found within specific DNA regulatory regions where most of our genes start to be read.

***

"...the researchers detected the Btg3-associated nuclear protein (BANP) as the only protein bound to the CGCG motif.

"'This protein has been known before, but it was thought to repress gene activity at the periphery of the nucleus," Grand says. "We show that it does quite the opposite: it's a very potent activator of gene expression."

"The team found that BANP has a high affinity for the CGCG motif, both in mouse and human cells. Removing BANP in stem cells causes a decrease in the expression of several genes, including essential ones involved in key biological processes such as transcription, DNA replication, and the assembly of chromatin—the complex of DNA and proteins that forms chromosomes. The researchers observed similar drops in gene expression also when BANP was removed in neurons.

"After binding to specific regulatory regions within the genome, BANP makes the DNA accessible to other proteins. This likely helps regulatory factors to bind and control gene expression. The findings, published today in Nature, could redefine how essential genes are controlled. "These genes, which are expressed in every cell of the body but at different levels, could be regulated by the same switch present in all cells rather than by a series of transcription factors across different cell types", Grand says."

Comment: More junk DNA bites the dust. Bit by bit, research teases apart the controls. Not by chance.

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5132 views

Picking apart the molecular mechanism:

https://phys.org/news/2021-07-capture-ribosome-action.html

The ribosome is the cellular organelle responsible for decoding messenger RNA to make proteins. Many antibiotics target the ribosome;...

***

Expression of the information encoded in DNA makes life possible. DNA is first transcribed into RNA; RNA is then translated into protein. The ribosome is the molecular machine responsible for this second step. It decodes messenger RNA and makes proteins. Importantly, the ribosome is responsible for the synthesis of cellular proteins in all forms of life.

***

Using these techniques, the researchers captured six high-resolution structures of the bacterial ribosomal complex, including messenger RNA, transfer RNA and elongation factor EF-G, an enzyme involved in reading RNA. The work reveals for the first time how EF-G engages with the ribosome complex. (my bold)

Comment:

Such complexity has to be designed, especially the enzyme noted in my bold. Enzymes are giant molecules of many amino acids in precise order to drive the reaction.

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5122 views

Structural cells play a major role in pathogen response:

https://medicalxpress.com/news/2020-07-smart-cells-body-immune-function.html

"In a Nature paper, CeMM researchers report on the epigenetic and transcriptional regulation in structural cells. They found widespread activity of immune genes, suggesting that structural cells are deeply involved in the body's response to pathogens. Moreover, the study uncovered an epigenetic potential that pre-programs structural cells to engage in the immune response against pathogens. These findings highlight an underappreciated part of the immune system and open up an exciting area for research and future therapies.

"The immune system protects our body from constant attack by viruses, bacteria, and other pathogens. Much of this protection is provided by hematopoietic immune cells, which are derived from the bone marrow and specialize in fighting pathogens. They include macrophages, which remove pathogens; T cells, which kill infected virus-producing cells; and B cells producing antibodies that neutralize pathogens. However, immune functions are not restricted to these 'specialists,' and many more cell types are able to sense when they are infected and contribute to the immune response against pathogens.

"Structural cells provide essential building blocks of the body and play an important role in shaping the structure of tissue and organs. Most notably, epithelial cells constitute the surface of the skin, while also separating tissues and organs from each other; endothelial cells coat the inside of all blood vessels; and fibroblast provide the connective tissue that keeps tissues and organs in shape. Structural cells are often regarded as simple and rather uninteresting components of the body, despite their well-established roles in autoimmune diseases (such as rheumatoid arthritis and inflammatory bowel disease) and in cancer. In their new study, Thomas Krausgruber, Nikolaus Fortelny and colleagues in Christoph Bock's laboratory at CeMM focused on elucidating the role of structural cells in immune regulation by pursuing a systematic, genome-wide analysis of epigenetic and transcriptional regulation of structural cells in the body.

***

"This dataset uncovered widespread expression of immune genes in structural cells as well as highly cell-type-specific and organ-specific patterns of gene regulation. Bioinformatic analysis detected genes that control a complex network of interactions between structural cells and hematopoietic immune cells, indicating potential mechanisms by which structural cells contribute to the response to pathogens.

***

"When the mice were infected with a virus (LCMV) that triggers a broad immune response, many of those genes that were epigenetically poised for activation became upregulated and contributed to the transcriptional changes that structural cells showed in response to viral infection. These results suggest that structural cells implement an "epigenetic potential" that pre-programs them to engage in rapid immune responses. As an additional validation, the researchers triggered an artificial immune response by injecting cytokines into mice, and they indeed found that many of the same genes were upregulated.

"The new study has uncovered a striking complexity of immune gene regulation in structural cells. These results highlight that structural cells are not only essential building blocks of the body, but also contribute extensively to its defense against pathogens. Moreover, the presented data constitute an important first step toward understanding what 'structural immunity' might mean for the immune system, and it may help develop innovative therapies for some of the many diseases that involve the immune system."

Comment: It is amazing how complex the immune system really is. But not surprising considering how dangerous some pathogens can be.

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6345 views

Certain molecules are involved:

https://medicalxpress.com/news/2020-07-protein-autoimmunity.html

"The immune system is supposed to protect from external microbial invaders, but sometimes it turns its efforts inward, potentially resulting in autoimmune diseases. In a new study, researchers from Osaka University have discovered how reversible modifications to DNA by certain proteins protect from autoimmune diseases, and conversely, how the absence of these proteins paves the way to autoimmunity.

***

"An important regulatory mechanism is the reversible addition (methylation) or removal (demethylation) of chemical bonds, so-called methyl groups, to segments of DNA. This modifies the readout of DNA segments. Proteins of the ten-eleven translocation (Tet) family are known DNA demethylases, which decrease the production of certain proteins in immune cells. How Tet proteins play into the development of autoimmune diseases has remained unknown until now.

"'Epigenetics deals with how reversible changes in DNA affect gene activity and protein expression," says corresponding author of the study Tomohiro Kurosaki. "Disrupting this machinery can have dramatic effects on cellular function. The goal of our study was to understand how epigenetic control in a specific type of immune cells, called B cells, affects the development of autoimmune diseases."

***

"'These findings suggest that Tet2 and Tet3, as well as proteins whose expression is regulated by Tet2 and Tet3, might play a fundamental role in the development of systemic lupus erythematosus," says lead author of the study Shinya Tanaka. "We wanted to gain a deeper molecular understanding of the mechanism behind the effects of Tet2 and Tet3 on the immune system."

"The researchers next investigated a different type of immune cell, called T cells, which often interact with B cells, and found that T cells were excessively activated in the Tet2/Tet3 knockout mice. By examining the molecular interaction between B and T cells closer, the researchers found that the protein CD86 was produced at higher levels in B cells of Tet2/Tet3 knockout mice, leading to aberrant T cell activation and autoimmunity.

"'These are striking results that show how Tet proteins suppress autoimmune diseases by inactivating B cells and thus ultimately preventing them from attacking our bodies," says Kurosaki. "Our findings provide new insights into the contribution of epigenetics to the development of autoimmune disease. Regulating Tet proteins and their downstream effectors could be a novel treatment for autoimmune diseases.'"

Comment: Our immune system should not attack us, but it does under some circumstances which are mistakes by the control systems. The mistakes are that the protections put in place do not work.

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6360 views

It has two driving parts:

https://www.sciencedaily.com/releases/2020/10/201002105756.htm

"An international research collaboration with The University of Queensland found the Y-chromosome gene that makes mice male is made up of two different DNA parts, not one, as scientists had previously assumed.

"'Expression of the Y chromosomal gene Sry is required for male development in mammals and since its discovery in 1990 has been considered a one-piece gene," he said.

"'Sry turns out to have a cryptic second part, which nobody suspected was there, that is essential for determining the sex of male mice. We have called the two-piece gene Sry-T."

"The scientists tested their theory and found that male mice (XY) lacking in Sry-T developed as female, while female mice (XX) carrying a Sry-T transgene developed as male.

"The success rate for the experiments was almost 100 per cent.

***

"'Sry is a master switch gene because it flicks the switch for male development, it gets the ball rolling for a whole series of genetic events that result in a baby being born as a male instead of female.

"'This new piece of the gene is absolutely essential for its function; without that piece, the gene simply doesn't work.

"'We've discovered something massively important in biology here, because without Sry there can be no sexual reproduction and hence no propagation and survival of mammalian species.'"

Comment: We do not understand how sexual reproduction first started or how it happened. Obviously male and female have to be present. Now we see both male and female DNA are needed in a special way. There is no way chance caused this arrangement since both parts must be simultaneously present. Only by design fits.

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5992 views

Another new study of ape genomes:

https://phys.org/news/2020-10-evolution-chromosome-great-apes-deciphered.html

"A team of biologists and computer scientists at Penn State sequenced and assembled the Y chromosome from orangutan and bonobo and compared those sequences to the existing human, chimpanzee, and gorilla Y sequences. From the comparison, the team were able to clarify patterns of evolution that seem to fit with behavioral differences between the species and reconstruct a model of what the Y chromosome might have looked like in the ancestor of all great apes.

***

"The Y chromosome is unusual. It contains relatively few genes, many of which are involved in male sex determination and sperm production; large sections of repetitive DNA, short sequences repeated over and over again; and large DNA palindromes, inverted repeats that can be many thousands of letters long and read the same forwards and backwards.

"Previous work by the team comparing human, chimpanzee, and gorilla sequences had revealed some unexpected patterns. Humans are more closely related to chimpanzees, but for some characteristics, the human Y was more similar to the gorilla Y.

"'If you just compare the sequence identity—comparing the As,Ts, Cs, and Gs of the chromosomes—humans are more similar to chimpanzees, as you would expect," said Kateryna Makova, Pentz Professor of Biology at Penn State and one of the leaders of the research team. "But if you look at which genes are present, the types of repetitive sequences, and the shared palindromes, humans look more similar to gorillas. We needed the Y chromosome of more great ape species to tease out the details of what was going on.'"

Comment: This adds more information but nothing else.

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5988 views

Very precise molecular interactions to allow or reduce methylation:

https://advances.sciencemag.org/content/7/4/eabb9149?utm_campaign=toc_advances_2021-01-...

"Abstract
5-Methylcytosine (5mC) oxidases, the ten-eleven translocation (TET) proteins, initiate DNA demethylation, but it is unclear how 5mC oxidation is regulated. We show that the protein SMCHD1 (structural maintenance of chromosomes flexible hinge domain containing 1) is found in complexes with TET proteins and negatively regulates TET activities. Removal of SMCHD1 from mouse embryonic stem (ES) cells induces DNA hypomethylation, preferentially at SMCHD1 target sites and accumulation of 5-hydroxymethylcytosine (5hmC), along with promoter demethylation and activation of the Dux double-homeobox gene. In the absence of SMCHD1, ES cells acquire a two-cell (2c) embryo–like state characterized by activation of an early embryonic transcriptome that is substantially imposed by Dux. Using Smchd1/Tet1/Tet2/Tet3 quadruple-knockout cells, we show that DNA demethylation, activation of Dux, and other genes upon SMCHD1 loss depend on TET proteins. These data identify SMCHD1 as an antagonist of the 2c-like state of ES cells and of TET-mediated DNA demethylation.

***

"Our data suggest that SMCHD1 is critical for Dux suppression in mESCs, thus controlling the 2c-like state. Furthermore, SMCHD1 plays a key role in de novo methylation of CpG islands on the inactive X chromosome during mouse development (23). Recent data have shown, however, that loss of SMCHD1 in somatic cells does not lead to X chromosome reactivation (24, 25). Together, the existing data suggest that SMCHD1 functions in promoting de novo DNA methylation during development rather than in mediating methylation maintenance, and we propose the following mechanism: SMCHD1 operates in these critical DNA methylation events by inhibiting TET-mediated 5mC oxidation and demethylation at its target regions, as we show in this study, thereby shifting the balance of methylation versus demethylation toward the methylated state (Fig. 7H). When SMCHD1 is lost, but DNA methylation remains high in the absence of TETs (reduced DNA methylation dynamics), Dux expression may not be occurring because of inhibition of transcription by DNA methylation. On the other hand, in absence of SMCHD1 and presence of TET activity, and thus higher methylation-demethylation dynamics, Dux will be activated. This pathway is important in inhibiting the totipotent (2c-like state) of ES cells. Although a role of SMCHD1 in inactivation of Dux in late 2c mouse embryos has recently been proposed (58), this event seems initially independent of DNA methylation inasmuch as the Dux promoter region is almost completely unmethylated in 2c and 4c mouse embryos (59); therefore, the de novo methylation events must occur later during development. Further studies are needed to confirm whether SMCHD1 is responsible for the remethylation of the Dux locus during early embryo development and whether inhibition of TET proteins plays an important role in this process."

Comment: The highly complex interactions are very difficult to study as the methods sections I've skipped over show. Only design can produce this type of control mechanism.

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5738 views

It controls how information is expressed:

https://phys.org/news/2021-02-core-complex.html

"Gene expression is a highly regulated process that involves several steps. These include transcription of DNA instructions into RNA, removal of non-coding segments from the RNA message, and its subsequent translation into proteins. All these steps involve specific molecular machineries responsible for conducting each process with high accuracy.

***

"During transcription, genetic information contained in the DNA is used to create a precursor messenger RNA (pre-mRNA) thanks to the action of an enzyme, RNA Polymerase II. To maintain only the necessary coding segments required to produce a protein, short fragments of the pre-mRNA are kept and others are removed . This process is known as pre-mRNA splicing and is catalyzed by a large and dynamic RNA-protein complex, the spliceosome.

***

"More than 100 proteins and five small nuclear RNAs (snRNAs) are involved in building the spliceosome complex and orchestrating pre-mRNA splicing. Before the snRNAs can be incorporated into the spliceosome, they need to undergo an endonucleolytic processing step (in other words, a process where an enzyme has to cut the RNA, also called 3'-end processing), which is catalyzed by the Integrator complex. Discovered fifteen years ago, Integrator remained largely uncharacterised structurally, which triggered the Galej group's interest.

***

"Recent investigation has revealed that the Integrator complex is broadly involved in the transcription attenuation process, meaning that it can make sure some genes are not expressed. Playing such an essential role in the regulation of gene expression gives even more reason to have a closer look at its molecular structure.

***

"Interestingly, Integrator has some similarities with other cellular machineries involved in the 3'-end processing of the messenger RNAs that encode proteins. However, the inner arrangement of the Integrator proteins is quite unique compared with the other 3'-end processing complexes, and some proteins are twisted in their positions. This peculiar architecture could have played an important role in the specialization of this complex, which evolved to fulfill different functions."

Comment: Such a complex arrangement of proteins, some twisted is a highly organized design, is never by chance. Designer required

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5684 views

Kind of two-faced in actions:

https://phys.org/news/2021-02-gene-destruction.html

"The family of ENDOU enzymes is found in most organisms, yet its functions are only poorly understood...[Researchers] suggest that the gene ENDU-2 could be responsible for triggering tumors in the body from a distance. In addition, the team discovered a novel, seemingly contradictive response: Under stress, ENDU-2 can contribute both to the protection of the organism and to its destruction.

***

"'ENDOU/ENDU-2 is not only selectively discharged from stressed cells and circulated throughout the body, but it can also bind to the messenger RNA (mRNA) of many genes at the site of origin and in the target cells," Qi explains. These mRNAs are the working copies of genes and are needed as blueprints for the production of all proteins and enzymes. What surprised the researcher was that ENDU-2 can perform two different functions under stress: at the site of origin, it cuts and destroys the mRNA, which reduces metabolism and prevents the already stressed organism from making faulty new proteins. At the destination, the RNA remains intact, and ENDU-2 helps these cells to survive. For this, however, it must be dosed precisely; otherwise it can cause tumor formation.

"One conclusion that can be drawn from this could be that the worm specifically protects the embryos, i.e. its offspring, in times of great stress. "In this way, it seems guaranteed that whenever the organism's self-healing powers are not sufficient for mother and child, it at least ensures the survival of the progeny," speculates Prof. Dr. Ralf Baumeister, who was also involved in the study and in whose department Qi leads a research group. The Freiburg scientists now know that the loss of ENDU-2 can also reprogram stem cells. These then lose their immortality within a few generations. Next, the team wants to explore which conditions cause ENDU-2 to distinguish between destruction and protection."

Comment: We can tell what activity a gene can cause, but not how it does it. Presented from the viewpoint that as we try to understand the genome, it is still a giant black box, and research is only scratching a giant surface.

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5706 views

All done by molecular motors:

https://www.nature.com/articles/d41586-021-00351-1?WT.ec_id=NATURE-20210225&utm_sou...

"Cells neatly compact their spaghetti of DNA in several ways. In cells with a nucleus, the DNA is first wrapped around cores of histone proteins to make structures called nucleosomes, which together form a chromatin fibre that looks like beads on a string. Loop extrusion is the subsequent compaction process, whereby a molecular motor binds a chromatin fibre and reels it in from the sides, forcing out a progressively larger loop in between.

"Although the process of loop extrusion was hypothesized decades ago, only in the past few years has it become clear that it is a universal mechanism that organizes DNA in organisms from bacteria to humans. In 2016, computational models showed that extrusion can compact DNA, turning a hairball of chromatin into detangled yet tightly packed chromosomes. Simulations also indicated that, when extrusion is stalled by barriers on the chromatin (a normal part of the process), it produces chromosomal domains seen in data from Hi-C — a technique used to characterize chromosome structure.

"These studies further suggested that ‘structural maintenance of chromosomes’ (SMC) complexes — once thought to be passive rings or staples — are actually loop-extruding motors. Moreover, proteins known as CCCTC-binding factors (CTCFs), which attach to specific DNA sequences, were proposed to be barriers that catch and stall SMC motors called cohesins (Fig. 1b). All in all, a range of experimental evidence — from in vivo depletion of SMCs and CTCFs, to direct visualization of single molecules — now supports the existence of loop extrusion8.

***

"Arnould et al. add to this list of possibilities, suggesting that loop extrusion safeguards the genome by supporting the repair of double-strand DNA breaks (DSBs).

"To repair severed DNA, cells must first establish a large (roughly one million base pair) region of modified H2AX histones flanking the break. Phosphate groups are added to the histones by certain enzymes, including one called ATM, producing a region of what are known as γH2AX histones. These histones signal the presence of the break to repair enzymes."

Comment: These motorized molecules are amazing. The excerpts are just a hint of the complexity described in this article, much of which is offering probabilities of h ow it all works at a molecular level. See the diagrams to help in understanding the findings. A marvelous example of the need to recognize a designer is necessary,

Post reply

5634 views

All done by molecular motors:

https://www.nature.com/articles/d41586-021-00351-1?WT.ec_id=NATURE-20210225&utm_sou...

"Cells neatly compact their spaghetti of DNA in several ways. In cells with a nucleus, the DNA is first wrapped around cores of histone proteins to make structures called nucleosomes, which together form a chromatin fibre that looks like beads on a string. Loop extrusion is the subsequent compaction process, whereby a molecular motor binds a chromatin fibre and reels it in from the sides, forcing out a progressively larger loop in between.

"Although the process of loop extrusion was hypothesized decades ago, only in the past few years has it become clear that it is a universal mechanism that organizes DNA in organisms from bacteria to humans. In 2016, computational models showed that extrusion can compact DNA, turning a hairball of chromatin into detangled yet tightly packed chromosomes. Simulations also indicated that, when extrusion is stalled by barriers on the chromatin (a normal part of the process), it produces chromosomal domains seen in data from Hi-C — a technique used to characterize chromosome structure.

"These studies further suggested that ‘structural maintenance of chromosomes’ (SMC) complexes — once thought to be passive rings or staples — are actually loop-extruding motors. Moreover, proteins known as CCCTC-binding factors (CTCFs), which attach to specific DNA sequences, were proposed to be barriers that catch and stall SMC motors called cohesins (Fig. 1b). All in all, a range of experimental evidence — from in vivo depletion of SMCs and CTCFs, to direct visualization of single molecules — now supports the existence of loop extrusion8.

***

"Arnould et al. add to this list of possibilities, suggesting that loop extrusion safeguards the genome by supporting the repair of double-strand DNA breaks (DSBs).

"To repair severed DNA, cells must first establish a large (roughly one million base pair) region of modified H2AX histones flanking the break. Phosphate groups are added to the histones by certain enzymes, including one called ATM, producing a region of what are known as γH2AX histones. These histones signal the presence of the break to repair enzymes."

Comment: These motorized molecules are amazing. The excerpts are just a hint of the complexity described in this article, much of which is offering probabilities of h ow it all works at a molecular level. See the diagrams to help in understanding the findings. A marvelous example of the need to recognize a designer is necessary,

Corrected typos in the title. Surprised you didn't note the cellular intelligence provided by God's coding DNA to handle this.

Post reply

5635 views

Amazingly exact and complex:

https://www.nature.com/articles/d41586-021-00512-2?WT.ec_id=NATURE-202103&sap-outbo...

"Accurate chromosome segregation in meiosis requires that each chromosome first identify and physically link to its homologous partner. These steps depend on a DNA-repair pathway called homologous recombination, which begins with programmed DNA breakage at a few randomly chosen sites along each chromosome. The broken DNA ends seek out similar sequences on other chromosomes, eventually identifying their homologous partner and establishing physical links called crossovers. Crossovers also enable the exchange of genetic information between homologous chromosomes, ensuring genetic variation between parents and offspring.

"The molecular mechanisms that control homologous recombination in meiosis have been studied for more than two decades, since the identification of a set of ten proteins in the budding yeast Saccharomyces cerevisiae that are required for the formation of DNA breaks during meiosis2. Four of these proteins make up the Spo11 core complex which breaks DNA. Three others form the MRX complex, which mediates post-breakage processing steps2. The roles of the remaining three proteins — Rec114, Mei4 and Mer2, together called the RMM complex — have remained mostly mysterious.

***

"The authors purified the S. cerevisiae RMM complex for the first time, revealing that Rec114 and Mei4 form a subcomplex that associates with Mer2. The authors then showed that the purified RMM proteins can condense on DNA into liquid-like droplets containing hundreds of copies of each protein.

***

"Taking advantage of this purified complex in the current work, the group showed that RMM condensates recruit the Spo11 core complex to DNA. A mutation in Rec114 that disrupts its binding to the Spo11 core complex also compromises DNA breakage in meiotic cells, indicating that the RMM complex recruits the Spo11 core complex to DNA break sites.

***

"Claeys Bouuaert and colleagues’ work marks the start of an exciting ‘phase’ of research into the fundamental mechanisms of meiotic recombination. Taken together with steady progress in our understanding of meiotic chromosome architecture and dynamics, the stage is set for further advances,..."

Comment: Mind-blowing c0mpexity. Not presented for full understanding but a glimpse into the intricate dance of these molecules. Only design fits.

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5622 views

A carefully designed system to modify but not suppress gene activity expression:

https://science.sciencemag.org/content/372/6539/292?utm_campaign=toc_sci-mag_2021-04-15...

"A transcriptional control mechanism in yeast that allows cells to respond to changes in nutrient concentrations works very much like a household light-dimmer switch. That is, the system separately controls whether gene expression is “on” or “off” and the extent of gene expression. The galactose-responsive pathway is activated when yeast need to switch from metabolizing glucose to metabolizing galactose. Ricci-Tam et al. found that, rather than using two separate elements for the switch and dimmer controls, yeast use a single transcription factor, Gal4p, separately regulating its abundance (through transcriptional regulation) and its catalytic activity (through interaction with a protein-binding partner). Such regulation may be common and can allow responses to the environment on physiological and evolutionary time scales.

"Abstract
Gene-regulatory networks achieve complex mappings of inputs to outputs through mechanisms that are poorly understood. We found that in the galactose-responsive pathway in Saccharomyces cerevisiae, the decision to activate the transcription of genes encoding pathway components is controlled independently from the expression level, resulting in behavior resembling that of a mechanical dimmer switch. This was not a direct result of chromatin regulation or combinatorial control at galactose-responsive promoters; rather, this behavior was achieved by hierarchical regulation of the expression and activity of a single transcription factor. Hierarchical regulation is ubiquitous, and thus dimmer switch regulation is likely a key feature of many biological systems. Dimmer switch gene regulation may allow cells to fine-tune their responses to multi-input environments on both physiological and evolutionary time scales.

***

"Our results support a “hierarchically decoupled regulation” model in which the abundance and activity of a single transcription factor, Gal4p, are regulated independently. In this model, transcriptional regulation of Gal4p abundance by the upstream transcription factor Mig1p mediates the response to glucose, whereas protein binding of Gal80p to Gal4p regulates Gal4p activity in response to the galactose:glucose ratio. Unlike our initial chromatin-decoupled regulation model, a single transcription factor, Gal4p, controlled both the switch and the rheostat at the final step of the pathway. In both models, decoupling was achieved by regulation working through two distinct mechanisms; this is reminiscent of other cases, such as the frequency versus amplitude modulation of the Msn2p-Msn4p stress responses in yeast. Our model is agnostic to mechanistic details of how Gal4p activates downstream GAL promoters and is thus compatible with recent observations that different Gal4p-binding sites have different functional roles.

"What physiological function could be served by decoupling the on-off switch of pathway activation from the expression level of the pathway? When faced with mixtures of sugars, yeast first use glucose, then less-preferred carbon sources, a phenomenon called diauxic growth. Yeast prepare by expressing GAL genes before glucose is depleted; the earlier a strain expresses GAL genes, the higher the fitness advantage it has once glucose is depleted. However, preparation comes at a fitness cost in the period before the glucose runs out. One possible function of the decoupled switch-and-rheostat design is to allow early activation of the pathway but with a reduced cost.

***

"Decoupled control is a useful property because it allows response features to be independently controlled physiologically and evolutionarily. Decoupling has often been proposed to involve independent transcription factor–binding sites on promoters and to be aided by chromatin. We show here that the same result can be accomplished by hierarchical regulation of the abundance and activity of a transcription factor. Because regulation of this kind is common, it is likely that decoupling of responses is also achieved by this mechanism in other systems."

Comment: Another very carefully designed system which creates gene expression activity depending on different sugar concentrations. We can see how is is done step by step, but still have no way of understanding the underlying mechanisms of control. That is still a total black box

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5467 views

Very fancy system allows researchers to watch:

https://phys.org/news/2021-05-key-early-gene-captured-real.html

"On scales too small for our eyes to see, the business of life happens through the making of proteins, which impart to our cells both structure and function. Cellular proteins get their marching orders from genetic instructions encoded in DNA, whose sequences are first copied and made into RNA in a multi-step process called transcription.

***

"Now, scientists led by postdoctoral researcher Linda Forero-Quintero have, for the first time, observed early RNA transcription dynamics by recording where, when and how RNA polymerase enzymes kick off transcription by binding to a DNA sequence.

***

"'This is the first time someone has looked at RNA polymerase phosphorylation dynamics in a single-copy gene," said Forero,

***

"...they observed the start of the transcription cycle that happens when the RNA polymerase II (RNAP2) transcription enzyme becomes phosphorylated, or decorated with phosphate groups, on its amino acid tail.

***

"The images obtained with this system translate into fluorescent intensity fluctuation. The researchers then used those signals to interpret the spatiotemporal organization of RNAP2 phosphorylation throughout the transcription cycle at a single-copy gene.

***

"By fitting this statistical model to reproduce all the experimental results, the computational team then extended their analyses to glean new mechanistic and quantitative information about the different molecules and their states through the transcription process.

"For example, they estimated how many individual RNA polymerase molecules collect to form transient clusters in the region of the DNA's promoter, how long these clusters persist, and how, when and where the polymerases distribute themselves along the DNA. They found, for example, that each burst of transcription activity produces a cluster of between five and 40 RNA polymerases to form around the promoter region of the gene, of which 46% eventually succeed to transcribe RNA. They also found that each RNA takes approximately five minutes to be fully transcribed and processed prior to release."

Comment: We are sneaking into a means of viewing the most intricate aspects of genome function. Not by chance.

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5312 views

DNA is like a huge library with many shelved areas containing exactly precise narrow regions of specific instructions must be reviewed while not using any other shelves/regions:

https://www.sciencedaily.com/releases/2021/06/210602153352.htm

"The organization of the human genome relies on physics of different states of matter -- such as liquid and solid -- a team of scientists has discovered. The findings, which reveal how the physical nature of the genome changes as cells transform to serve specific functions,

"The genome is the library of genetic information essential for life. Each cell contains the entire library, yet it uses only part of this information. Special types of cells, such as a white blood cell or a neuron, have only certain "books" open -- those containing information relevant for their function. Researchers have long sought to determine how the genome manages these enormous libraries and allows access to the "books" that are needed, while storing away the ones not in use.

***

'"We found that the parts of the genome that are being used are liquid, while the unused parts form solid-like islands," explains Alexandra Zidovska, an assistant professor in New York University's Department of Physics and the senior author of the study. "These solid-like islands serve as library bookshelves storing the books with genes not currently in use, while the liquid genome part acts like an 'open book,' which is readily accessible and used for a cell's life and function."

***

"Here they found that stem cells keep their genome "open" -- making it as accessible as an open book, with "genetic pages" being easily reachable.

However, the mapping also showed that once a stem cell becomes a specialized cell, e.g. a neuron, this specialized cell keeps readily accessible only parts of the genome that are needed for its specific function. It puts away the unused parts of the genome on "bookshelves." This leaves more space for information that is being actively read out and processed.

"'These motions tell us exactly how accessible the genome is in a given place in the cell nucleus," explains Zidovska. "Moreover, these motions reveal the physical state of different parts of the genome, with liquid parts corresponding to loosely packed DNA, and solid-like parts corresponding to tightly packed DNA gels. The genome packing in these different states of matter directly impacts the genome's accessibility; the liquid parts are accessible, in contrast to the solid-like parts. The amazing thing is that this organization relies on physics of different states of matter, liquid and solid."

"'Measuring motions of distinct parts of the genome allowed us to show these different physical properties of different parts of the genome, and thus understand the genome organization -- the cell's 'library system,' " she adds.

"A proper cellular filing system is vital for human health, the researchers note.

"'Considering the vast number of cell types in the human body, if a book is missing or misplaced in this cellular library, it may lead to missing or unnecessary information, possibly leading to developmental and inherited disorders as well as afflictions such as cancer," explains Zidovska. "Therefore, revealing how the genome is organized inside the cell nucleus is critical to our understanding of these conditions and diseases. Moreover, such knowledge may help us in designing future therapies and diagnostics of such disorders.'"

Comment: Having liquid and more solid phases to pinpoint usable areas in DNA is an extremely clever clever design, as cells in general do this in multiple ways making wall-less organelles in the body of the cell by liquid or solid phase transitions isolating manufacturing processes to very specific regions. To twist an old saying 'cleverless is equal to Godliness'. :-)

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5283 views

More study on the bacteriophage with this strange DNA:

https://phys.org/news/2021-07-biosynthesis-pathway-dna-nucleobase-elucidated.html

"...in a bacteriophage, another base, represented by the letter Z, exists. This exception, the only one observed to date, has long remained a mystery. Scientists from the Institut Pasteur and the CNRS, in collaboration with the CEA, have now elucidated the biosynthesis pathway of this base.

***

"Cyanophage S-2L is a bacteriophage, in other words a virus that infects bacteria. In this phage, adenine is completely replaced by another base, 2-aminoadenine (represented by the letter Z). The latter forms three hydrogen bonds with thymine (Z-T), instead of the usual two bonds between adenine and thymine. This higher number of bonds increases the stability of the DNA at high temperatures and changes its conformation, meaning that the DNA is less well recognized by proteins and small molecules.

"Since it was discovered in 1977, cyanophage S-2L has been the only known exception, and the biosynthesis pathway of 2-aminoadenine has remained unknown. Scientists from the Institut Pasteur and the CNRS, in collaboration with the CEA, recently elucidated this biosynthesis pathway and demonstrated its enzymatic origins. They achieved this by identifying a homolog of the known enzyme succinoadenylate synthase (PurA) in the genome of cyanophage S-2L. A phylogenetic analysis of this enzyme family revealed a link between the homolog, known as PurZ, and the PurA enzyme in archaea. This indicates that the homolog is an ancient enzyme that probably conferred an evolutionary advantage. The research was carried out using the Institut Pasteur's Crystallography Platform.

"The new Z-T base pair and the discovery of the biosynthesis pathway show that new bases can be enzymatically incorporated into genetic material."

Comment: It needs a special enzyme. As I've always noted, enzymes are giant specialize molecules which are hard to imagine appearing by chance. It still suggests design. See this previous entry: Friday, April 30, 2021, 20:05

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5078 views

Another review:

https://www.quantamagazine.org/dna-has-four-bases-some-viruses-swap-in-a-fifth-20210712/

"A few decades ago, researchers found viruses that had swapped one of the four bases in their DNA for a novel fifth one. Now, in a trio of papers published in Science in April, three teams have identified dozens of other viruses that make this substitution, as well as the mechanisms that make it possible. The discoveries raise the thought-provoking possibility that this kind of fundamental genomic change could be much more widespread and important in biology than anyone imagined.

***

"In 1977, for instance, researchers in the Soviet Union found something peculiar while looking at a virus that infects photosynthetic bacteria: All the A’s in the genome had been replaced with an alternative base, 2-aminoadenine, which was later dubbed Z. Usually, C pairs with G and T pairs with A to form double-stranded DNA. But in this virus, with no A’s to be found, T paired with Z. (During gene transcription, T-Z was still treated as though it were T-A.)

"The Z base looks like a chemical modification of A; it’s an adenine nucleotide with an extra attachment. But that modest change allows Z to form a triple hydrogen bond with T, which is more stable than the double bond that holds together A-T.

***

"The scientists have now reported finding the Z substitution in more than 200 phages. Further analysis of the viral genomes allowed the research groups to uncover a key enzyme for making Z, as well as an enzyme that degrades free-floating A nucleotides, making Z more likely to be taken up during DNA synthesis.

"But the biggest surprise was that the viruses had a polymerase enzyme dedicated to pairing Z bases with T’s during DNA replication. “It was like a fairy tale,” said Marlière, who had been hoping to find such a polymerase. “Our wildest dreams came true.” (my bold)

"That’s because while scientists have uncovered other examples of bacteriophages making nucleotide substitutions, this “is the first polymerase that is really shown to selectively exclude a canonical nucleotide,” said Peter Weigele, a researcher at New England Biolabs who studies the biosynthesis of noncanonical bases. The system evolved to allow “a reprogramming,” Romesberg said — one that could potentially provide new insights into how polymerases function, and how to engineer them.

"Z and other modified DNA bases seem to have evolved to help viruses evade the defenses with which bacteria degrade foreign genetic material. The eternal arms race between bacteriophages and their host cells probably provides enough selection pressure to affect something as seemingly “sacrosanct” as DNA, according to Romesberg. “Right now, everyone thinks the modifications are just protecting the DNA,” he said. “People almost trivialize it.”

"But something more may be at work: The triple bond of Z, for instance, might add to DNA’s stability and rigidity, and perhaps influence some of its other physical properties. Those changes could carry advantages beyond hiding from bacterial defenses and could make such modifications more broadly significant.

***

"We need to “stop taking the components of molecular biology as we know them for granted,” Freeland said. “Purely because our instrumentation has gotten better and we’ve looked harder, everything that we thought was standard and universal is just falling away.'”

Comment: This really adds to our knowledge of this new style DNA. That a special enzyme must be produced to create the Z base brings the issue of design to the fore, as my bold above shows. Remember enzymes support reactions by having stations for the reacting molecules, literally forcing them to react. T his required the design of huge molecules made up of thousands of amino acids in special sequences, not happening by chance. This also relates to Shapiro's discovery that bacteria DNA. He never discovered how they do it. Again, enzymes?

The last comment by the author is important. We do not know what we do not yet know, and conclusions are not in cement. Known genome complexity will vastly increase with time, and it will require a designer.

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5057 views

Describes a necessary protein in the enzyme process:

https://phys.org/news/2021-07-mrna-transcription-difficulties.html:

"'mRNAs are a central component of all living things on our planet. Without them life as we know it would not function," says Elmar Wolf.

"Information becomes protein

"Transcription: If one can still remember their biology lessons, then they know that it is the process by which the genetic information in the DNA is translated into messenger RNA—or as how scientists like to call it: mRNA. Only the mRNA is capable of transmitting the information from the genetic material of the DNA in the nucleus of the cell to the sites of protein biosynthesis outside the nucleus. "The mRNA composition thus decides how the cells of our body look and how they function," Wolf says.

"The transcription process from DNA to mRNA sounds relatively simple: "You can think of transcription as an obstacle race. The RNA polymerase starts the reading process at the beginning of the gene, then moves through the entire gene and, finally reach the finish line," Wolf explains. If the polymerase makes it through to the end, the mRNA has been produced. Scientists have long known that a lot can go wrong in this process. After all, many genes are a long 'race track' with plenty of obstacles.

"In order to better understand what happens at the molecular level during the race, Wolf and his team took a close look at the process of transcription. "We studied an important component of the RNA polymerase: the protein SPT6," explains Wolf. The question they explored is: "Is SPT6 important for the process of transcription and—if so—in what way?"

"What do the scientists do when they want to learn about the function of a protein: they remove it from the cells and see what happens. That's exactly what Wolf and his team did. The result was quite clear: "Interestingly, RNA polymerase starts making mRNA even in the absence of SPT6," Wolf described. But then it regularly gets stuck in difficult places—you could say that it falls over an obstacle.

"This failure has two consequences that have a negative impact on cell function: On one hand, hardly any RNA polymerase makes it to the destination, which is why hardly any mRNA is produced. On the other hand, however, the gene itself is also affected. "Without SPT6, the polymerase destroys the obstacles and the racetrack, which is why functional RNA polymerases are then unable to find their way," says Wolf. Thus, it is clear that the SPT6 protein is a central element in the production of mRNA in cells."

Comment: Once again we see protein molecular specifity required. Only a designer can do this.

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5099 views

A rare syndrome with defective production of dopamine and serotonin in the brain is helped by gene therapy:

https://www.sciencemag.org/news/2021/07/gene-therapy-restores-missing-dopamine-children...

"After 8 years of living with an ultrarare genetic brain disorder that left her unable to walk or talk, a girl enrolled in a clinical trial whose new results suggest gene therapy can alter the course of such inherited diseases, even after many years, STAT reports. The patient had AADC deficiency, a disorder that keeps the brain from generating dopamine and serotonin, essential molecules that allow brain cells to communicate back and forth. Researchers injected harmless viruses carrying healthy copies of the AADC gene into her brain so cells would make a missing enzyme. Within months, the patient—and six other children in the trial—recovered the ability to generate dopamine, researchers report this week in Nature Communications. That has let many of them walk on their own—and talk with assistance—for the first time. The results also suggest the brain has an unexpected ability to make new connections once a missing enzyme is restored."

Comment: we have the brains to help when molecular mistakes happen..

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5076 views

Strange new genes found in Archaea allow methane consumption:

https://www.biorxiv.org/content/10.1101/2021.07.10.451761v1

Borgs are giant extrachromosomal elements with the potential to augment methane oxidation

"Summary
Anaerobic methane oxidation exerts a key control on greenhouse gas emissions 1, yet factors that modulate the activity of microorganisms performing this function remain little explored. In studying groundwater, sediments, and wetland soil where methane production and oxidation occur, we discovered extraordinarily large, diverse DNA sequences that primarily encode hypothetical proteins. Four curated, complete genomes are linear, up to ~1 Mbp in length and share genome organization, including replicore structure, long inverted terminal repeats, and genome-wide unique perfect tandem direct repeats that are intergenic or generate amino acid repeats. We infer that these are a new type of archaeal extrachromosomal element with a distinct evolutionary origin. Gene sequence similarity, phylogeny, and local divergence of sequence composition indicate that many of their genes were assimilated from methane-oxidizing Methanoperedens archaea. We refer to these elements as “Borgs”. We identified at least 19 different Borg types coexisting with Methanoperedens in four distinct ecosystems. Borg genes expand redox and respiratory capacity (e.g., clusters of multiheme cytochromes), ability to respond to changing environmental conditions, and likely augment Methanoperedens capacity for methane oxidation (e.g., methyl coenzyme M reductase). By this process, Borgs could play a previously unrecognized role in controlling greenhouse gas emissions."

***

"Conclusions
Borgs are enigmatic extrachromosomal elements that can approach (and likely exceed) 1 Mbp in length (Table 1). We can neither prove that they are archaeal viruses or plasmids or mini-chromosomes, nor can we prove that they are not. Regardless of the name, they are clearly different from anything that has been reported previously. It is fascinating to ponder their possible evolutionary origins. Are they giant linear viruses or plasmids unlike anything previously reported? Alternatively, are they auxiliary chromosomes? Perhaps they were once a sibling Methanoperedens lineage that underwent gene loss and established a symbiotic association within Methnoperedens, as might be indicated by the monophyly of some of their Methanoperedens-like genes (Figs. S9, S10). We suspect that different Borgs tend to associate with different Methanoperedens species, yet Borg homologous recombination may indicate movement among hosts, thus their possible roles as gene transfer agents. It has been noted that Methanoperedens have been particularly open to gene acquisition from diverse bacteria and archaea 6, and Borgs may have contributed to this. The existence of Borgs encoding MCR demonstrates for the first time that MCR and MCR-like proteins for metabolism of methane and short-chain hydrocarbons can exist on extrachromosomal elements and thus could potentially be dispersed across lineages, as is inferred to have occurred several times over the course of archaeal evolution 17,29. Borgs carry numerous metabolic genes, some of which produce variants of Methanoperedens proteins that could have distinct biophysical and biochemical properties. Assuming that these genes extend and augment Methanoperedens energy metabolism, Borgs may have far-reaching biogeochemical consequences, including reducing methane fluxes, with important and unanticipated climate implications."

Comment: What the researchers have found is a form of genome not seen before. Archaea bacteria are the originators of life, under current theory. They are newly found and their secrets are slowly being uncovered. These extrachromosomal genes are possibly present in more advanced forms, awaiting their discovery.

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5125 views

From a new study:

https://www.sciencenews.org/article/only-a-tiny-fraction-of-our-dna-is-uniquely-human

"The genetic tweaks that make humans uniquely human may come in small parcels interspersed with DNA inherited from extinct ancestors and cousins.

"Only 1.5 percent to 7 percent of the collective human genetic instruction book, or genome, contains uniquely human DNA, researchers report July 16 in Science Advances.

"That humans-only DNA, scattered throughout the genome, tends to contain genes involved in brain development and function, hinting that brain evolution was important in making humans human. But the researchers don’t yet know exactly what the genes do and how the exclusively human tweaks to DNA near those genes may have affected brain evolution.

***

"The results don’t mean that individual people are mostly Neandertal or Denisovan, or some other mix of ancient hominid. On average, people in sub-Saharan Africa inherited 0.096 percent to 0.46 percent of their DNA from ancient interbreeding between their human ancestors and Neandertals, the researchers found (SN: 4/7/21). Non-Africans inherited more DNA from Neandertals: about 0.73 percent to 1.3 percent. And some people inherited a fraction of their DNA from Denisovans as well.

***

"The team compiled results from those individual genomes into a collective picture of the human genome. For each spot, the team determined whether the DNA came from Denisovans, Neandertals or was inherited from a common ancestor of humans and those long-lost relatives.

"Although each person may carry about 1 percent Neandertal DNA, “if you look at a couple hundred people, they mostly won’t have their bit of Neandertal DNA in the same place,” says Kelley Harris, a population geneticist at the University of Washington in Seattle who wasn’t involved in the work. “So if you add up all the regions where someone has a bit of Neandertal DNA, that pretty soon covers most of the genome.”

"In this case, about 50 percent of the collective genome contains regions where one or more people inherited DNA from Neandertals or Denisovans, the researchers discovered. Most of the rest of the genome has been passed down from the most recent common ancestor of humans and their extinct cousins. After whittling away the ancient heirloom DNA, the team looked for regions where all people have human-specific tweaks to DNA that no other species have. That got the estimate of uniquely human DNA down to anywhere between 1.5 percent and 7 percent of the genome.

"The finding underscores just how much interbreeding with other hominid species affected the human genome, says coauthor Nathan Schaefer, a computational biologist now at the University of California, San Francisco. The researchers confirmed previous findings from other groups that humans bred with Neandertals and Denisovans, but also with other extinct, unknown hominids (SN: 2/12/20). It’s not known whether those mysterious ancestors are the groups that included “Dragon Man” or Nesher Ramla Homo, which may be closer relatives to humans than Neandertals.

***

"The tweaks that make the uniquely human DNA distinctive arose in a couple of evolutionary bursts, probably around 600,000 years ago and again about 200,000 years ago, the team found. Around 600,000 years ago is about the time that humans and Neandertals were forming their own branches of the hominid family tree."

Comment: Fascinating. At least we can be thankful the study doesn't try to make us advanced chimps. That 98% of our DNA bases are the same as chimp bases is not the same kind of study as this one, that looked at the specific or der of DNA segments.

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5099 views

The molecules responsible are described:

https://science.sciencemag.org/content/373/6557/876

How translation stops
Protein synthesis concludes when a ribosome encounters a stop codon in a transcript, which triggers the recruitment of highly conserved release factors to liberate the protein product. Lawson et al. used traditional biochemical methods and single-molecule fluorescence assays to track the interplay of release factors with ribosomes and reveal the molecular choreography of termination. They identified two distinct classes of effectors, small molecules and mRNA sequences, that directly inhibited the release factors and promoted stop codon readthrough. These findings may buttress ongoing efforts to treat diseases caused by premature stop codons, which cause 11% of all heritable human diseases.

Abstract
Translation termination, which liberates a nascent polypeptide from the ribosome specifically at stop codons, must occur accurately and rapidly. We established single-molecule fluorescence assays to track the dynamics of ribosomes and two requisite release factors (eRF1 and eRF3) throughout termination using an in vitro–reconstituted yeast translation system. We found that the two eukaryotic release factors bound together to recognize stop codons rapidly and elicit termination through a tightly regulated, multistep process that resembles transfer RNA selection during translation elongation. Because the release factors are conserved from yeast to humans, the molecular events that underlie yeast translation termination are likely broadly fundamental to eukaryotic protein synthesis.

***

The fidelity of translation elongation is driven in part by kinetic proofreading, in which EF-Tu/eEF1A preferentially rejects noncognate tRNAs in two sequential steps to boost overall accuracy. Although the basis of termination fidelity is unknown, we consider kinetic proofreading a plausible model. eRF3 is essential for termination fidelity, because its inclusion boosts specificity by 2600-fold. Here, we show that eRF3 conformationally unlocks and delivers eRF1 to ribosomes and facilitates eRF1 accommodation in an eRF3 GTPase–dependent manner, thus providing eRF3 with multiple opportunities to favor genuine stop codons. Further study of termination substep kinetics at cognate and near-cognate stop codons will reveal whether proofreading governs eukaryotic termination fidelity.

Comment: Note the bold. Another example of irreducible complexity, designed all at once for the parts to work together. The final paragraph shows the specific editing for error controls found so far.

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4900 views

An other study:

https://phys.org/news/2021-09-transcription-elongation-checkpoint.html

"According to the study, the presence of a protein called SPT5 serves as a "passport," determining whether a polymerase complex is allowed to proceed down the length of DNA or is instead degraded and destroyed.

"Only RNA Polymerase IIs with SPT5 are allowed to leave the station," said Ali Shilatifard, Ph.D., the Robert Francis Furchgott Professor, chair of Biochemistry and Molecular Genetics and senior author of the study.

***

"During transcription elongation, the RNA polymerase II complex "walks" along one strand of DNA, copying genetic elements to a strand of RNA. Shilatifard's laboratory has previously discovered pauses in this process linked to regulatory checkpoints. Now, using this new method of gene deletion, they've discovered a crucial checkpoint before elongation even starts.

"In cells with SPT5 depleted, polymerase never begin its journey down the strand of DNA. Instead, it is recognized as faulty and degraded. How exactly it is recognized remains unknown, but it's clear that SPT5 serves as a badge of approval, according to Yuki Aoi, Ph.D., a postdoctoral fellow in the Shilatifard laboratory and lead author of the study.

"'If there are issues here, and the polymerase is allowed to go, there could be more issues down the line," Aoi said. "It's only allowing polymerases that are certified to leave because they have SPT5."

"The investigators also discovered that a protein called CUL3 is part of the pathway that destroys polymerases lacking SPT5."

Comment: More evidence for design. This system cannot arise by stepwise additions. It must be complete at its start. Think of it this way: only a complete organ system can work and therefore be judged by natural selection. An incomplete or partial system isn't working and cannot be evaluated.

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4880 views

Six feet coiled into a tiny space:

https://evolutionnews.org/2021/09/hierarchical-systems-in-biology-dna-packaging/

"So how do you package one meter of information content into a space 1/100,000 that size? Very carefully and quite ingeniously. The storage of DNA is very much like hierarchical file systems on Windows and Linux desktop computers compressed into a .zip file. In the same manner that there are folders within folders within folders in a desktop computer, with the actual files at the terminal level, individual genes within a DNA molecule are equivalent to “files” that in this case specify the building of a protein needed for the cell to function. DNA packaging is far more complex, however, with several levels of packaging into a highly compressed and compact structure called chromatin. Essentially, there are three orders of DNA packaging: the first order is the nucleosome, the second order is the solenoid fiber, and the third order is the scaffold loop chromatids chromosome. The diagram below demonstrates the levels of packaging.

***

"The first level of packaging of DNA is where the double-stranded DNA is wrapped around spools of histone, a family of positively charged proteins that function primarily in packaging DNA, to form nucleosomes, creating the appearance of “beads” on a string. The nucleosomes themselves are then coiled into a 10 nm (10 billionths of a meter) fiber. Each nucleosome “core” consists of eight histone molecules. The nucleosomes are then further folded into the second order supercoiled solenoid fiber, which is 30 nm in width. The third order is the forming of looped domains of solenoid fibers that average 300 nm in width which are then further compressed down to 250 nm to form chromatin fiber. The chromatin fibers are further folded into 700 nm chromatids, and finally we have the highest order of structure that forms the characteristic shape of a chromosome which is 1400 nm in width as seen above.

It is hard to fathom that such a highly complex, hierarchical mechanism of information storage on a microscopic scale could come about purely by chance, which more importantly demonstrates a clear case of the classic “chicken and egg” problem. This complex, highly orchestrated packaging model, coordinated by the machinery of enzymes (topoisomerases) and various types of histones that are proteins themselves coded in DNA, must have come prior to DNA and prior to the random variation mechanism of evolution itself. The DNA packaging model is programmed with the knowledge of what regions of the chromosome to keep tightly supercoiled and what regions to keep more loosely packed to aid in DNA transcription. Moreover, if a region needed for transcription is supercoiled, it will unwind that region and compensate for the unwinding with a compensating supercoil in a prior region. Thus, there is an astounding process of coordination taking place within the process of transcribing DNA.

"Interestingly, there are companies that recognize the genius of DNA and its packaging model who are investigating using DNA molecules as a means of creating molecular-level archival data storage to solve the problem of an ever-increasing amount of digital data that is surpassing the amount of physical storage available using modern magnetic and optical media. For example, tech giant Microsoft is currently engaged in this research, noting the following on their website: “Using DNA to archive data is an attractive possibility because it is extremely dense (up to about 1 exabyte per cubic millimeter) and durable (half-life of over 500 years).” When one considers the fact that the world’s finest software engineers look to the DNA packaging topology to dramatically increase storage capability by orders of magnitude, it is reasonable to conclude that the packaging and processing of DNA is the product of a purposeful designer with a degree of engineering knowledge simply unmatched by humans."

Comment: When humans look to how DNA works for computer ideas, it is obvious a designer wass at work to create it.

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4855 views

A new huge survey in mammals:

https://www.science.org/content/article/chemical-switches-genes-may-help-explain-why-la...

"When it comes to how long a mammal can live, a bigger body is usually better: The typical mouse life span is less than 4 years, whereas a bowhead whale may make it to 211. But within a species, this relationship can flip: Large dog breeds tend to have shorter life spans than smaller canines.

***

"The analysis looked at a DNA modification called methylation, which can control whether genes are turned on or off. The patterns of methylation the team found add a new layer of information to better understood differences in the DNA sequences of genes themselves, the authors say. “It’s kind of a gold mine for people who either want to study what is unique about a certain species or conversely what is shared,” says aging researcher Steve Horvath of the University of California,

***

"In DNA methylation, a molecule called a methyl group attaches to a base, usually cytosine. Horvath is known for showing that patterns of these methyl groups change as a person ages, and for creating an “epigenetic clock” that uses a DNA sample to estimate a person’s age within 3.6 years.

***

"They used the data to devise an epigenetic clock that can be used to estimate the age of any living mammal from a DNA sample. This clock turned up some new genes that may govern aging, first author Ake Lu reports in a poster at the ASHG meeting this week and a January preprint.

"The consortium also wondered whether other individual or species-specific traits could be tied to DNA methylation. To explore this, computational biologist Amin Haghani, a postdoc in Horvath’s lab, first simply looked for methylation patterns. He found 55 clusters of methylated cytosines—between 33 and 1864 sites per cluster—many of which turned out to correlate with species-specific traits such as maximum life span, average adult weight, and age at sexual maturity. And others matched up with individual traits, such as age, sex, and tissue type.

"The team also showed, in work reported in a poster and a March preprint, that evolutionary trees constructed using cytosine methylation largely mirror phylogenies based on their gene sequences. “This is really interesting because it shows our DNA methylation is tracking evolution,” Haghani says.

"The genes switched on or off by the methylated bases near them may help control that trait—for example, the life span methylation cluster may govern stem cell genes important early in development, the team proposes. “Chances are, these cytosine sites are part of pathways or cell types that are important,” Horvath says.

***

"Not all epigenetics researchers are surprised by the consortium’s findings. It’s logical that methylation patterns track with evolution because the process itself is controlled by genes with evolving sequences, says plant epigenomics researcher Frank Johannes of the Technical University of Munich. Horvath’s trees are “a molecular readout … of genetic diversity,” says Johannes, who notes that similar “phyloepigenetic” trees were constructed for plants 10 years ago. Still, he says, the new study offers “a large resource for comparative epigenomics.'”

Comment: makes lots of sense seeing this stronger view of epigenetics as mixed up in making evolution proceed. Lamarck is now reasonable. Perhaps methyl groups are God's controls?

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4663 views

A new study on 'junk' DNA:

https://news.berkeley.edu/2021/10/18/so-called-junk-dna-plays-critical-role-in-mammalia...

"Nearly half of our DNA has been written off as junk, the discards of evolution: sidelined or broken genes, viruses that got stuck in our genome and were dismembered or silenced, none of it relevant to the human organism or human evolution.

***

"The study shows that at least one family of transposons — ancient viruses that have invaded our genome by the millions — plays a critical role in viability in the mouse, and perhaps in all mammals. When the researchers knocked out a specific transposon in mice, half their mouse pups died before birth.

"This is the first example of a piece of “junk DNA” being critical to survival in mammals.

"In mice, this transposon regulates the proliferation of cells in the early fertilized embryo and the timing of implantation in the mother’s uterus. The researchers looked in seven other mammalian species, including humans, and also found virus-derived regulatory elements linked to cell proliferation and timing of embryo implantation, suggesting that ancient viral DNA has been domesticated independently to play a crucial role in early embryonic development in all mammals.

"According to senior author Lin He, UC Berkeley professor of molecular and cell biology, the findings highlight an oft-ignored driver of evolution: viruses that integrate into our genome and get repurposed as regulators of host genes, opening up evolutionary options not available before.

“The mouse and humans share 99% of their protein coding genes in their genomes — we are very similar with each other,” He said. “So, what constitutes the differences between mice and humans? One of the major differences is gene regulation — mice and humans have the same genes, but they can be regulated differently. Transposons have the capacity to generate a lot of gene regulatory diversity and could help us to understand species-specific differences in the world.”

***

"In a paper appearing last week in the journal Cell, He and her team identify the key regulatory DNA involved: a piece of a transposon — a viral promoter — that has been repurposed as a promoter for a mouse gene that produces a protein involved in cell proliferation in the developing embryo and in the timing of implantation of the embryo. A promoter is a short DNA sequence that is needed upstream of a gene in order for the gene to be transcribed and expressed.

***

"While transposons are generally specific to individual species — humans and mice, for example, have largely different sets — the researchers found that different species-specific transposon families were turned on briefly before implantation in all eight mammals, including the opossum, the only mammal in the group that does not employ a placenta to implant embryos in the uterus.

“'What’s amazing is that different species have largely different transposons that are expressed in preimplantation embryos, but the global expression profiles of these transposons are nearly identical among all the mammalian species,” He said."

Comment: so transposons are not DNA junk. But more than that viral elements are involved in driving evolution, a point mentioned before in entries here. Why any viruses since some are dangerous? Why any bacteria because some are dangerous? Viruses arev seen her as useful andv we know bacteria perform all sorts of vital functions.

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4650 views

A logical event:

https://knowablemagazine.org/article/living-world/2021/the-curious-case-shrinking-genome

"...the fungus gnat does something bizarre. Early in the embryo’s development, most of the cells jettison two specific chromosomes — enormous ones, compared with the others — so the pair never ends up in the lion’s share of the gnat’s body. Only the cells that become germ cells retain the bonus DNA and pass it on to the next generation.

"How and why this feature evolved remains largely mysterious, though biologists first spotted it a century ago. And black-winged fungus gnats aren’t the only genetic screwballs. A surprisingly wide array of creatures, all the way up to some vertebrates, dump significant stretches of DNA during early development, so the stretches don’t end up in most of their body cells.

***

"To date, scientists have observed the phenomenon in various insects, in lampreys and hagfish, in hairy one-celled life forms called ciliates, in parasitic roundworms and tiny crustaceans called copepods. They’ve seen it in rat-like marsupials called bandicoots and in songbirds — probably all songbirds, according to recent work. And they expect to find many more cases.

“'A lot of these weird genomic features tend to be fairly rare, but they do evolve repeatedly,” Ross says. “It’s not just one freak event.” Presumably, then, there must be some selective advantage to the creatures that go down that evolutionary route. But what is it?

***

"Guaranteeing that genes are active at certain times but not others, or in some tissues but not others, is a critical function for any living thing. Think of the many different cell types in our bodies: All contain the same DNA sequence, but our heart cells produce different proteins than our skin cells do, so that each can do its specialized job. And even within a particular type of cell, the proteins that are produced vary during a creature’s lifespan.

"Perhaps what these dropped genes do would be so damaging to adult cells that eliminating them is a better-safe-than-sorry device, Davis says. “It’s total speculation, though — because there’s no proof of anything.'”

Comment: Makes perfect sense. Much of the DNA that drives the developing fetus are not needed during regular developed life. So just keep them in germ cells.

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4613 views

Non-coding RNA makes compartments of info:

https://phys.org/news/2021-11-vast-library-cells.html

"The human genome can be thought of as a massive library, containing over 20,000 different "instruction manuals": your genes. For example, there are genes which contain information to build a brain cell, a skin cell, a white blood cell, and so on. There are even genes that contain information about regulating the genome itself—like books that explain how to organize a library. The ability to regulate gene expression—in other words, the cell's ability to turn various constellations of genes on or off—is the basis of why different cells (such as a muscle cell or a brain cell) have different forms and functions.

"For any library to be useful to a reader, it needs to be organized in an easily searchable way. For example, all the books pertaining to world history may be on one shelf, whereas the cookbooks may be in an entirely different section of the library. In a cellular nucleus, there is over six feet of genetic material packed into a space 50 times smaller than the width of a human hair. How is the "library" in the nucleus organized? When a cell needs to regulate certain genes, how does the cellular machinery find the right ones amongst 20,000 others?

***

"Led by former Guttman lab graduate student Sofia Quinodoz (Ph.D. '20)—now a Hanna Gray postdoctoral fellow at Princeton University—the team found that molecules of non-coding RNA are responsible for establishing "compartments" within the nucleus and shepherding in key molecules to precise regions in the genome. Noncoding RNA are molecules that do not encode for proteins, and instead have an array of functions that are often still mysterious to biologists. In the library analogy, non-coding RNA molecules act as the "shelves" that organize different groups of genes and the machinery that interacts with them.

"Understanding how genetic material is organized spatially is a crucial part of understanding the basic workings of life. Dysfunction within the nucleus is a hallmark of many diseases, including cancer, neurodegenerative disorders, and others."

Comment: "Instruction manuals" means information. This is another example of the 3-D understanding of how DNA works to offer coded information. Not by chance

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4572 views

High speed reaction times in setting up transcription machinery:

https://www.sciencedaily.com/releases/2021/11/211105134631.htm

"It is essential for cells to control precisely which of the many genes of their genetic material they use. This is done in so-called transcription factories, molecular clusters in the nucleus. Researchers have now found that the formation of transcription factories resembles the condensation of liquids. Their findings will improve the understanding of causes of diseases and advance the development of DNA-based data storage systems.

"It is essential for cells to control precisely which of the many genes of their genetic material they use. This is done in so-called transcription factories, molecular clusters in the nucleus. Researchers of Karlsruhe Institute of Technology (KIT), Friedrich-Alexander-Universität Erlangen-Nuremberg (FAU), and Max Planck Center for Physics and Medicine (MPZPM) have now found that the formation of transcription factories resembles the condensation of liquids.

***

"Human genetic material contains more than 20,000 different genes. But each cell only uses a fraction of the information stored in this genome. Hence, cells have to control precisely which genes they use. If not, cancer or embryonal growth disorder may develop. So-called transcription factories play a central role in the selection of active genes. "These factories are molecular clusters in the nucleus that combine the correct selection of active genes and the read-out of their sequence at a central location," Lennart Hilbert explains.

***

"In their publication, the researchers point out that condensation to form transcription factories resembles steamy glasses or windows. Liquid condenses in the presence of a receptive surface only, but then very quickly. In the living cell, specially marked areas of the genome are used as condensation surfaces. The liquid-coated areas allow for the adhesion of relevant gene sequences and additional molecules that eventually activate the adhering genes. These findings were obtained by interdisciplinary cooperation.

***

"'Our work shows how the biological cell organizes such processes rapidly and reliably.'"

Comment: Same old story. Transcription processes are extremely rapid and accurate, but as discussed in the theodicy thread, mistakes by rapidly changing molecules can happen occasionally. God added editing systems to correct these as much as they could.

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4536 views

Some organisms use an entirely different form of DNA:

https://www.the-scientist.com/news-opinion/screen-of-250-000-species-reveals-tweaks-to-...

"A massive screen of bacterial and archaeal genomes revealed five previously unknown instances where an organism uses an alternate code to translate genetic blueprints into proteins.

***

"Prior to the new study, all known alternate genetic codes in bacteria involved changing a “stop” codon that instructs cellular machinery that it’s reached the end of a protein into one associated with an amino acid. The new results reveal the first alternate genetic codes in bacteria that represent a sense codon reassignment—that is, changing a codon from one amino acid to another.

"Identifying these alternate codes is important, Eddy says, because scientists who predict what proteins an organism will synthesize based on its genome do so under the assumption that the standard genetic code is at play. Accounting for deviations, then, will improve the accuracy of those predictions and prevent errors from being codified into databases as more and more genomes are sequenced.

***

"Part of the reason changes do happen, Shulgina explains, is that some bacterial genomes may have a low composition of certain nucleotides compared to others. That brings the usage of codons that rely on those nucleotides down to nearly zero, making it easier for an organism to survive shifts without altering too many proteins in a drastic way.

“'At least in bacteria, it seems like these sorts of forces might explain why the genetic code evolved this way,” Shulgina says. “This might be totally different if we looked in other forms of life like eukaryotes.” Exceptions to the standard genetic code have been found in single-celled eukaryotes such as yeast, but experts expect alternate codes to be rare in more complex eukaryotic organisms.

"Tracing down why these alternate genetic codes emerged during evolutionary history is difficult, multiple researchers tell The Scientist, in no small part because humans couldn’t watch it happen. But the authors do have some hypotheses.

"In one case, Shulgina identified a bacterium that uses the same alternate code as a bacteriophage virus that infects it, indicating that the bacteria seemingly evolved an alternate code that prevented its cellular machinery from being hijacked—and that the phage may have then made the same adaptation to follow its host."

Comment: So DNA is not absolutely set in stone in simple organisms. No studies have been done on more advanced complex eukaryotes.

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4572 views

Held in tight bounds:

https://www.science.org/doi/10.1126/science.abi7489

"Centromeres are key for anchoring chromosomes to the mitotic spindle, but they have been difficult to sequence because they can contain many repeating DNA elements. These repeats, however, carry regularly spaced, distinctive sequence markers because of sequence heterogeneity between the mostly, but not completely, identical DNA sequence repeats. Such differences aid sequence assembly. Naish et al. used ultra-long-read DNA sequencing to establish a reference assembly that resolves all five centromeres in the small mustard plant Arabidopsis. Their view into the subtly homogenized world of centromeres reveals retrotransposons that interrupt centromere organization and repressive DNA methylation that excludes centromeres from meiotic crossover repair. Thus, Arabidopsis centromeres evolve under the opposing forces of sequence homogenization and retrotransposon disruption. (my bold)

"The centromeres of eukaryotic chromosomes assemble the multiprotein kinetochore complex and thereby position attachment to the spindle microtubules, allowing chromosome segregation during cell division. The key function of the centromere is to load nucleosomes containing the CENTROMERE SPECIFIC HISTONE H3 (CENH3) histone variant [also known as centromere protein A (CENPA)], which directs kinetochore formation. Despite their conserved function during chromosome segregation, centromeres show radically diverse organization between species at the sequence level, ranging from single nucleosomes to megabase-scale satellite repeat arrays, which is termed the centromere paradox. Centromeric satellite repeats are variable in sequence composition and length when compared between species and show a high capacity for evolutionary change, both at the levels of primary sequence and array position along the chromosome. However, the genetic and epigenetic features that contribute to centromere function and evolution are incompletely understood, in part because of the challenges of centromere sequence assembly and functional genomics of highly repetitive sequences. New long-read DNA sequencing technologies can now resolve these complex repeat arrays, revealing insights into centromere architecture and chromatin organization.

***

"Our Col-CEN assembly and functional genomics analysis have implications for understanding centromere sequence evolution in eukaryotes. We propose that a recombination-based homogenization process, occurring between allelic or nonallelic locations on the same chromosome, maintains the CEN180 library close to the consensus optimal for CENH3 recruitment. The advantage conferred to ATHILA retrotransposons by integration within the centromeres is presently unclear. They may be engaged in centromere drive, supporting the hypothesis that centromere satellite homogenization acts as a mechanism to purge driving elements. Each Arabidopsis centromere appears to represent different stages in cycles of satellite homogenization and ATHILA-driven diversification. These opposing forces provide both a capacity for homeostasis and a capacity for change during centromere evolution. In the future, assembly of centromeres from multiple Arabidopsis accessions and closely related species may further clarify how centromeres form and the evolutionary dynamics of CEN180 and ATHILA repeats."

Comment: Note my bolds. Such tight controls are automatic, and in life provide persisting homeostasis, which is why so much energy is required by life. Staying alive is a constant biochemical battle.

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4553 views

If absent, proper development of tissues is damaged:

https://phys.org/news/2021-11-histone-modification-essential-tissue.html

"Chemical modifications of histones, the small proteins around which DNA is wrapped, are known to affect gene expression. In a study conducted in C. elegans, researchers from the Gasser group show that the defining modification of the tightly packed form of DNA called heterochromatin selectively blocks the expression of genes in differentiated tissues. The loss of the enzyme that mediates this modification leads to a loss of tissue integrity and early aging.

"Histone methylation is a process by which methyl groups are transferred to select amino acids of histones, the proteins that act as spools around which DNA winds to create the structural units called nucleosomes. The methylation of lysine 9 in histone H3 (H3K9me), an example of histone methylation, is the key modification that defines heterochromatin, a tightly packed form of DNA that is most commonly found on repetitive "junk" DNA. Heterochromatin is also thought to silence tissue-specific genes during development, however it has been poorly characterized how this is achieved.

***

"In the resulting study published in Nature Cell Biology, co-first authors Methot and Padeken show that the loss of H3K9me in worms leads to a tissue specific misexpression of genes. Not only were specific genes aberrantly expressed, but the animals became less mobile and were short-lived. The scientists showed that in the absence of H3K9me, cell-type specific transcriptional activators are necessary to drive the misexpression of genes. This occurs primarily at tissue-specific genes whose expression normally occurs in other cell types. For instance, genes that should be expressed in neurons or intestine cells become aberrantly expressed in muscle upon the loss of H3K9me. This histone modification, and the enzyme that mediates it, are therefore essential for ensuring the integrity of differentiated tissues."

Comment: Such specificity requires exact design, not likely to be developed by natural mutational processes.

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4505 views

A review of genome complexity in one activity:

https://christianscholars.com/guest-post-latest-discoveries-in-the-field-of-structural-...

"Transcription is the biochemical process that occurs in every cell in the human body when protein synthesis is initiated. It is a complex series of steps that begin in the nucleus when a gene—a section on a strand of DNA—expresses instructions for a specific protein to be produced.

"...In simple terms, the portion of the DNA molecule where the gene is located is unzipped resulting in a strand of mRNA (messenger RNA). mRNA can be thought of as a digital tape that contains a sequence of 3-letter codes called codons that dictate the precise sequence of amino acids for the protein it is about to produce.

The mRNA leaves the nucleus and enters the site of protein synthesis called a ribosome. It is here that the codons are read and the specific amino acids are delivered by a second RNA molecule, tRNA (transfer RNA) which has its own 3-letter sequences called anti-codons that match the codons on the mRNA. The process continues; the ribosome continues assembling the amino acids one-by-one until the protein has been assembled according to the instructions originally encoded on the gene.

***

"They discovered it involves something called a preinitiation complex (PIC); an ensemble of transcription factors, an enzyme called RNA polymerase II (Pol II), more transcription factors, and a mediator complex that stabilizes the structure. In all there are about 75 different proteins.

"In order to image the PIC, it first had to be produced. This entailed building “on years of painstaking work by research teams that not only established methods for isolating all of the PIC’s protein components in the lab but coaxed those pieces into assembling in just the right way, without the whole complex falling apart.”1

"There is a deeper, philosophical question here: How can such a complex molecular machine, crucial for the synthesis of proteins and hence life, be itself dependent on 75 different proteins for its function? Where did those proteins come from in the first place if there was no PIC to initiate protein synthesis? (my bo ld)

"Or what came first—the chicken or the egg?"

Comment: any reasonable person, reading this article, would recognize the need for design, so why not accept a designer at work? Not at the 'maybe' level of thought!

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4474 views

Two female X chromosomes in somatic cells must be reduced to one for control:

https://evolutionnews.org/2021/11/new-studies-reveal-the-exquisite-designs-of-the-nucle...

"While males have both an X and Y chromosome, females have two X chromosomes. As if to avoid a double dose of X chromosome genes, females inactivate one of their two X chromosomes during embryonic development. As for which of the two X chromosomes is inactivated, this appears to be done randomly in each cell. This means that females, unlike males, have two different functional genomes operating in their bodies, making for a fascinating twist to female genetics. That is, in some cells of the female, the first X chromosome is active whereas in the remainder of the cells the other X chromosome is active.

"Exactly how the developing female embryo inactivates one of the X chromosomes has not been well understood. What has been clear is that the story involves a region on the X chromosome itself, and information in that region that codes for a long RNA molecule, known as Xist. The name Xist stands for X-inactive specific transcript, a direct reference to its function of inactivating the X chromosome. But a genetic region that, ultimately, causes the inactivation of the entire chromosome must be handled very carefully. It is present on all X chromosomes but causes inactivation not of the single male X chromosome, and not of one of the two female X chromosomes. Importantly it causes inactivation only of the other female X chromosome.

"In addition to the fact that Xist must be very carefully controlled, new research1 is shedding light on how this single molecule can produce such a significant result. While it seemed that a very large number of Xist molecules must be required to inactivate the much larger X chromosome, the researchers studied mouse embryonic stem cells and found that only about one hundred Xist’s are required. The Xist’s, operating in pairs, recruit a large number of proteins. The result is about 50 complexes, each consisting of two Xist’s and an army of proteins, spaced along the X chromosome. Some of the proteins twist and condense the overall chromosome, compressing it so that most of the genes are close to one of the 50 complexes. Other proteins act to silence those nearby genes, thus essentially inactivating the entire X chromosome. Obviously, there are many important, coordinated, steps in this inactivation process, allowing for a small number of Xist’s to manage this big job. As the paper’s lead author remarked, “It was kind of shocking to us that from just 50 sites, Xist manages to silence a thousand genes.'”

From the paper itself:

https://phys.org/news/2021-11-xist-rna-molecule-silences-chromosome.html

"Instead of interacting directly with every gene on the chromosome, Markaki and Plath showed, these Xist pairs act as hubs, or protein magnets, recruiting thousands of proteins to their spots on the chromosome. Then, specialized proteins pull the chromosome into a tightly condensed shape so that every section is in the vicinity of one of these 50 large clouds of proteins. From there, gene silencing proteins within these complexes bind to each gene, shutting it off.

"'The key insight here is that Xist RNA is not acting directly on the X chromosome but is more of an architectural molecule that sets up proteins to do their job," Plath said.

"The team also identified the proteins, called Polycomb group proteins, responsible for twisting the X chromosome into the necessary shape. Without the Polycomb proteins, only those sections of the X chromosome already near one of the 50 Xist sites become inactivated, the researchers found."

Comment: sexual reproduction may bring enhanced evolution potential, but obviously creates problems such as double X's. After seeing this exquisite design, try and tell me a designing mind does not exist.

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4414 views

A review as junk DNA disappears:

https://www.the-scientist.com/features/adapting-with-a-little-help-from-jumping-genes-6...

"The notion that TEs are vital to genomes, and not parasites or trash, harks back to the 1950s and Barbara McClintock, who won a Nobel Prize in 1983 for the discovery of transposons in maize: she proposed that TEs play an important role in gene expression in the very first paper on them. But the idea that genetic elements could be mobile clashed with the prevailing view of an organism’s genome as fixed. It would be decades before transposons were described from other organisms and their near-universal presence in genomes became clear. By then, researchers had figured out that these bits of DNA coopt a cell’s machinery, and the parasite framing emerged. Further, research showing that TEs don’t code for essential cellular proteins meant that, at best, they got lumped in with other kinds of noncoding DNA as genetic junk.

***

"But with long-read sequencing methods enabling scientists to document the transposon content—the “mobilome”—of individual organisms, TEs are entering the spotlight. And, it turns out, they can and do regulate genes. McClintock was right.

***

"There are numerous ways that mobile genetic elements can affect evolution. For example, many transposable elements (TEs), often called transposons, contain genes that code for their jumping or copying machinery, and over time these may be “domesticated” through mutation and selection, becoming integral parts of the organisms’ genome. The RAG1 and RAG2 enzymes that mix up DNA segments in immune proteins (antibodies and T cell receptors) are a notable example. “Wild” TEs can also have adaptive potential, creating genetic diversity as they leap. If TEs land inside a gene, they can directly alter coding regions, mRNA splice sites, or expression-related motifs (left). And because transposons often contain transcription factor binding sites and other regulatory sequences, they can alter a gene’s expression even if they land nearby (right). The transposable elements can also alter the genome in other ways—such as by picking up huge chunks of DNA as they jump (not pictured)—that scientists suspect are similarly altering the course of evolution.

"Arguably the most immediate and dramatic impacts TEs have on genomes occur when they insert into active genes. They can jump into coding regions, altering protein sequences, or they can insert into noncoding regions and alter gene splicing or expression. This is what happened in peppered moths, when a 22-kb TE inserted into the cortex gene and led to overproduction of melanin, turning dark the normally lightly bespeckled moths and improving their survival in polluted environments.

***

"In addition to a growing body of evidence that transposons can generate diversity in host genomes to drive change over millions of years, Mirouze says TEs are likely major drivers of rapid evolution—changes measured in terms of generations rather than millennia.

***

"Chuong, who says his group’s unpublished work in cattle has suggested that TEs can be activated by immune responses after eons of being silenced, says it’s plausible that TEs are a “major source of variation . . . that could be selected upon” during times of extreme stress, especially when that stress is novel and sudden, such as infection with a deadly pathogen. In such cases, he says, “I think transposons and their activity are much more likely to provide an outsized source of variation compared to littler mutations.'”

Comment: Perhaps transposons are God's dabble mechanism. Enormous article worth reading.

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4096 views

A vital function demonstrated:

https://thedaily.case.edu/case-western-reserve-university-research-team-identifies-new-...

"In this study, the team discovered 53BP1 has a biological function in mediating the structure of DNA, specifically at a highly compacted region called heterochromatin.

"The researchers found that this new function involves a new form of activity of 53BP1, in which the protein accumulates at the condensed DNA regions and forms small liquid droplets—a process called liquid-liquid phase separation, similar to mixing oil with water for salad dressing.

"The team determined how 53BP1 can form liquid droplets: They found that this process requires the participation of other proteins known to support the structure of those highly condensed DNA. But, in turn, they discovered that 53BP1 actually stabilized the gathering of these proteins at these DNA regions, which is important for keeping the overall function of the DNA.

“'More excitingly, through these comprehensive analyses, we found that this new protective activity of 53BP1 is independent of the widely known role of this protein in repairing DNA damage, indicating a totally new function of 53BP1,” Zhang said. “Our study suggests that, in addition to DSB repair modulation, 53BP1 contributes to the maintenance of genome stability through the formation of these liquid droplets.'”

Comment: this editing system is irreducibly complex and must be designed. An example of an editing system to protect DNA. Distorted DNA results in cancer.

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4033 views

Mutation rates vary in different regions of the genome:

https://www.the-scientist.com/news-opinion/essential-genes-protected-from-mutations-69643

"...a new study cements the countering idea that the process of mutation isn’t evenly distributed across genomes. The work, published in Nature on January 12, finds that there’s a discrepancy in the rates of mutations among genes in model plant Arabidopsis thaliana. Specifically, genes playing a crucial role in survival and reproduction mutate far less often than those that are less important. (my bold)

"Arabidopsis is a small flowering plant that has a comparatively small genome, making it a popular system for genetic research. The study, which began at the Max Planck Institute for Biology in Germany and was carried over to University of California, Davis, when lead author and plant scientist J. Grey Monroe got a job there, finds a 58 percent lower mutation rate within genes than in the areas of the genome around them. On top of that, genes considered essential had a 37 percent lower mutation rate than those in which modifications would be less likely to prove disastrous.

"Mutations are distributed in a way that seems to be beneficial to the plant, Monroe tells The Scientist. The finding is “part of an ongoing movement that’s been happening since we started being able to sequence DNA,” which challenges the idea that mutations are equally likely throughout the genome and clarifies how evolution occurs, Monroe says. He adds that his paper is the first comprehensive analysis in a eukaryotic species that connects the mechanisms driving the variability in mutation rate at the cellular level with the finding that more important genes seem protected from mutation.

"Monroe and his colleagues found evidence of specific epigenetic characteristics such as cytosine methylation that prevent mutations from occurring in those regions, not unlike protective barriers. These structures and the variability in mutation rates within a single organism’s genome, Monroe says, suggest that “evolution created mechanisms that changed how evolution works.”

"Scientists have been demonstrating that mutations don’t occur randomly for nearly a century. Monroe, then, isn’t the first to show a mutation bias—previous studies to do so include a Journal of Molecular Evolution paper from 2005 demonstrating an increased mutation rate out near chromosomes’ telomeres, a 2011 publication in Nature Reviews Genetics suggesting the existence of a mutation bias across the human genome, and a 2012 review in BioEssays that suggests organisms may develop higher mutation rates in areas of the genome where changes would be most advantageous. With methodological improvements and a thorough epigenetic analysis, Monroe’s team added another piece to the puzzle."

Comment: The article contains many guesses as to why these protections exist, with no clear answer. I have one. These protections stabilize the existence of species, and do not allow speciation, which would then require a very special set of events as if a designer stepped in.

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4088 views

Very quickly in order to have speedy reactions:

https://www.sciencedaily.com/releases/2022/01/220127141550.htm

"In an article in the scientific journal Science, researchers at Uppsala University show how a DNA-binding protein can search the entire genome for its target sequence without getting held up on the way. The result contradicts our current understanding of gene regulation -- the genetic code affects how often the proteins bind, but not for how long.

"Over an organism's lifetime, its genome changes very little. What does change, constantly, are which proteins the cell produces in response to damage, changes in the environment, or stages in the reproductive cycle. The protein production is regulated by DNA-binding proteins that have evolved the ability to turn different genes on or off. Because the environment can change quickly, rapid adaptation is key. The DNA-binding proteins must find the correct DNA code among millions of base pairs, and do so fast.

"When DNA-binding proteins search the genetic code for their target sequence, they slide along the DNA helix to speed up the process. When they finally find the right spot, they stay there; the interaction with the "correct" sequence prevents them from sliding along. This mechanism has been widely accepted to describe the search process. It is an appealing hypothesis, yes, but it presents an annoying problem -- the DNA code is full of "almost correct" sequences. If the time a protein resides on a particular DNA motif was determined by the sequence, the searching proteins would constantly linger on sequences that resembled their target.

***

"The result was striking. Contradicting previous assumptions, the DNA sequence had little effect on how long LacI remained bound to the DNA. However, it was much more likely that the sliding LacI was held up briefly when the sequence was similar to the target sequence. In other words, DNA-binding proteins often leave also the sequence they are intended to regulate, but at the target site, they all but always make a very short journey before finding their way back again. On the macroscopic time scale, this looks like a stable interaction.

"'Our result, that DNA-binding proteins bind often rather than protractedly, explains how LacI can slide on the DNA sequence in search of its target without getting held up unnecessarily. LacI regulates the uptake of lactose in bacteria, but is of course just an example. The hundreds of different transcription factors that regulate our own genes likely act according to a similar principle," says Johan Elf, Professor at the Department of Cell and Molecular Biology at Uppsala University.

Comment: I always point out all reactions occur at high speed. How the molecule knows its target is still not known. But it has to work this way

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4035 views

From a new way of analysis:

https://phys.org/news/2022-01-uncovers-evidence-long-term-directionality-human.html

"A new study by a team of researchers from Israel and Ghana has brought the first evidence of nonrandom mutation in human genes, challenging a core assumption at the heart of evolutionary theory by showing a long-term directional mutational response to environmental pressure. Using a novel method, researchers led by Professor Adi Livnat from the University of Haifa showed that the rate of generation of the HbS mutation, which protects against malaria, is higher in people from Africa, where malaria is endemic, than in people from Europe, where it is not.

***

"Unlike other findings on mutation origination, this mutation-specific response to a specific environmental pressure cannot be explained by traditional theories. "We hypothesize that evolution is influenced by two sources of information: External information that is natural selection, and internal information that is accumulated in the genome through the generations and impacts the origination of mutations," said Livnat.

***

"However, the only alternative at the fundamental level conceived of up until now consisted of variants of Lamarckism—the idea that organisms can somehow respond directly to their immediate environments with beneficial genetic change. Since Lamarckism has not worked in general, the notion of random mutation remained the prevailing view.

***

"In breaking a new accuracy record, their method allowed something not previously possible—counting of de novo mutations for particular points of interest in the genome.

***

"Contrary to the widely accepted expectations, the results supported the nonrandom pattern. The HbS mutation originated de novo not only much faster than expected from random mutation, but also much faster in the population (in sub-Saharan Africans as opposed to Europeans) and in the gene (in the beta-globin as opposed to the control delta-globin gene) where it is of adaptive significance. These results upend the traditional example of random mutation and natural selection, turning it into an example of a nonrandom yet non-Lamarckian mutation.

"'Mutations defy traditional thinking. The results suggest that complex information that is accumulated in the genome through the generations impacts mutation, and therefore mutation-specific origination rates can respond in the long-term to specific environmental pressures," said Prof. Livnat. Previous studies, motivated by Lamarckism, only tested for an immediate mutational response to environmental pressures. "Mutations may be generated nonrandomly in evolution after all, but not in the way previously conceived. We must study the internal information and how it affects mutation, as it opens the door to evolution being a far bigger process than previously conceived," Livnat concluded.

"Until now, investigators have been limited by technology to measuring mutation rates as averages across many positions in the genome. Overcoming this barrier, the new method developed by Livnat and Melamed allowed the HbS mutation to be the first to have its mutation-specific origination rate measured, opening up new vistas for studies on mutation origination. These studies have the potential to affect not only our fundamental understanding of evolution, but also our understanding of diseases that are caused by mutations, namely genetic disease and cancer."

Comment: Livnat says complex information accumulates in the genome to guide it. Did God create the mechanism to accumulate information? What is not covered is the effect of dying from malaria causing a growth of immune survivors by subtraction from the original population.

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4010 views

In Arabidopsis thaliana, or thale plants:

https://phys.org/news/2022-01-evolutionary-theory-dna-mutations-random.html

"Researchers spent three years sequencing the DNA of hundreds of Arabidopsis thaliana, or thale cress, a small, flowering weed considered the "lab rat among plants" because of its relatively small genome comprising around 120 million base pairs. Humans, by comparison, have roughly 3 billion base pairs.

***

"'At first glance, what we found seemed to contradict established theory that initial mutations are entirely random and that only natural selection determines which mutations are observed in organisms," said Detlef Weigel, scientific director at Max Planck Institute and senior author on the study.

"Instead of randomness they found patches of the genome with low mutation rates. In those patches, they were surprised to discover an over-representation of essential genes, such as those involved in cell growth and gene expression.

"'These are the really important regions of the genome," Monroe said. "The areas that are the most biologically important are the ones being protected from mutation."

"The areas are also sensitive to the harmful effects of new mutations. "DNA damage repair seems therefore to be particularly effective in these regions," Weigel added.

"The scientists found that the way DNA was wrapped around different types of proteins was a good predictor of whether a gene would mutate or not. "It means we can predict which genes are more likely to mutate than others and it gives us a good idea of what's going on," Weigel said.

"The findings add a surprising twist to Charles Darwin's theory of evolution by natural selection because it reveals that the plant has evolved to protect its genes from mutation to ensure survival.

"'The plant has evolved a way to protect its most important places from mutation," Weigel said. "This is exciting because we could even use these discoveries to think about how to protect human genes from mutation.'"

Comment: It seems chance mutations can be protected from affecting plants. Was this designed or a natural event? I'll stick with design.

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4043 views

Very important to proper reproduction:

https://www.sciencedaily.com/releases/2022/02/220202111811.htm

"A research team, led by the John Innes Centre found that the enzyme DNA topoisomerase VI (topo VI) performs a critical role in removing chromosome tangles that occur in the cell nucleus of plants.

"This function enables the process of endoreduplication where the DNA content is doubled. Endoreduplication is the source of polyploidy, where a plant has multiple sets of chromosomes, including in some major crops.

"Topo VI was discovered, many years ago, in archaea, a type of single-celled organism without a nucleus. It was only found in plants and parasites such as malaria, more recently leading to the scientific question: what is the function of this enzyme in eukaryotes, organisms whose cells contain a nucleus?

"'Our study shows that topo VI in plants functions to remove chromosome tangles that occur during the endoreduplication process. This potentially explains its presence in plants where during endoreduplication, entanglements are most likely to occur," explains lead author Dr Shannon McKie."

Comment: My usual point: enzymes are giant complex working molecules necessary for life. Thisone was first found in Archaea so it had to have appeared with the first DNA, and must have been designed in anticipation of tangle problems. God knew there could be errors.

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4043 views

The making of mRNA is studied:

https://phys.org/news/2022-02-blueprint-proteins-mrna.html

"Proteins need to interact in a complex manner for a so-called "messenger RNA" (mRNA) to be created in human cells from a precursor molecule. mRNA provides a blueprint for proteins; the first vaccines against the coronavirus are also based on mRNAs. A team from Martin Luther University Halle-Wittenberg (MLU) and the Max Planck Institute (MPI) of Biochemistry in Martinsried has discovered how an essential final step in the production of mRNA precisely works.

"Proteins are responsible for all of the body's essential processes. In a sense, the genes in the human genome act as building instructions for them. However, an intermediate step is necessary before new proteins can be created: "First the DNA must be transcribed: A chain-like precursor RNA is produced which is an exact copy of the DNA. From this, several steps are required to create the mature mRNA.

***

"There is no room for error in this complicated process—even the smallest changes in the structure of a protein can impair its function and lead to the development of diseases. "The mRNA not only determines the structure of a protein, but also how much of it is produced. Therefore, it is important that its structure is also precisely controlled," Wahle adds. The proteins involved in reading out and transcribing DNA into precursor RNA are already known to scientists. However, an important sub-step in the process of creating mature mRNA has only been vaguely understood until now. First, the chains of the mRNA precursors are cleaved at a specific point to create uniform products. Then, a long molecular chain, the so-called poly(A) tail, is attached to one end of the strand. This ensures that the mRNA is not directly degraded again in the cells, and it is also important for protein synthesis.

***

"'We basically reproduced the conditions in a normal cell, although the natural process is probably even more complex," explains Wahle. Sixteen proteins are involved in creating the final molecules. "The process is universal, affecting every cell and every mRNA molecule in the body," says Felix Sandmeir from the MPI of Biochemistry." (my bold)

Comment: totally automatic and precisely controlled. Irreducibly complex, which means designed. This process is in every cell in our bodies, acting at necessarily high speed.

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4007 views

New basic major research:

https://phys.org/news/2022-02-distinct-domains-munc-non-coding-rna.html

Distinct structural domains in MUNC long non-coding RNA regulate gene expression.

"An lncRNA is an RNA longer than 200 bases that is not translated into a functional protein. It appears that humans have many tens of thousands of these RNAs that seem to play key roles in gene regulation through interactions with DNA, RNA or proteins.

***

"The researchers studied MUNC lncRNA in mouse myoblasts, precursor cells that can differentiate into skeletal muscle cells. MUNC lncRNA is known to play an important role in this skeletal muscle tissue formation through differentiation, a process called myogenesis. The MUNC lncRNA has two isoforms, one with 1,083 nucleotides that has two exons and one intron, and one with 518 nucleotides, where the intron has been cut out and the two exons spliced together.

***

"In the current study of MUNC lncRNA, the researchers found two important results when they did chemical structural determinations of the two isoforms. First, those structures had multiple structural domains that were not detected by computer predictions. This shows the need to determine structures experimentally. Second, those domains were largely conserved between the two isoforms, indicating the stability of the domains. The domains included six common "hairpins," where the RNA folds back on itself to make a double strand, found in each isoform. The spliced isoform had one additional hairpin and one loop not seen in the unspliced isoform.

***

"Both isoforms, when overexpressed in mouse myoblast cells, were promyogenic, meaning they promoted expression of genes involved in muscle cell differentiation, likely through activation of a common set of transcription factors. However, while 645 genes were upregulated by both forms of MUNC, 2,730 other genes were upregulated by only one isoform or the other. Thus, they control different sets of genes.

"The researchers made variants of the spliced isoform that either lacked one specific structural domain or had a defined mutation in a single domain. Each variant was overexpressed in mouse myoblast cells to see how disruption of individual structural domains affected expression of promyogenic factors. The resulting changes in gene expression revealed that different RNA domains of MUNC were important for binding to and regulating different genes. Thus, they could act independently, suggesting that the spliced MUNC is something like a Swiss Army knife that contains different tools in one pocketknife.

***

"The researchers also tested how loss or mutation of the domains affected binding of MUNC to two different promoter sites on the chromosome for the gene Myod1, which encodes a protein that acts as a master switch for myogenesis. Such binding at either site leads to enhanced Myod1 gene expression. Experiments showed that three of the hairpins were required for binding at both sites. In addition, six other domains were important for binding, but with a difference—three influenced binding at one site, and the other three influenced binding at the other site. Thus, different domains mediate distinct features of MUNC promyogenic activity. (my bold)

"To add to this complex story, Dutta and colleagues tested whether structure or the sequence of RNA bases was responsible for the functional roles of common-hairpin-1 and common-hairpin-4 in promyogenic gene expression. They did this by making mutants of the two hairpins, where different stretches of RNA base sequence were changed without altering the hairpin structure. The result? The mutants retained their function of inducing Myod1, indicating that the shape, not the RNA sequence, was key. "Based on the results from eight independent sequence mutants, we conclude that MUNC function attributed to common-hairpin-1 and common-hairpin-4 is primarily driven by structure," Dutta said. (my bold)

"'Overall," Dutta said, "the multi-modal mechanisms of regulation of gene expression by MUNC involve different domains of MUNC, and likely different protein partners. MUNC recruits varying cooperative machinery depending on the genomic context, and this behavior is likely exemplary of other lncRNAs that regulate gene expression.'"

Comment: tis key study shows how precise the genome is designed to control the information for formations of organs it produces. It certainly emphasizes the role of shape in the folding of shape.

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3980 views

In rotifers:

https://phys.org/news/2022-02-scientists-dna-modification-animals-captured.html

"In humans and other eukaryotes, two principal epigenetic marks are known. A team from the Marine Biological Laboratory (MBL) has discovered a third, novel epigenetic mark—one formerly known only in bacteria—in bdelloid rotifers, small freshwater animals.

"We discovered back in 2008 that bdelloid rotifers are very good at capturing foreign genes," said senior author Irina Arkhipova, senior scientist in the MBL's Josephine Bay Paul Center. "What we've found here is that rotifers, about 60 million years ago, accidentally captured a bacterial gene that allowed them to introduce a new epigenetic mark that was not there before." This is the first time that a horizontally transferred gene has been shown to reshape the gene regulatory system in a eukaryote.

"'This is very unusual and has not been previously reported," Arkhipova said. "Horizontally transferred genes are thought to preferentially be operational genes, not regulatory genes. It is hard to imagine how a single, horizontally transferred gene would form a new regulatory system, because the existing regulatory systems are already very complicated."

"'It's almost unbelievable," said co-first author Irina Yushenova, a research scientist in Arkhipova's lab. "Just try to picture, somewhere back in time, a piece of bacterial DNA happened to be fused to a piece of eukaryotic DNA. Both of them became joined in the rotifer's genome and they formed a functional enzyme. That's not so easy to do, even in the lab, and it happened naturally. And then this composite enzyme created this amazing regulatory system, and bdelloid rotifers were able to start using it to control all these jumping transposons. It's like magic." (my bold)

***

"In the two previously known epigenetic marks in eukaryotes, a methyl group is added to a DNA base, either cytosine or adenine. The team's newly discovered mark is also a cytosine modification, but with a distinct bacterial-like positioning of the methyl group—essentially recapitulating evolutionary events of over two billion years ago, when the conventional epigenetic marks in early eukaryotes emerged.

***

"...the Arkhipova lab was surprised to find a gene in the rotifer genome that resembled a bacterial methyltransferase (a methyltransferase catalyzes the transfer of a methyl group to DNA). "We hypothesized that this gene conferred this new function of suppressing transposons, and we spent the last six years proving that, indeed, it does," Arkhipova said."

Comment: Note my bold. Appeared magically or by God's design?

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3932 views

Using identifying marks on non-DNA areas of the nucleus:

https://phys.org/news/2022-03-rna-mammalian-cell-nucleus-reveals.html

"Most people are familiar with the cell nucleus from grade school biology as a storage compartment for DNA. But the nucleus also contains several distinct structures, called nuclear bodies or domains, whose roles scientists are just beginning to understand.

"Some of these structures are brimming with genes' messages, also known as RNA transcripts.

Now, U of T researchers have reported the first large-scale survey of RNA transcripts that are associated with different nuclear bodies in human cells. Their work suggests that these structures act as hubs to coordinate gene regulation and cell division.

"'It was known that some nuclear domains contain RNA, but the composition of that RNA was not systematically probed in previous studies," said Benjamin Blencowe, senior author...

***

"The team discovered swaths of novel RNAs, from several hundred to thousands, across the nuclear bodies. Previously, only a handful of transcripts were known to be associated with some of these structures, said Barutcu, whose research was supported by the Banting Postdoctoral Fellowship and a fellowship from the Canadian Institutes of Health Research (CIHR).

"One piece of data immediately struck the researchers. The nuclear bodies known as the speckles were associated with surprisingly high numbers of RNA transcripts with retained introns, segments which do not code for proteins.

"When a gene is transcribed into RNA, introns must be spliced out in the nucleus before the transcript can be released into the cell's interior to serve as a template for making proteins.

"The finding led them to realize that speckles are associated with a class of introns with delayed splicing. The nature of the transcripts provided a clue to their function. They were transcribed from genes that control various aspects of gene regulation and the cell division cycle. Genes controlling cell cycle progression must be activated in a timely manner so that their protein products are made only when they are needed. Errors in this process are well known drivers of cancer.

"The researchers came up with a model in which the role of the speckles might be to coordinate intron removal from transcripts in order to regulate their release from the nucleus, and their subsequent translation into protein factors required for gene regulation and the cell cycle. This mechanism would help ensure a rapid response to cellular signals to make the right kinds of proteins at the right time.

"Furthermore, when speckles were disrupted, this altered the splicing of the retained introns, including those located in genes that are directly involved in control of the cell cycle, supporting the idea that the speckles are linked to cell cycle progression.

"The model opens up new ways of thinking about cell cycle regulation with implications for cancer research, said Blencowe, who holds Canada Research Chair in RNA Biology and Genomics and Banbury Chair in Medical Research.

"'We've uncovered a mechanism involving differential intron retention linked to speckle integrity that could play an important role in not just normal cell division but also how it goes wrong in cancers," he said.

"In addition to the speckles, the team also found large numbers of intron-retained transcripts associated with the nuclear lamina, which forms at the periphery of the nucleus, but the functional significance of this observation remains unclear."

Comment: Still very early, but the degree of complexity keeps increasing as I've predicted previously, which leads to the obvious point, when does demonstrated complexity reach the tipping point to force everyone to admit, a designer has to be present?

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3914 views

Another article on humans:

https://genome.cshlp.org/content/early/2022/01/14/gr.276103.121

"Abstract:
While it is known that the mutation rate varies across the genome, previous estimates were based on averaging across various numbers of positions. Here we describe a method to measure the origination rates of target mutations at target base positions and apply it to a 6-bp region in the human hemoglobin subunit beta (HBB) gene and to the identical, paralogous hemoglobin subunit delta (HBD) region in sperm cells from both African and European donors. The HBB region of interest (ROI) includes the site of the hemoglobin S (HbS) mutation, which protects against malaria, is common in Africa and has served as a classic example of adaptation by random mutation and natural selection. We found a significant correspondence between de novo mutation rates and past observations of alleles in carriers, showing that mutation rates vary substantially in a mutation-specific manner that contributes to the site frequency spectrum. We also found that the overall point mutation rate is significantly higher in Africans than in Europeans in the HBB region studied. Finally, the rate of the 20A→T mutation, called the 'HbS mutation' when it appears in HBB, is significantly higher than expected from the genome-wide average for this mutation type. Nine instances were observed in the African HBB ROI, where it is of adaptive significance, representing at least three independent originations; no instances were observed elsewhere. Further studies will be needed to examine mutation rates at the single-mutation resolution across these and other loci and organisms and to uncover the molecular mechanisms responsible." (my bold)

From a review of the article:

https://www.eurekalert.org/news-releases/941828

"The results show that the HbS mutation is not generated at random but instead originates preferentially in the gene and in the population where it is of adaptive significance,” said Prof. Livnat. Unlike other findings on mutation origination, this mutation-specific response to a specific environmental pressure cannot be explained by traditional theories. “We hypothesize that evolution is influenced by two sources of information: external information that is natural selection, and internal information that is accumulated in the genome through the generations and impacts the origination of mutations,” said Livnat.

***

"Contrary to the widely accepted expectations, the results supported the nonrandom pattern. The HbS mutation originated de novo not only much faster than expected from random mutation, but also much faster in the population (in sub-Saharan Africans as opposed to Europeans) and in the gene (in the beta-globin as opposed to the control delta-globin gene) where it is of adaptive significance. These results upend the traditional example of random mutation and natural selection, turning it into an example of a nonrandom yet non-Lamarckian mutation. (my bold)

***

"Previous studies, motivated by Lamarckism, only tested for an immediate mutational response to environmental pressures. “Mutations may be generated nonrandomly in evolution after all, but not in the way previously conceived. We must study the internal information and how it affects mutation, as it opens the door to evolution being a far bigger process than previously conceived,” Livnat concluded.

Comment: Wow! Here we see just the mechanism dhw proposes in a very specific limited example, changing hemoglobin into form malaria cannot enter. And it doesn't seem a chance random mutation. But this is not at the level of complex phenotypical or physiological design dhw wants God to give organisms.

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3945 views

Mind blowing complexity:

https://www.sciencemagazinedigital.org/sciencemagazine/18_march_2022/MobilePagedArticle...

Abstract:
"The tail of replication-dependent histone H3.1 varies from that of replication-independent H3.3 at the amino acid located at position 31 in plants and animals, but no function has been assigned to this residue to demonstrate a unique and conserved role for H3.1 during replication. We found that TONSOKU (TSK/TONSL), which rescues broken replication forks, specifically interacts with H3.1 via recognition of alanine 31 by its tetratricopeptide repeat domain. Our results indicate that genomic instability in the absence of ATXR5/ATXR6-catalyzed histone H3 lysine 27 monomethylation in plants depends on H3.1, TSK, and DNA polymerase theta (Pol θ). This work reveals an H3.1-specific function during replication and a common strategy used in multicellular eukaryotes for regulating post-replicative chromatin maturation and TSK, which relies on histone monomethyltransferases and reading of the H3.1 variant".

Conclusion:
"Overall, this work uncovers a role for the TPR domain of TSK in selectively interacting with the H3.1 variant. Previous work in human cell lines has shown that the TSK ortholog TONSL copurifies with H3.1 in affinity purification/biochemical fractionation assays (Display footnote number:28), and that TONSL-mediateddoublestranded DNA break repair depends on the H3.1 chaperone CAF-1 (Display footnote number:2). These findings, combined with our identification of the TPR domain of TSK/TONSL acting as an H3.1 reader, point to a model where post-replicative chro-matin maturation in plants and animals relies on similar mechanisms involving H3.1 and clade-specific enzymes that monomethylate histones to prevent TSK/TONSL binding (Fig. 4G). In plants, monomethylation occurs at H3.1 Lys27 via ATXR5/6 and prevents binding of TSK through the TPR domain. In animals, SET8-mediated monomethylation at H4 Lys20 interferes with TONSL binding via the ARD domain (Display footnote number:9). However, in both plants and animals, recruitment of TSK/TONSL to chromatin likely relies on the ability of the conserved TPR domain to preferentially interact with the H3.1 variant. Thus, our work reveals the importance of selectively incorporating H3.1 variants during DNA replication, as it confers a window of opportunity during the cell cycle for the TSK/TONSL DNA repair pathway to resolve broken replication forks."

Comment: This is obviously difficult to follow for those of us not working in this field. This mechanism is used by both plant and animal organisms with sexual reproduction in which DNA is wrapped around histone core molecules and is specifically designed to repair mistakes in which DNA is broken. This mechanism had to be present when sexual reproduction first appeared in evolution, or these forms of life would not have survived. Only comprehensive design can produce this.

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3922 views

A different explanation than the original article in a second study:

https://www.sciencedaily.com/releases/2022/03/220321132210.htm

"The fact [is] that our DNA requires constant upkeep to maintain its integrity. Were it not for dedicated DNA repair machinery that routinely fixes mistakes, the information within DNA would be rapidly degraded.

"This repair happens at cell cycle checkpoints that are activated in response to DNA damage. Like a quality assurance agent on an assembly line, proteins that participate in the DNA damage checkpoint assess the cell's DNA for mistakes and, if necessary, pause cell division and make repairs. When this checkpoint breaks down -- which can happen as a result of genetic mutations -- DNA damage builds up, and the result is often cancer.

***

"As a result of this effort, his lab has purified several components of the repair machinery, including 9-1-1 proteins and proteins that facilitate the binding of 9-1-1 to DNA.

***

"Much like the gears and levers of a machine, it's these movements of amino acids that allow proteins to serve as the workhorses of the cell, including those that repair DNA.

"'Using cryo-EM, we're able to not only determine one structure but an ensemble of structures. By putting these structures together in a logical pattern, based on the new data and previous biochemical data, we can come up with a proposal for how this clamp works."

***

"Much like the gears and levers of a machine, it's these movements of amino acids that allow proteins to serve as the workhorses of the cell, including those that repair DNA.

"'When Dirk came to us, we realized that many of the tools that our lab has developed over the past few years were perfectly suited to answering this question," Dr. Hite says. "Using cryo-EM, we're able to not only determine one structure but an ensemble of structures. By putting these structures together in a logical pattern, based on the new data and previous biochemical data, we can come up with a proposal for how this clamp works."

***

"'It had been thought from all studies prior to this that clamps would open in the manner of lock washer, where basically the two open ends of the clamp would rotate out of plane to create a narrow gap," Dr. Remus says. "But what Rich observed is that the 9-1-1 clamp opens much more widely than anticipated, and it opens completely in plane -- there's no twisting like in the lock-washer scenario."

***

"Another surprise was that the 9-1-1 clamp loader complex was observed to bind DNA in the opposite orientation from other clamp loader complexes that act on undamaged DNA during normal DNA replication. This observation explained how 9-1-1 is specifically recruited to sites of DNA damage."

Comment: this repair mechanism had to have been designed when DNA code was first designed. The possibility of breaks was recognized and protected against. There would be no DNA- dependent life surviving without it. Basically, you can't have one without the other. Necessarily inseparable.

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3874 views

Great new study:

https://phys.org/news/2022-03-unprecedented-videos-rna.html

"Similar to a light switch, RNA switches (called riboswitches) determine which genes turn "on" and "off." Although this may seem like a simple process, the inner workings of these switches have confounded biologists for decades.

"Now researchers led by Northwestern University and the University at Albany discovered one part of RNA smoothly invades and displaces another part of the same RNA, enabling the structure to rapidly and dramatically change shape. Called "strand displacement," this mechanism appears to switch genetic expression from "on" to "off."

"Using a simulation they launched last year, the researchers made this discovery by watching a slow-motion simulation of a riboswitch up close and in action. Affectionately called R2D2 (short for "reconstructing RNA dynamics from data"), the new simulation models RNA in three dimensions as it binds to a compound, communicates along its length and folds to turn a gene "on" or "off."

***

"Although RNA folding takes place in the human body more than 10 quadrillion times per second—every time a gene is expressed in a cell—researchers know very little about the process. To help visualize and understand the mysterious yet crucial process, Lucks and Chen unveiled R2D2 last year, in a paper published in the journal Molecular Cell. (my bold)

***

"Riboswitches have two basic parts. One part binds to a compound. Then, depending on how the compound is bound, the second part causes the RNA to fold into a shape that allows it to control gene expression. While these two parts are intertwined and overlapping in many riboswitches, the Bacillus subtilis is different.

"'What's strange is that they are separated by a long distance, but the bound molecule can cause large functional changes," Lucks said. "If the chemical binds at one end, then how is that communicated downstream to the other end of the RNA? It's been a mystery."

***

"Lucks, Chen and their teams found the riboswitch likely communicates downstream through the strand displacement mechanism. In response to the chemical binding, the strand exchange process triggers structural switching between "on" and "off" states."

Comment: Another level of complexity in genome design in control of gene activation or suppression. Another of God's designed switch mechanisms for precise controls. Note the required speed! Not surprising, a mistake can happen. dhw doesn't understand the import in theodicy discussions.

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3935 views

More complex than ever:

https://phys.org/news/2022-03-global-dna.html

"Widely accepted work, including studies that led to a 2015 Noble Prize, had argued that TCR played a relatively small role in repair because it relied on a putative TCR factor that made only a marginal contribution to DNA repair. A parallel process, global genome repair (GGR), was assumed to scan and fix most of DNA independent of transcription. Both processes were thought to set the stage for nucleotide excision repair (NER), in which a damaged stretch of DNA was snipped out and replaced by an accurate copy.

***

"Contrary to the conventional dogma, the study found that RNA polymerase serves as the scaffold for the assembly of the entire NER complex, and as the primary sensor of DNA lesions. It turned out that the principal NER enzymes UvrA and UvrB do not locate most lesions on their own, but are delivered to them by RNA polymerase. This fundamental TCR process is independent of Mfd, say the authors.

"The second study, published in Nature Communications, again in living cells, used a high-throughput sequencing technology called CPD-seq to track the appearance of DNA lesions upon exposure to UV light, and the rate of repair with a resolution down to a single letter (nucleotide) in the DNA code. CPD-seq showed that interfering with bacterial transcription using the antibiotic rifampicin shuts down repair throughout the bacterial genome. The study findings argue that NER is tightly coupled to transcription everywhere in the bacterial chromosome, the DNA infrastructure that houses all the genes.

"In another fascinating leap, experiments showed that bacterial cells, in the face of DNA damage, inhibit the action of the protein Rho, the global termination signal which tells RNA polymerase to stop reading. With the stop signals dialed down, RNA polymerases read on and on, delivering the repair enzymes to DNA damage anywhere it was encountered throughout the genome.

"'Given our findings, we theorize that eukaryotes, including human cells, also use RNA polymerase for efficient repair globally, as the bacterial TCR complexes described here have human analogs," says co-first author of the Nature study Binod Bharati, Ph.D., a post-doctoral scholar in Nudler's lab. "Moving forward, our team plans to confirm the presence of global TCR in human cells, and if confirmed, to explore whether in the future repair might be safely boosted to counter diseases of aging.'"

Comment: this is an irreducibly complex repair mechanism that had to be designed when DNA was designed. since broken DNA means life cannot continue. How much design in living biology is needed before the existence of the designer is accepted???

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3940 views

Two proteins involved:

https://phys.org/news/2022-04-two-faced-protein-inhibits-cell-receptor.html

"In a study published in March in Science Signaling, researchers from Tokyo Medical and Dental University (TMDU) have revealed that CD22, a crucial molecule in B cell signaling, switches from an inhibitory role to an activating role when B cell receptor (BCR) signaling is compromised due to a genetic defect that causes an immune disorder.

"Contact between BCRs and foreign invaders prompts B cells to make antibodies, and CD22 inhibits BCR signaling to keep B cells from inappropriately releasing antibodies. Interestingly, previous research suggests that this inhibition is regulated by binding of CD22 to other factors expressed on the same cell. In contrast, a protein called CD45 is a main activator of BCR signaling, and defects in the gene encoding CD45 cause an immunodeficiency syndrome.

"'CD45 normally enhances BCR signaling," explains Chizuru Akatsu, lead author on the study. "When CD45 is missing in laboratory cell lines, BCR signaling is dramatically decreased; however, signaling is not affected as severely in mice when CD45 is missing, which suggests that there is some kind of compensatory mechanism at work."

***

"As it turns out, the cells in which signaling was restored expressed unusually high levels of BCR, which accounted for their ability to continue functioning relatively normally. BCR signaling occurs at low levels even in the absence of stimulation by foreign antigens, and this low-level steady-state signaling is required for B cell development and survival. Because BCR is an endogenous ligand of CD22, continuous CD22 binding to its ligands facilitates inhibition of steady-state BCR signaling by CD22. If BCR signaling is compromised by a defect such as CD45 deficiency, steady-state signaling is markedly reduced by the signaling defect together with the signal inhibition by CD22; therefore, only B cells that express high levels of BCR survive. Through this mechanism, CD22 paradoxically restores BCR signaling in immune-deficient B cells."

Comment: for some reason scientists are always surprised at how complicated controls are in managing the immune system response with antibodies. The molecules and the cells do not think, but are managed by carefully designed feedback loops for accuracy in production when required. The controls are damaged in autoimmune diseases.

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3885 views

In studies of COPD patients:

https://phys.org/news/2022-04-cell-human-lung-regenerative-properties.html

"The researchers, who report their findings today in Nature, analyzed human lung tissue to identify the new cells, which they call respiratory airway secretory cells (RASCs). The cells line tiny airway branches, deep in the lungs, near the alveoli structures where oxygen is exchanged for carbon dioxide. The scientists showed that RASCs have stem-cell-like properties enabling them to regenerate other cells that are essential for the normal functioning of alveoli. They also found evidence that cigarette smoking and the common smoking-related ailment called chronic obstructive pulmonary disease (COPD) can disrupt the regenerative functions of RASCs—hinting that correcting this disruption could be a good way to treat COPD.

***

"In the new study, Morrisey and his team uncovered evidence of RASCs while examining gene-activity signatures of lung cells sampled from healthy human donors. They soon recognized that RASCs, which don't exist in mouse lungs, are "secretory" cells that reside near alveoli and produce proteins needed for the fluid lining of the airway.

"'With studies like this we're starting to get a sense, at the cell-biology level, of what is really happening in this very prevalent disease," said senior author Edward Morrisey, Ph.D., the Robinette Foundation Professor of Medicine, a professor of Cell and Developmental Biology, and director of the Penn-CHOP Lung Biology Institute at Penn Medicine.

"Observations of gene-activity similarities between RASCs and an important progenitor cell in alveoli called AT2 cells led the team to a further discovery: RASCs, in addition to their secretory function, serve as predecessors for AT2 cells—regenerating them to maintain the AT2 population and keep alveoli healthy.

"AT2 cells are known to become abnormal in COPD and other lung diseases, and the researchers found evidence that defects in RASCs might be an upstream cause of those abnormalities. In lung tissue from people with COPD, as well as from people without COPD who have a history of smoking, they observed many AT2 cells that were altered in a way that hinted at a faulty RASC-to-AT2 transformation."

Comment: it makes perfect sense for a designer to anticipate damaging gases entering a constantly breathing lung and putting a repair mechanism in place when lungs were first designed.

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3850 views

The results are sketchy and in trouble to gain acceptance:

https://www.the-scientist.com/features/does-human-epigenetic-inheritance-deserve-a-clos...

"The concept of epigenetic inheritance has long been controversial. Some researchers hope that new data on cross-generational effects of environmental exposures will help settle the debate.

"This question of what’s passed down from parent to child is complex and has often been socially and politically charged, says Baccarelli, who now chairs the environmental health sciences department at Columbia University’s Mailman School of Public Health (and who attributes his truffle love to his childhood in Umbria). The nuances of inheritance are perhaps most commonly framed as the age-old debate of nature versus nurture, the pervasive idea of a tug-of-war between deterministic genetic sequences and changing environmental influences—a dichotomy that scientists have long criticized as an oversimplification, given the complex interactions between genetics and the environment. Over the last couple of decades, however, scientific and public conversations about inheritance have grappled with an apparently separate, non-genetic dimension of inheritance.

***

"As data trickle in, arguments about which, if any, aspects of epigenetic inheritance hypotheses are likely to apply to humans continue to simmer in the literature. Many scientists still lament what they view as hype, misreporting, and an unhelpful blurring of definitions in the field, particularly when it comes to distinguishing between inter- and transgenerational effects. Some researchers in this field, meanwhile, say they feel their work’s been unduly maligned. Many people don’t appreciate how much effort it’s taken to get research on epigenetic inheritance recognized, Mansuy says over email, adding that “collecting data and publishing [in this discipline] require more efforts and time than in more classical fields.” She also points to struggles that she and some of her colleagues have had obtaining funding for projects on epigenetic inheritance in mammals in recent years.

"Other scientists say they’re still prepared for concepts of epigenetic inheritance to fail, either because the relevant mechanisms turn out to be vanishingly rare in humans or because their effects end up being negligible compared to everything else influencing development. “I don’t think we’ll ever point to a single study across multiple generations [and say], ‘They finally showed it!’” Breton says. “I think it’s going to end up being the cumulative evidence. The more papers that show the same set of relationships, that’s where we’re going to end up saying, ‘OK, I think we start to believe this’—or maybe we don’t. Maybe in the end it was all the other life stuff that was getting in the way that really made it look like an association, and really it isn’t.”

"For LUMC’s Heijmans, reduced interest in epigenetic inheritance now as compared to several years ago offers a welcome opportunity for epigeneticists to focus efforts on more-fruitful research directions, he says, noting that “there are more-relevant nuts to crack.” He has been studying how prenatal or early-life environments might influence the epigenome, and whether epigenetic alterations can be used as biomarkers to predict disease risk within a person’s lifetime. This could in theory “help us in identifying vulnerable individuals, and also monitoring [their] health,” he says—in other words, “helping them using epigenetics. That’s where I think it can be quite relevant.'”

Comment: A huge article which hashes out all the conflicting results, which I have skipped to simply show us recent thinking without reading enormous discussions of minor relevance. It is obviously not a solution for the problem of understanding how speciation works. It appears to be related to very minor alterations.

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3876 views

Very transient full and partial loops create gene expression:

https://phys.org/news/2022-04-genome-loops-dont-cells-theories.html

"In human chromosomes, DNA is coated by proteins to form an exceedingly long beaded string. This "string" is folded into numerous loops, which are believed to help cells control gene expression and facilitate DNA repair, among other functions. A new study from MIT suggests that these loops are very dynamic and shorter-lived than previously thought.

"In the new study, the researchers were able to monitor the movement of one stretch of the genome in a living cell for about two hours. They saw that this stretch was fully looped for only 3 to 6 percent of the time, with the loop lasting for only about 10 to 30 minutes. The findings suggest that scientists' current understanding of how loops influence gene expression may need to be revised, the researchers say.

***

"Using computer simulations and experimental data, scientists including Mirny's group at MIT have shown that loops in the genome are formed by a process called extrusion, in which a molecular motor promotes the growth of progressively larger loops. The motor stops each time it encounters a "stop sign" on DNA. The motor that extrudes such loops is a protein complex called cohesin, while the DNA-bound protein CTCF serves as the stop sign. These cohesin-mediated loops between CTCF sites were seen in previous experiments.

***

"The researchers used their method to image a stretch of the genome in mouse embryonic stem cells. "If we put our data in the context of one cell division cycle, which lasts about 12 hours, the fully formed loop only actually exists for about 20 to 45 minutes, or about 3 to 6 percent of the time," Grosse-Holz says.

"'If the loop is only present for such a tiny period of the cell cycle and very short-lived, we shouldn't think of this fully looped state as being the primary regulator of gene expression," Hansen says. "We think we need new models for how the 3D structure of the genome regulates gene expression, DNA repair, and other functional downstream processes."

"While fully formed loops were rare, the researchers found that partially extruded loops were present about 92 percent of the time. These smaller loops have been difficult to observe with the previous methods of detecting loops in the genome.

"In this study, by integrating our experimental data with polymer simulations, we have now been able to quantify the relative extents of the unlooped, partially extruded, and fully looped states," Brandão says.

***

"The researchers hypothesize that these partial loops may play more important roles in gene regulation than fully formed loops. Strands of DNA run along each other as loops begin to form and then fall apart, and these interactions may help regulatory elements such as enhancers and gene promoters find each other.

"'More than 90 percent of the time, there are some transient loops, and presumably what's important is having those loops that are being perpetually extruded," Mirny says. "The process of extrusion itself may be more important than the fully looped state that only occurs for a short period of time."

***

"Since most of the other loops in the genome are weaker than the one the researchers studied in this paper, they suspect that many other loops will also prove to be highly transient. They now plan to use their new technique study some of those other loops, in a variety of cell types.

"'There are about 10,000 of these loops, and we've looked at one," Hansen says. "We have a lot of indirect evidence to suggest that the results would be generalizable, but we haven't demonstrated that. Using the technology platform we've set up, which combines new experimental and computational methods, we can begin to approach other loops in the genome.""

Comment: This study supports my statement that life's biochemistry must run at high speed. DNA cannot remain in tight coils, so a loop mechanism is a design must. How the cell is instructed to find the right spot to loop at the correct nanosecond is yet to be found. Only design can accomplish this complexity of action.

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3863 views

Studies in C. elegans worms raise issues:

https://www.quantamagazine.org/in-worms-inheritance-beyond-genes-can-help-evolution-202...

"As a mostly hermaphroditic species (with a few males thrown in for variety), a C. elegans worm usually self-fertilizes its eggs until its sperm stash is depleted late in life; only then does it produce a pheromone to attract males and stay in the reproductive game. But when environmental conditions become stressful, the worms become sexually attractive much sooner. For them, sex is the equivalent of a Hail Mary pass — a desperate gamble that if their offspring are more genetically diverse, some will fare better under the new, rougher conditions.

***

“'Epigenetics has this double function: They’re inheritance systems, but they’re also response systems. You respond to the environment not by waiting for a mutation but by changing the way you express your genes,” said Eva Jablonka, a geneticist and philosopher of science at Tel Aviv University, who was not involved in the study. (my bold)

***

"If DNA sequences are the words in the book of life, then epigenetics is the punctuation, marking the difference between “Let’s eat, Grandma!” and “Let’s eat Grandma!” By telling the cell’s protein translation machinery where to work and how active to be, epigenetic signals can work either in addition to existing genetic signals or as the manifestation of these genetic commands. This layer of regulation provides an interface between the genome (which rarely changes) and the environment (which is always in flux), explained Eric Greer, an epigeneticist at Harvard Medical School.

“'Epigenetics exists at the interface between the environment and the genetics,” he said.

***

"In the years since, researchers have found evidence in invertebrates for the RNA-based epigenetic inheritance of pathogen avoidance, response to olfactory cues, longevity and more. Precisely how the gene silencing is inherited is still under study, but somehow either RNAi molecules or the instructions for making them pass from parents to offspring.

“'Only in the last few years have we started being able to really provide some evidence that small RNAs themselves can be the vessel that is actually transferring information from one generation to the next,” said Lamia Wahba, a postdoctoral fellow in the Fire lab at Stanford.

***

"Toker and Rechavi first needed to confirm that small RNAs were responsible for the inherited mating effect. This proved to be true: When the researchers prevented short interfering RNAs from being transmitted between generations, the offspring didn’t express the pheromone to attract mates prematurely.

***

"Nevertheless, Coleen Murphy of Princeton University, who also studies transgenerational epigenetic inheritance in worms, isn’t yet convinced that the observed effect is relevant to the real world. For 10 generations (roughly a month), Rechavi and Toker had to keep the worms in a narrow temperature range between 25 C and 27 C: hot enough to see the precocious mating effect become heritable but not so hot that it triggered the worms to enter what’s called a “dauer” state of stasis instead of reproducing.

“'I don’t know how to interpret that significance,” she said.

"Toker agrees that designing laboratory experiments to reflect real-world phenomena more accurately is a big issue for the field, and one that scientists have yet to resolve. Showing that this epigenetic inheritance can happen in the lab is only the first step toward understanding its overall significance, he said.

"Another major question that biologists are beginning to face is whether multigenerational epigenetic inheritance happens in vertebrates. Although scientists have found tantalizing clues that this might be happening in mammals, and even in humans, many scientists remain unconvinced.

Comment: This won't satisfy dhw's desires for bacteria's DNA editing ability to be widespread in advanced animals or plants. All we are sure of is epigenetics by methylation or small RNA's offers temporary adaptations within species, nothing more.

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3832 views

An interplay of enzymes:

https://phys.org/news/2022-05-crystal-dna-mystery.html

"When cells reproduce, the internal mechanisms that copy DNA get it right nearly every time. Rice University bioscientists have uncovered a tiny detail that helps understand how the process could go wrong.

"Their study of enzymes revealed the presence of a central metal ion critical to DNA replication also appears to be implicated in misincorporation, the faulty ordering of nucleotides on new strands.

***

"Rice structural biologist Yang Gao, graduate student Caleb Chang and alumna Christie Lee Luo used time-resolved crystallography to analyze the flexible enzymes called polymerase as they bend and twist to rapidly reassemble complete strands of DNA from a pool of C, G, A and T nucleotides.

"All of the proteins involved in DNA replication rely on metal ions—either magnesium or manganese—to catalyze the transfer of nucleotides to their proper positions along the strand, but whether there were two or three ions involved has long been a topic of debate.

"The Rice team seems to have settled that through studying a polymerase known as eta, a translesion synthesis enzyme that guards against ultraviolet-induced lesions.

***

"Gao said typical polymerases resemble a right-handed shape, and he thinks of them in terms of an actual hand: "They have a palm domain that holds the active site, a finger domain that closes up to interact with the new base pair, and a thumb domain that binds the primer/template DNA," he said.

***

"The study led to their theory that the first of the three metal atoms in eta supports nucleotide binding, and the second is the key to keeping the nucleotide and primer on track by stabilizing the binding of loose nucleotides to the primer located on the existing half of the new strand (aka the substrate). Primers are short DNA strands that mark where polymerases start stringing new nucleotides.

"'Only when the first two metal ions are in check can the third one come and drive the reaction home," said Chang, suggesting the process may be universal among polymerases.

"The researchers also noted poly-eta contains a motif that makes it prone to misalignment of primers, leading to a greater chance of misincorporation.

"'This is, first, about a basic mechanism of life," Gao said. "DNA has to be copied accurately, and errors can lead to human disease. People who study these enzymes know that for DNA synthesis, they always do much, much better than they should because there's a very limited amount of energy available for them to choose the right base pair.'"

Comment: cell division is an ancient process going back to the first dividing cell divisions. The enzymes involved are giant exactly designed molecules. All of this mechanism has to be designed together at the same time. There is no way stepwise chance mutations could create such arrangement. It is irreducibly complex and must be formed by a designer, at the start of life's first cells.

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Another view of cell splitting:

https://evolutionnews.org/2022/05/cell-fate-another-hurdle-for-evolution/

"Researchers at University of California at Riverside investigated what happens when stem cells divide and specialize. UCR’s reporter Iqbal Pittawala describes how “genome organization influences cell fate.”

"Understanding the molecular mechanisms that specify and maintain the identities of more than 200 cell types of the human body is arguably one of the most fundamental problems in molecular and cellular biology, with critical implications for the treatment of human diseases. Central to the cell fate decision process are stem cells residing within each tissue of the body.

"The two daughter cells face a massive organization problem. Even though they contain the same DNA code, they will take on separate roles in the cell. This means that the accessibility of genes between the two cells must radically differ.

"Chromatin — a package of DNA wrapped around histone proteins — makes some genes accessible for transcription but hides others from the transcription factors (additional proteins) that switch on transcription. Begin to get a sense of how difficult this will be. There are tens of thousands of genes, and 200 cell types that utilize specific genes but not others. What process determines how chromatin will package the specialist daughter cell to make genes available if it will be a nerve cell as opposed to a muscle cell or heart cell? And how does the system keep the other daughter cell unaltered from the original stem cell?

"Biochemist Sihem Cheloufi at UCR, together with colleague Jernej Murn, researched a protein complex involved in the process named “chromatin assembly factor 1” or CAF-1. As you read their description, think of the challenge a librarian faces with the card catalog for a large library.

“'To help CAF-1 secure correct chromatin organization during cell division, a host of transcription factors are attracted to open regions in a DNA sequence-specific manner to serve as bookmarks and recruit transcription machinery to correct lineage-specific genes, ensuring their expression,” she said. “We wondered about the extent to which CAF-1 is required to maintain cell-specific chromatin organization during cell division.”

***

"Recalling the 200 cell types in the human body, how does CAF-1 organize chromatin for each type? How does it know what genes to make accessible for a kidney cell, an astrocyte in the brain, or a liver cell? The UCR work is peeking into a keyhole of a library with a big operation inside. They don’t yet know how CAF-1 “preserves the chromatin state at specific sites and whether this process works differently across different cell types.” Think of our librarian just starting to get a handle on the job of arranging books in one wing and then finding 200 more wings to manage. Maybe a different analogy will expose the magnitude of this challenge.

“'Like a city, the genome has its landscape with specific landmarks,” Cheloufi said. “It would be interesting to know how precisely CAF-1 and other molecules sustain the genome’s ‘skyline.’ Solving this problem could also help us understand how the fate of cells could be manipulated in a predictive manner. Given the fundamental role of CAF-1 in packaging the genome during DNA replication, we expect it to act as a general gatekeeper of cellular identity. This would in principle apply to all dividing cells across numerous tissues, such as cells of the intestine, skin, bone marrow, and even the brain.”

***

"Expecting random mutations to somehow emerge then be “selected” by some blind, aimless, uncaring “agentless act” (as Neil Thomas has put it) to construct this complex system seems beyond rational consideration. Intelligent design scientists, though, could make testable predictions to guide further research. Knowing how comparable systems are made by intelligent engineers — that is, systems involving coordinated reorganization of information for multiple applications — they could expect to find new types of sensors, feedback circuits, quality-control checkpoints, or other functional modules at work. These might consist of proteins, protein complexes, small RNAs, sugars, ions, or combinations of them capable of storing or conveying information. (Note: even if automated, these are not “agentless acts.” The agency is one step removed from mind to program, but a mind with foresight was necessary for its origin.) (my bold)

"For example, an ID research team might look for a comparable system in industry that faces the same kind of challenge. They could identify the minimum number of job descriptions required to make the system work, then look for molecules performing those roles in the cellular analogue. Even if the match is imperfect, the ID approach can advance science, because what the researchers learn can feed back into biomimetic design, leading to improved applications in industry.

"Poor Darwin. With his crude awareness of cells dividing that looked like bubbles separating, he had no idea what he would be in for in the 21st century."

Comment: Simple cell splitting in the previous entry. This shows how big the evolutionary gap is in the Cambrian explosion. Stem cells at work from sexual reproduction!!!! It is not just the new animals' forms that comprise the gap. Darwin had no idea. A nice taste if ID thinking. Note the bold.

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A part of chromosome construction for cell division controls:

https://phys.org/news/2022-05-key-protein-cell-division-puzzles.html

"Human cell division involves hundreds of proteins at its core. Knowing the 3D structure of these proteins is pivotal to understand how our genetic material is duplicated and passed through generations. The groups of Andrea Musacchio and Stefan Raunser at the Max Planck Institute of Molecular Physiology in Dortmund are now able to reveal the first detailed structure of a key protein complex for human cell division known as CCAN. By using cryo-electron microscopy, the researchers show important features of the complex's 16 components and challenge previous assumptions about how the complex is able to recognize the centromere, a crucial region of chromosomes in cell division.

"The centromere is a constriction in the chromosome, made of DNA and proteins. Most importantly, the centromere is the dock for the kinetochore, a machinery of about 100 proteins that drives the separation of two identical chromosomes during cell division and their delivery to the daughter cells. Previous research has shown that the kinetochore docks onto the centromere through the CCAN complex: The CCAN interacts with the centromere protein A, the landmark protein of the centromere. CCAN is also responsible for replenishing the centromere protein A once the cell division has taken place. Yet, the details of the interaction between CCAN and the centromere protein A remain elusive.

***

"In the new publication, the MPI groups have been able to determine the 3D structural details of the human CCAN complex, highlighting its unique features and the implications for an interaction with the centromere protein A.

"'Contrary to what was expected, this structure does not directly recognize the centromere protein A in the standard configuration," says Musacchio.

"The centromere protein A is most commonly packed with DNA and other proteins as a nucleosome, the standard unit of the genetic material. The authors are now suggesting that the centromere protein A may be embedded in the centromere with a different configuration that may facilitate the crucial interaction with CCAN. They plan to identify conditions that could lead to this new configuration and prove their hypothesis."

Comment: this is a giant structure that must be designed all at once to be properly functional. It is irreducibly complex. Since it controls cell splitting accuracy, it was present very early in life well before sexual reproduction appeared.

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Goes back to Archaea:

https://phys.org/news/2022-05-mcm-molecules-impede-formation-dna.html

"'In this current study, they have now jointly identified the minichromosome maintenance (MCM) complex as a new class of barriers in the formation of DNA loops. In the process of DNA loop formation, also called loop extrusion, three proteins or protein complexes are mainly involved: first cohesin, second the zinc finger protein CTCF, and third the MCM complex. Cohesin binds to DNA and initiates the formation of a loop. Cohesin coils the DNA and this results in the progressive growth of a loop.

"'Loop extrusion stops when cohesin encounters the DNA-bound protein CTCF, which was the only known loop extrusion barrier prior to this work. "Although the details differ, one can imagine that it is a little like placing a ring on a ribbon and threading the ribbon through the ring, which remains at the base of the loop," says Matthias Scherr, co-first author of the study. Kikuë Tachibana explains: "Unlike CTCF, which is a vertebrate-specific barrier, MCMs are conserved across eukaryotes and archaea. It is therefore fascinating to consider that this might be an ancestral barrier to loop extrusion." The work raises the possibility that the encounters of loop extruding cohesin complexes with MCM complexes are part of a fundamental mechanism that organizes the genome folding of a wide variety of organisms."

Comment: folding six feet of DNA into the tiny nucleus must have carefully controlled folding. Logically the development of very long DNA molecules in evolution had to accompanied by the folding mechanism. They had to be desi gned together. How could it have happened stepwise?

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3742 views

Another way to look at all the information coded into various sub-sets of control:

https://evolutionnews.org/2022/05/in-life-one-code-or-many/

Examples follow:

"What researchers found was that not only does the sequence of the amino acids matter, but so does the speed of the process in which the amino acids are put together into a functional protein.

“'Our results uncovered a new ‘code’ within the genetic code. We feel this is quite important, as the finding uncovers an important regulatory process that impacts all biology,” said Dr. Yi Liu, Professor of Physiology.

"The researchers say that the speed of translation affects how the protein will fold. This will affect its shape, and ultimately its function. So while a point mutation may change a nucleotide in a gene without altering the amino acid its codon produces, the resulting messenger RNA may be translated at a different speed. Consequently, the protein may fold differently and have a different function — or cause disease.

"If this is a code, it rides on the genetic code. The triplet sequence will determine the amino acid used, but a different synonymous sequence will affect the protein that results. Conceivably one could say this is all one genetic code and leave it at that.

***

"The University of Copenhagen found a new function for histones, the proteins that wrap DNA and control access to genes (this compares with Wells’s “epigenetic code”). They compare their discovery to revealing “undiscovered white dots on the map.” Sounds like more information has been discovered; let’s see.

"The four core histones have so-called tails, and among other things they signal damageto the DNA and thus attract the proteins that help repair the damage. Between the histone “yarn balls” we find the fifth histone, Histone H1, but up until now its function has not been thoroughly examined.

"Using a so-called mass spectrometer, a technique developed in collaboration with fellow researchers at the Novo Nordisk Foundation Centre for Protein Research, Niels Mailand and his team have discovered that, surprisingly, the H1 histone also helps summon repair proteins.

"Scientists at the University of Barcelona, meanwhile, claim to be “Shaking up the fundamentals of epigenetics” — a bit of hyperbole, perhaps — by showing that chromatin marks do not always have the same effect on gene expression during development. From modENCODE data, they found that some genes in worms and fruit flies were highly expressed during development without the chromatin marks that the “accepted view” expects should have been there. This is a work in progress that possibly suggests deeper regulations than are currently understood.

"At Caltech, researchers found another layer of regulation in gene expression. “Cells Rhythmically Regulate Their Genes,” the headline reads...What they found was another source of informational guidance in the combinatorial code of transcription factors. It’s a time-based method of gene regulation that is “largely unexplored” —

"Previously, researchers have thought that the relative concentrations of multiple transcription factors in the nucleus determine how they regulate a common gene target–a phenomenon known as combinatorial regulation. But the new study suggests that the relative timing of the pulses of transcription factors may be just as important as their concentration.

“'Most genes in the cell are regulated by several transcription factors in a combinatorial fashion, as parts of a complex network,” says Cai. “What we’re now seeing is a new mode of regulation that controls the pulse timing of transcription factors, and this could be critical to understanding the combinatorial regulation in genetic networks.”

"...it seems fair to categorize codes separately if they contain unique information and produce unique results. Even if histones are built from DNA, once they are assembled, they no longer rely on the genetic code. They follow their own rules of tagging genes with “tails” made of other molecules. Transcription factors and their pulsations, similarly, act apart from the language of DNA triplet codons. How much more the sugar code, membrane code, and bioelectric codes that are not even made up of amino acids?

"It would be as ridiculous to lump all of these into a single genetic code as it would be to lump Morse Code into the genetic code on the grounds that the fingers of a telegraph operator contain proteins built from DNA. Codes are distinguished by the information they contain and the rules that they follow. As Jonathan Wells cogently argues, there’s more information in life than can be explained by one genetic code. He identifies “at least” six codes, never implying that the extent of coded information in life stops there."

Comment: of course, there is one master code in a zygotes' DNA. What is done here is to demonstrate sub-sections of coded controls. There are so many active processes occurring all at the same time, there must be these sub-sets of controlling coded information. Not by chance.

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A newly discovered facet of 'junk' DNA:

https://phys.org/news/2022-05-arms-genome.html

"In a new study, biologists at the University of Pennsylvania show, for the first time, evidence of a two-sided genomic arms race involving stretches of repetitive DNA called satellites. "Opposing" the rapidly evolving satellites in the arms race are similarly fast-evolving proteins that bind those satellites.

"While satellite DNA does not encode genes, it can contribute to essential biological functions, such as formation of molecular machines that process and maintain chromosomes. When satellite repeats are improperly regulated, impairments to these crucial processes can result. Such disruptions are hallmarks of cancer and infertility.

"Using two closely related species of fruit flies, researchers probed this arms race by purposefully introducing a species mismatch, pitting, for example, one species' satellite DNA against the other species' satellite-binding protein. Severe impairments to fertility were a result, underscoring evolution's delicate balance, even at the level of a single genome.

"'We typically think of our genome as a cohesive community of elements that make or regulate proteins to build a fertile and viable individual," says Mia Levine, an assistant professor of biology in Penn's School of Arts & Sciences and the senior author on the work, published in Current Biology. "This evokes the idea of a collaboration between our genomic elements, and that's largely true.

"'But some of these elements, we think, actually harm us," she says. "This disquieting idea suggests that there needs to be a mechanism to keep them in check."

"The researchers' findings, likely to also be relevant in humans, suggest that when satellite DNA occasionally escapes the management of satellite-binding proteins, significant costs to fitness can occur, including impacts on molecular pathways required for fertility and perhaps even those relevant in the development of cancer.

"'These findings indicate that there is antagonistic evolution between these elements that can impact these seemingly conserved and essential molecular pathways," says Cara Brand, a postdoc in Levine's lab and first author on the work. "It means that, over evolutionary time, constant innovation is required to maintain the status quo."

***

""If genes are words and you were to read the story of our genome, these other parts are incoherent," she says. "For a long time, it was ignored as genomic junk."

"Satellite DNA is part of this so-called "junk." In Drosophila melanogaster, the fruit fly species often used as a scientific model organism, satellite repeats make up roughly half the genome. Because they evolve so rapidly without any apparent functional consequence, however, scientists used to believe satellite repeats were unlikely to be doing anything useful in the body.

***

"In 2001, a group of scientists put forward a theory, suggesting that coevolution was taking place, with the satellites rapidly evolving and satellite binding proteins evolving to keep up. In the two decades since, scientists have offered support to the theory. With genetic manipulation, these studies have introduced a satellite-binding protein from one species into the genome of a closely related species and observed what happens as a result of the mismatch.

"'Often these gene swaps cause dysfunction," says Brand, "particularly disrupting a process that is usually mediated by regions of the genome that are enriched with repetitive DNA."

***

"Another fruit fly species, Drosophila simulans, lacks a satellite repeat that spans a whopping 11 million nucleotide base pairs found in its close relative, D. melanogaster. This satellite was known to occupy the same cellular location as a protein called Maternal Haploid (MH). The researchers also had access to a mutant strain of D. melanogaster that lack the 11 million base pair repeat.

"'It turns out the fly can live and reproduce just fine without this repeat," Levine says. "So it gave us a unique opportunity to manipulate both sides of the arms race."

***

"Looking to the closest relative of the MH protein in humans, a protein called Spartan, gave the scientists a clue as to the mechanism behind these results. In humans, Spartan is understood to digest proteins that can get stuck on DNA, posing an obstacle to various processes and packaging that DNA must undergo. "After everything we'd discovered thus far," Levine says, "we thought, maybe this wrong species version of the protein is chewing up something it shouldn't."

"One of the proteins often targeted by Spartan is Topoisomerase II, or Top2, an enzyme that can help resolve tangles in tightly wound and entangled DNA. To see whether the negative effects of the MH gene mismatch owed to inappropriate degradation of Top2, they overexpressed Top2 and found fertility was restored. Reducing Top2, on the other hand, exacerbated the reduction in fertility.

"'This repair process that MH is involved in happens in yeast, in flies, in humans, across the tree of life," says Brand. "Yet we're seeing rapid or adaptive evolution of these proteins involved. That suggests that this seemingly conserved and essential pathway requires evolutionary innovation." In other words, coevolution must proceed apace, just to maintain this essential pathway."

Comment: a complex study revealing another layer of coding controls hidden in the so-called junk

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3701 views

Got to pack DNA tight:

https://phys.org/news/2022-05-linker-histone-partnership-single-stranded-dna.html

"To keep order in the tight quarters of the cell nucleus, our DNA is neatly clamped in place around a central disk by H1 linker histone, which helps shepherd DNA into the tidy chromatin fibers that comprise chromosomes. Linker histone, however, is far more than a mere protein clip. Without sufficient H1, the process of gene transcription falters and the intricate dance of DNA repair screeches to a halt. Perched unassumingly atop our nucleosomes, the humble linker histone appears to somehow conduct multiple processes central to genome maintenance.

"Now, a new study in Nature Structural & Molecular Biology suggests that linker histone can distinguish between different forms of nucleic acids, with a clear preference for forming condensates with single-stranded DNA over double-stranded DNA. This discriminating feature provides yet more evidence that H1's role stretches far beyond that of chromatin compaction, and may help explain the protein's contribution to DNA repair and a number of human diseases.

***

"Scientists have long suspected that linker histone plays a key role in multiple genomic processes. Besides the evidence that H1 is involved in DNA repair and transcription, the existence of many different types of linker histone in our cells implies an expanded role for the protein. "We wouldn't need 11 different subtypes of linker histone if its role was purely structural," says Rachel Leicher, a former graduate student in Liu's lab

***

"...our assumption was that H1 would only interact with double-stranded DNA and nucleosomes," Leicher says. "But when we stretched DNA, we fortuitously observed the accumulation of H1 around the portions of the molecule that had popped into single strands. That was when we realized that H1 not only binds single-stranded DNA, but likes it better than double-stranded DNA."

"Since one feature of DNA damage is the breakdown of double strands into frayed single strands, the findings tie in nicely with H1's proposed role in DNA repair. If H1 is involved in responding to DNA damage, one would expect it to show a special affinity for single-stranded DNA. The current study focused on one particular H1 subtype, also one of the most abundant. Future studies will investigate how the other linker histone subtypes interact with damaged DNA, continuing to capitalize on the optical tweezer technique that allowed the lab to investigate the material properties of molecular condensates in ways that traditional techniques cannot."

Comment: the role of complex layers of the genome and their functions continue to amaze. Not by chance

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3703 views

A non-coding RNA 's role in mitochondria:

https://phys.org/news/2022-06-non-coding-7s-rna-gene-human.html

A new study published in the journal Cell shows that a non-coding RNA molecule regulates mitochondrial gene expression in human cells.

***

"Mitochondria are the powerhouses of cells and are crucial for converting energy from our food into the form of energy required for various cellular functions. A peculiar aspect of mitochondria is the existence of a separate mitochondrial genome, which, when damaged, can cause serious diseases, affecting high-energy tissues like the brain and heart.

***

"Human mitochondrial 7S RNA belongs to a large family of non-coding RNA molecules essential for proper development in mammals. It was previously known that levels of mitochondrial 7S RNA vary depending on the metabolic needs of the eukaryotic cell, but the molecular basis and functional implications for these changes were unknown. In their work, the scientists developed methods to study the effects of 7S RNA both on purified proteins and mitochondrial gene activity in cells.

"'The most exciting thing about the study is that we identify a completely new mechanism for regulation of mitochondrial activity. Our findings reveal the function of 7S RNA, a molecule identified already 40 years ago. Despite 7S RNA being abundant and frequently measured in studies of mitochondrial function, its physiological role has remained an enigma until now. We are thrilled that we, in collaboration, could determine a cryo-EM structure that shows the probable mechanism for how 7S RNA inhibits mitochondrial gene activity," says Xuefeng Zhu. Xuefeng, and Xie Xie, both at University of Gothenburg, share the first authorship of the article with Hrishikesh Das at Karolinska Insititutet.

"Non-coding RNA molecules play an important role in regulation of various processes in the nucleus, but a defined role in regulation of mitochondrial function has not previously been reported. "Our finding reveals a new and physiologically relevant level of regulation in human mitochondria. The challenge now is to understand how 7S RNA levels are fine-tuned in response to the metabolic needs of the human cell.

***

"'This is a new principle for regulating mitochondrial activity and future therapies targeting 7S RNA production, can be valuable," says Maria Falkenberg, professor at the University of Gothenburg, who led the study together with Martin Hällberg at Karolinska Insititutet. However, the practical implications of the work will take years to explore."

Comment: As usual there is tight regulation of gene expression in a carefully dsigned system

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3588 views

Aids in protection DNA from problems:

https://phys.org/news/2022-06-dna-steadily-interphase-cells-robust.html

"Researchers in Japan have discovered that the local DNA motion inside of human cells remains steady throughout interphase, where the cell grows and replicates its DNA for cell division. The study suggests that this steady-state DNA motion allows cells to conduct housekeeping tasks under similar environments during interphase.

***

"Maeshima and colleagues have revealed that the local chromatin motion remains steady throughout interphase, although genome DNA is doubled by DNA replication and the nucleus grows. The researchers also have shown that nuclear growth without replication did not affect the steady-state motion of chromatin. Thus, local chromatin motion is independent of such nuclear changes during interphase.

"'This is an important finding because the steady-state motion allows cells to conduct their routines, such as RNA transcription and DNA replication, under similar nuclear environments," the first author Shiori Iida said. "Local chromatin motion can govern genomic DNA accessibility for target searching or recruiting a piece of machinery. The steady-state motion of chromatin provides a robust cellular system in which DNA functions are unaffected by various nuclear changes."

"'Cells can transiently change the chromatin motion from the steady state to perform their ad hoc jobs in response to DNA damages, among many other tasks," Maeshima said. He and his team aim to further explore how DNA motion is regulated, which proteins are involved in the regulation process, and how DNA behaves during cell division. "Our ultimate goal is to understand how human genomic DNA inside the cell behaves to read-out genetic information in it," Maeshima said."

Comment: an irreducibly complex system for DNA protection from errors whikle undergoing cell division. Must be designed all at once.

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3659 views

A study of chromatin's role:

https://www.sciencedaily.com/releases/2022/09/220902122735.htm

"Researchers have discovered that the motion of chromatin, the material that DNA is made of, can help facilitate effective repair of DNA damage in the human nucleus -- a finding that could lead to improved cancer diagnosis and treatment.

***

"DNA damage happens naturally in human body and most of the damage can be repaired by the cell itself. However, unsuccessful repair could lead to cancer.

***

"Liu and his colleagues found that chromatin on the site of DNA damage moves much faster than those away from the DNA damage. They also found that the chromatin in cell nuclei is not moving randomly. It's a coherent movement, with the DNA moving as a group over a short distance.

"The researchers also found evidence that DNA damage may affect the DNA's group movement by reducing the coherence. These findings indicate that chromatin motion is under tight control when DNA is damaged. This is important to prevent the damaged DNA from harmful contact and to improve the accuracy and efficacy of DNA repair, Liu said.

***

"In the future, the researchers hope to study single DNA molecules and how they are moving, and how individual and group dynamics differ and change in response to DNA damage. They'd also like to learn more about DNA movement in specific genes that are known to be more vulnerable to DNA damage."

Comment: it is obvious these DNA damage controls had to exist. Our knowledge is still incomplete, but our body's cells come with precise protective feedback loops and repair mechanisms at all levels of biological complexity way beyond what natural evolution could possibly produce. ID is correct.

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3161 views

According to the latest:

https://phys.org/news/2022-09-transmission-epigenetic-memory-multiple.html

"A new study by researchers at UC Santa Cruz shows how a common type of epigenetic modification can be transmitted via sperm not only from parents to offspring, but to the next generation ("grandoffspring") as well. This is called "transgenerational epigenetic inheritance," and it may explain how a person's health and development could be influenced by the experiences of his or her parents and grandparents.

"The study, published the week of September 26 in the Proceedings of the National Academy of Sciences (PNAS), focused on a particular modification of a histone protein that changes the way DNA is packaged in the chromosomes. This widely studied epigenetic mark (called H3K27me3) is known to turn off or "repress" the affected genes and is found in all multicellular animals—from humans to the nematode worm C. elegans used in this study.

"'These results establish a cause-and-effect relationship between sperm-transmitted histone marks and gene expression and development in offspring and grandoffspring," said corresponding author Susan Strome, professor emerita of molecular, cell and developmental biology at UC Santa Cruz.

"Histones are the main proteins involved in the packaging of DNA in the chromosomes. The epigenetic mark known as H3K27me3 refers to methylation of a particular amino acid in the histone H3. This leads to the DNA being more densely packaged, making the genes in that region less accessible for activation.

***

"'In the germline of the offspring, some genes were aberrantly turned on and stayed in the state lacking the repressive mark, while the rest of the genome regained the mark, and that pattern was passed on to the grandoffspring," Strome explained. "We speculate that if this pattern of DNA packaging is maintained in the germline, it could potentially be passed on for numerous generations."

"In the grandoffspring, the researchers observed a range of developmental effects, including some worms that were completely sterile. This mix of outcomes is due to how chromosomes get distributed during the cell divisions that produce sperm and eggs, resulting in many different combinations of chromosomes that can be passed on to the next generation.

"Researchers in Strome's lab have been studying epigenetic inheritance in C. elegans for years, and she said this paper represents the culmination of their work in this area. She noted that other researchers studying mammalian cells in culture have reported results very similar to her lab's findings in worms, although those studies did not show transmission across multiple generations.

"'This looks like a conserved feature of gene expression and development in animals, not just a weird worm-specific phenomenon," she said. "We can do amazing genetic experiments in C. elegans that can't be done in humans, and the results of our experiments in worms can have broad implications in other organisms.'"

Comment: at a wimple worm level but possible in ours. My Grandpa's varicose veins are in my legs Which shows such a skip, since my mother did not have varicose veins.

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3107 views

Ahttps://www.the-scientist.com/news-opinion/mitochondrial-dna-sneaks-into-nuclear-genom... new finding in a large population study

"...in 2018, a study challenged this simple picture of maternal mitochondrial inheritance, describing paternal mtDNA in 17 individuals and suggesting that the organelle might be inherited from either parent. “This was a really wild idea,” Patrick Chinnery, a neurologist at the University of Cambridge in the UK, tells The Scientist. “We had a healthy skepticism about the discovery and went looking for other explanations.”

***

"Chinnery and his colleagues’ initial analysis of people testing positive for paternal mtDNA revealed that they hadn’t inherited the organelle itself from their fathers. Instead, pieces of paternal mtDNA had plastered themselves onto the nuclear genome. In the new study, the team scoured whole genome sequences from around 66,000 participants in Genomics England’s 100,000 Genomes Project. The researchers specifically searched for sections of DNA where one half could be mapped to the nucleus and the other half to the mitochondria.

"The search turned up a total of 1,637 mitochondrial fragments in the nuclear genome, with more than 99 percent of people harboring at least one. An average person possesses around five inserts that have not been previously described, suggesting they hopped onto the genome recently in human evolution, the team reports.

"The results suggest that “these transfers of genomic information from the mitochondria to the nucleus are still happening today,” says cell biologist Cole Haynes of the University of Massachusetts Chan Medical School, who was not involved in the study.

***

"The study has broad implications for eukaryotic evolution, says Iain Johnston, a computational biologist at the University of Bergen in Norway who was not involved in the work. Instead of mitochondria being frozen in time, their information transfer with the nucleus is “continuous and dynamic,” he adds.

"Fragments of mtDNA were usually found next to binding sites for PRDM9, a protein involved in repairing double-stranded breaks in DNA. This suggests that mtDNA may integrate into the genome at sites where both DNA strands are severed, the authors write in their paper. “Bits of mitochondrial DNA preferentially stick in these holes and act as a kind of Band-Aid to repair the nuclear genome,” says Chinnery."

Comment: An early discovery and how it might affect evolution is an important issue.

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3088 views

A new developing field of study:

https://www.quantamagazine.org/how-supergenes-fuel-evolution-despite-harmful-mutations-...

"Birds and other predators avoid Heliconius butterflies because they are toxic to eat, with a bitter taste. The mimics were not toxic, but because they looked so much like the foul-tasting Heliconius, they were less likely to be eaten. The closer the resemblance, the more potent the protection.

"What Bates and many later evolutionary biologists couldn’t explain was how this mimicry was possible.

***

"Today we know that in many species the answer is supergenes — stretches of DNA that lock several genes together into a single inheritable unit. “They’re kind of a wild card,” said Marte Sodeland, a molecular ecologist at the University of Agder in Norway. This aggregated form of inheritance “has obvious advantages, because it allows rapid adaptation, but there’s a lot we don’t know yet.”

"Supergenes once seemed like an evolutionary oddity, but the rise of genetic sequencing has shown that they are far more common than researchers believed. Not all supergenes may serve a function, but work in just the past few years has revealed that traits in a wide range of animal and plant species might be driven by these groups of genes that function like a single gene.

***

"Supergenes seem to hold explanations for many long-standing mysteries of evolution, such as how species can sometimes adapt to new environments rapidly, how populations can sometimes evolve in different directions even while living close together, and why some species have “balanced lethal systems” of breeding, such that they must have two different versions of a chromosome to survive.

***

"But supergenes aren’t all-powerful. Recent work on the evolution of supergenes is painting a nuanced picture of their effects. These theoretical models and studies of real populations have shown that supergenes often accumulate harmful mutations far more rapidly than other pieces of DNA do, and this can gradually lead to degenerative effects that undermine the original benefits.

***

"...researchers have been probing how supergenes arise and what the consequences for species might be as their supergenes continue to evolve. Understanding the origin of a supergene is “one of the most challenging questions,” said Tanja Slotte , an evolutionary geneticist at Stockholm University who studies supergenes in plants. “And it’s not a given that it’s even always possible.”

"In one recent effort, Katie Lotterhos, an evolutionary marine biologist at Northeastern University, built a computer model to study the first tentative steps taken on the path from inversion to supergene. Her model, published in the Philosophical Transactions of the Royal Society B in August as part of a special issue on supergenes, showed that the larger the initial DNA flip-flop, the more likely a supergene was to evolve. The reason was simple: A larger inverted fragment of DNA was more likely to capture multiple genes and lock them together as a single entity. Any beneficial mutations arising within the inversion could then promote its spread as a supergene.

"But the more important insight from Lotterhos’ model was that inversions themselves do not necessarily provide an evolutionary advantage. If a suite of genes is already well adapted to its surroundings, locking it into an inversion will not suddenly allow it to take off as a supergene. That fact may help to explain why complex vital traits aren’t routinely secured as supergenes: Ordinary selection pressures are often sufficient to preserve the traits.

***

"For supergenes, however, that isn’t true. Since they rarely recombine, any harmful mutations they acquire tend to stay in place. The benefits of supergenes, then, could be accompanied by significant disadvantages."

Comment: presented to reveal a whole new area of genome research.

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3055 views

New finding in mice:

https://www.the-scientist.com/news-opinion/micrornas-can-boost-gene-expression-study-70759

"MicroRNAs—snippets of nucleic acids a couple dozen base pairs in length—are so small that they went unnoticed for decades despite wielding enormous influence in our cells. It’s now known that they suppress the expression of thousands of genes through a process called RNA interference, in which they bind to messenger RNAs (mRNAs) and prevent their translation. But a study published November 9 in ACS Central Science finds that microRNAs (miRNAs) can also amplify gene expression.

“'It changes the landscape of microRNA,” Lara Mahal, a chemist at the University of Alberta in Canada tells The Scientist. “There isn’t one mode of microRNA regulation: There are two.”

***

"They discovered that while the miRNAs that interact with ST6GAL2 downregulate its expression, those that interact with ST6GAL1 boost its expression and therefore increase levels of 2,6-sialic acid attachment. “We were floored. We thought it was a mistake,” says Mahal.

***

"Mahal believes that miRNA-mediated upregulation may have gone largely unnoticed because most groups tend to focus on transcripts that are far more abundant. When there are lots of copies of a protein being made, its effects can be straightforwardly fine-tuned by metering translation. But for genes already expressed at low levels, like the ones that regulate glycosylation, downregulation doesn’t make as much biological sense, she says.

“'It’s an exciting study,” says Pinar Uysal Onganer, a cancer biologist at the University of Westminster in the UK who was not involved in the work. Similar high-throughput studies are essential for validating miRNA interactions, enabling researchers to make better predictions of their effects, she says."

Comment: I don't understand the surprise. In biological systems, what is sent up. most also be sent down to maintain equilibrium. God makes complete designs.

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2976 views

Old viruses hiding in our DNA:

https://www.sci.news/genetics/human-genome-retroviruses-11332.html

"Like modern HIV, ancient human endogenous retroviruses (HERVs) had to insert their genetic material into their host’s genome to replicate.

***

"There are around 30 different kinds of HERVs in people today, amounting to over 60,000 proviruses in the human genome.

"They demonstrate the long history of the many pandemics humanity has been subjected to over the course of evolution.

"Scientists think these viruses once widely infected the population, since they have become fixed in not only the human genome but also in chimpanzee, gorilla and other primate genomes.

"Research has demonstrated that HERV genes are active in diseased tissue, such as tumors, as well as during human embryonic development. But how active HERV genes are in healthy tissue was still largely unknown.

***

"The fact that thousands of pieces of ancient viruses still exist in the human genome and can even create protein has drawn a considerable amount of attention from researchers, particularly since related viruses still active today can cause breast cancer and AIDS-like disease in animals.

"Whether the genetic remnants of human endogenous retroviruses can cause disease in people is still under study.

"Researchers have spotted viruslike particles from HML-2 in cancer cells, and the presence of HERV genetic material in diseased tissue has been associated with conditions such as Lou Gehrig’s disease, or amyotrophic lateral sclerosis, as well as multiple sclerosis and even schizophrenia.

"The new study adds a new angle to these data by showing that HERV genes are present even in healthy tissue.

"This means that the presence of HERV RNA may not be enough to connect the virus to a disease.

***

"The most famous HERV embedded in human and animal genomes, syncytin, is a gene derived from an ancient retrovirus that plays an important role in the formation of the placenta.

"Pregnancy in all mammals is dependent on the virus-derived protein coded in this gene.

"Similarly, mice, cats and sheep also found a way to use endogenous retroviruses to protect themselves against the original ancient virus that created them.

"While these embedded viral genes are unable to use their host’s machinery to create a full virus, enough of their damaged pieces circulate in the body to interfere with the replication cycle of their ancestral virus if the host encounters it.

"Scientists theorize that one HERV may have played this protective role in people millions of years ago.

***

"The new study reveals a level of HERV activity in the human body that was previously unknown, raising as many questions as it answered.

"There is still much to learn about the ancient viruses that linger in the human genome, including whether their presence is beneficial and what mechanism drives their activity.

"Seeing if any of these genes are actually made into proteins will also be important.

"Answering these questions could reveal previously unknown functions for these ancient viral genes and better help researchers understand how the human body reacts to evolution alongside these vestiges of ancient pandemics."

Comment: this is a discovery with still unknown meaning. It shows we were previously infected with pandemics and may have affected our evolution. Considering the issue of theodicy and 'nasty' viruses, we do not know how these guys fit. From a design standpoint, God may have used viruses to edit DNA changes. Time will tell.

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2964 views

In a heat cell response from the very first cells:

https://phys.org/news/2022-11-primordial-super-enhancers-early-snapshot-mechanisms.html

"Transcriptional condensates are membrane-less compartments—almost like organelles, but lacking a membrane—within the nucleus of the cell that bring together and concentrate transcriptional machinery to allow for the rapid and high-level transcription of specific critical genes under certain conditions, such as to specify a cell lineage or in response to stress.

"In response to high environmental temperatures, cells turn on molecular chaperones, which act to help maintain protein stability. This heat shock response can be hijacked by cancer cells to help mutated proteins stay folded, and it gets broken down in neurodegenerative diseases such as Alzheimer's disease, where a lack of molecular chaperones leads to excessive protein aggregation.

***

"Previous research in mammalian cells had shown that eukaryotes use these membrane-less compartments to drive high-level gene expression by creating hubs where relevant DNA sequences and transcriptional activators can collect and drive transcription. In the current study, the researchers used a series of genetic mutations to demonstrate that yeast cells use the same mechanism to coordinate the heat shock response.

"'In our prior research, we saw that the genes being regulated in response to heat stress coalesce in 3D space to be activated," said Surabhi Chowdhary, a postdoctoral scholar in the Pincus lab at UChicago. "This study provides evidence that these genes are driven together in 3D space by these biomechanical condensates to facilitate gene transcription."

"This is the first time these condensates have been seen in a non-eukaryotic species, demonstrating that these structures are very ancient, dating back to a very early common ancestor and conserved across species. "This means that cells have been doing this high-level gene expression for a billion years," said Pincus. "And when these condensates form, they're not forming at an individual gene, but instead have the capacity to bring a bunch of genes together to activate them all at the same time."

Comment: the fact that this mechanism existed at the start of life strongly support design theory in that it is a design prepared for future use. A wise designer will set the process up this way.

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2954 views

They all look different but have the same genomic ancestor:

https://phys.org/news/2022-11-genome-uncover-fungal-evolution.html

"About 600 seemingly disparate fungi that never quite found a fit along the fungal family tree have been shown to have a common ancestor, according to a University of Alberta-led research team that used genome sequencing to give these peculiar creatures their own classification home.

"'They don't have any particular feature that you can see with the naked eye where you can say they belong to the same group. But when you go to the genome, suddenly this emerges," says Toby Spribille, principal investigator on the project and associate professor in the Department of Biological Sciences.

"'I like to think of these as the platypus and echidna of the fungal world."

***

"Using DNA-based dating techniques, the team found that this new class of fungi, called Lichinomycetes, descended from a single origin 300 million years ago, or 240 million years before the extinction of dinosaurs.

"David Díaz-Escandón, who performed the research as part of his Ph.D. thesis, explains that these "oddball" fungi were previously sprinkled across seven different classes—a high-level grouping that in animals would be equivalent to the groups called mammals or reptiles.

"Working with a team of researchers from seven countries to get material from the fungi, he sequenced 30 genomes and found that all classes but one descended from a single origin.

"'They were classified, but they were classified into such different parts of the fungal side of the tree of life that people never suspected they were related to each other," says Díaz-Escandón.

"These fungi include forms as varied as earth tongues—eerie tongue-shaped fungi that shoot up vertically out of the ground—beetle gut microbes, and a fungus found in tree sap in northern Alberta. They also include some unusual lichens that survive in extreme habitats such as South America's Atacama Desert, the driest non-polar desert in the world.

"'What is really fascinating is that despite these fungi looking so different, they have a lot in common at the level of their genomes," says Spribille. "Nobody saw this coming."

"Based on their genomes, which are small compared with those of other fungi, the team predicts that this group of fungi depend on other organisms for life.

"'Their small genomes mean this class of fungi have lost much of their ability to integrate some complex carbohydrates," said Spribille. "When we go back to look at each of these fungi, suddenly we see all of them are in a kind of symbiosis.'"

Comment: this is a major consideration in thinking about evolution. The relationships are at the genome, DNA, level, not at the outward appearance level. It puts to rest dhw's weirdly illogical worry about the Cambrian gap destroying my theory about how God evolved us from Archaea. WE have Archaea genes as previously noted.

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3004 views

Backup controls to herd chromosomes:

https://www.cell.com/current-biology/fulltext/S0960-9822(22)01828-0?dgcid=raven_jbs_aip...

"Summary
The complete separation of sister chromatids during anaphase is a fundamental requirement for successful mitosis. Therefore, divisions with either persistent DNA-based connections or lagging chromosome fragments threaten aneuploidy if unresolved. Here, we demonstrate the existence of an anaphase mechanism in normally dividing cells in which pervasive connections between telomeres of segregating chromosomes aid in rescuing lagging chromosome fragments. We observe that in a large proportion of Drosophila melanogaster neuronal stem cell divisions, early anaphase sister and non-sister chromatids remain connected by thin telomeric DNA threads. Normally, these threads are resolved in mid-to-late anaphase via a spatial mechanism. However, we find that the presence of a nearby unrepaired DNA break recruits histones, BubR1 kinase, Polo kinase, Aurora B kinase, and BAF to the telomeric thread of the broken chromosome, stabilizing it. Stabilized connections then aid lagging chromosome rescue. These results suggest a model in which pervasive anaphase telomere-telomere connections that are normally resolved quickly can instead be stabilized to retain wayward chromosome fragments. Thus, the liability of persistent anaphase inter-chromosomal connections in normal divisions may be offset by their ability to maintain euploidy in the face of chromosome damage and genome loss."

Comment: pulling chromosomes by thin tendrils can break them. These backups had to be in place when cell division by this method appeared. It is irreducibly complex and had to be designed all at once. Reactive evolution after the problem appeared would have taken too long

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2973 views

It helps prevent problems in cold water:

https://www.sciencenews.org/article/squid-edit-rna-cold-adaptation

"Squid don’t have thermostats to control ocean temperatures. Instead, the cephalopods tweak RNA to adjust to frigid waters, a study suggests.

"Usually, genetic instructions encoded in DNA are faithfully copied into messenger RNA, or mRNA, and then into proteins. But squid and other soft-bodied cephalopods edit many of their mRNAs so that the resulting proteins contain some different building blocks than are inscribed in DNA.

“'In these animals, 60 percent or more of their proteins are actually recoded. This is astonishing in comparison to how [rarely RNA] editing is used in mammals,” molecular biologist Kavita Rangan said December 5 at Cell Bio 2022, the annual joint meeting of the American Society for Cell Biology and the European Molecular Biology Organization.

"Rangan, of the University of California, San Diego, examined the consequences that editing has on proteins called kinesins. Those molecular motors ferry cargo throughout cells along protein tracks called microtubules. Problems on the cellular railway can lead to cells’ disfunction or death and may contribute to disease.

"Squid hatchlings put in chilly 6° Celsius water for a day edited mRNAs for a kinesin protein differently and more heavily than hatchlings placed in warm 20° C water, Rangon found.

"She then made an unedited version and several edited versions of kinesin in the laboratory and compared the proteins’ movements on microtubules. In the cold, unedited kinesin moved more slowly, traveled shorter distances and fell off microtubule tracks more often than it did when warm.

"Two of the edited kinesins, like those made by squid in cold water, moved a little slower than the unedited protein. But the renovated versions grabbed on to microtubules more often and had longer runs than unedited kinesin. “This suggests that recoding can allow kinesin to stay on its tracks and travel farther” in the cold, Rangan said.

"Changing some made-on-demand RNAs instead of permanently altering DNA may give squid more flexibility to adjust to fluctuating ocean temperatures, she said.

Comment: this is the simple epigenetics of methylation of some spots. This satisfies dhw's thought that God might design this process in higher organism than bacteria.

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2851 views

Just discovered:

https://www.sciencedaily.com/releases/2022/12/221222123123.htm

'After an intrepid, decade-long search, Johns Hopkins Medicine scientists say they have found a new role for a pair of enzymes that regulate genome function and, when missing or mutated, are linked to diseases such as brain tumors, blood cancers and Kleefstra syndrome -- a rare genetic, neurocognitive disorder.

***

"The location of the mark is on histone proteins, which act as spools that tightly wind DNA, often turning off genes and protecting DNA from damage. If Tetrahymena are not able to add the marks -- a process called methylation, which adds chemical tags to a part of histones called H3K23 -- the DNA becomes damaged and the cells grow poorly.

"In a follow up study published in 2016, Taverna found that the H3K23 location is conserved between Tetrahymena and mammals, including humans. However, the enzymes that control how the chemical tags are placed on H3K23 differ between the species.

***

"Taverna, recent Ph.D. graduate David Vinson and Srinivasan Yegnasubramanian, M.D., Ph.D., professor of oncology and pathology at the Johns Hopkins Kimmel Cancer Center, led a new study to search for the mammalian enzymes that add the chemical tags to H3K23.

"After screening many enzymes that write methylation, Vinson found just one pair of enzymes, EHMT1/GLP and EHMT2/G9a, which placed chemical tags on the H3K23 histone location.

"When the researchers used drug inhibitors and genetic mutations directed against the enzyme pair in human brain cells (neurons) grown in the laboratory, the ability of the enzymes to place methylation tags on the H3K23 histone location reduced significantly.

"'With this initial precedent established in human neuronal cells, the door is now wide open to study the role of these enzymes and the H3K23 modification in numerous contexts of health and disease, including human cancer," says Yegnasubramanian.

"Now that the researchers know that EHMT1/GLP and EHMT2/G9a place chemical tags on the H3K23 histone location, they are aiming to understand the precise mechanism of how they do so and develop drugs that target this activity."

Comment: these enzymes offer tight control over DNA errors when wound on histones. I'll remind, enzymes are giant very specified molecules. To work they must be designed all at once, and never could evolve stepwise.

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2887 views

Usually only mutations in genetic cells are used:

https://www.the-scientist.com/news-opinion/corals-upend-longstanding-idea-about-genetic...

"Corals native to Caribbean waters may have broken a basic tenet of biology. When a mutation occurs in the body cells of nearly any animal on Earth, it’s not passed on to offspring via reproductive cells. But these corals do pass on such mutations, according to a new study.

***

"Baums is also interested in the genetic diversity of corals, so she studies how they reproduce. Elkhorn coral reproduces both sexually and asexually. During asexual reproduction, a portion of the parent coral either breaks or buds off and attaches to the seabed nearby. Sexual reproduction is a bigger event: Every August, shortly after the full moon, all of the corals in a reef sync up to release their reproductive cells at once, which can then merge in the water. Eggs typically require fertilization by sperm from different colonies, then turn into larvae and swim up to hundreds of miles away to establish a new colony. “It’s an absolutely stunning experience,” says Baums. “It looks like it snows, but the wrong way around, from the bottom.”

***

"During the process of comparing the genomes of the parent corals with the offspring that arose via self fertilization and the nearby clones that arose via budding, she and her team realized “that this really old clone had accumulated a number of somatic mutations, and those somatic mutations ended up in those [offspring],” she says. Since the corals had self-fertilized, limiting the number of genetic possibilities that could occur in the offspring, the researchers could relatively easily search for somatic mutations. They found 268 somatic mutations in the parent clone, with each nearby clone that arose from the parent sharing between 2 and 149 of these mutations. Around 50 percent of the mutations found in the parent clone also showed up in offspring that were produced via self-fertilization. “It’s really unusual for an animal,” says Baums.

***

"Previously, it was thought that in order for mutations to be passed on to offspring in animals, they need to be present in the reproductive or germline cells. Mutations that develop throughout life are thought to remain only in our body cells. Baums says that the researchers aren’t sure how germ cells are acquiring these mutations, but they hypothesize that the somatic cells may have dedifferentiated into stem cells, and then redifferentiated into germ cells.

“'This is an observation we made that’s just really stunning. It’s just unexpected,” Baums says. She says that somatic mutations might be a previously-unrecognized source of genetic diversity for corals, which might influence how they adapt in response to stressors such as ocean warming and acidification. “We really want to understand what evolutionary impact the somatic mutations might have. Are they really a source for novelty and an adaptation for these corals that might be significant, given the huge stressors these corals are exposed to at the moment?'”

Comment: Somatic mutations should not do this, but they did. An odd finding.

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2783 views

Another enormous article which shows epigenetic changes in simple forms do not occur in complex human forms:

https://www.the-scientist.com/features/do-epigenetic-changes-influence-evolution-70591?...

"The idea that epigenetic changes can be inherited across multiple generations in animals only began to crystallize relatively recently, with the first case in C. elegans reported in 2006, for instance. Examples of such phenomena have been reported in mice, too, although some studies have suggested that certain types of epigenetic inheritance might be rare in the rodents. Mammalian cells undergo two rounds of epigenetic reprogramming during gamete production and early embryo development, removing the majority of methylation marks from the DNA and reshaping the histone modification landscape, explains molecular biologist Joan Barau of the Institute of Molecular Biology in Mainz, Germany. He adds that in his view, the evidence so far suggests that mammals lack RNA-dependent RNA polymerases (RdRPs), the enzymes that propagate RNA signals across multiple generations in C. elegans. The difficulty in deciphering the mechanism of transmission of epigenetic marks has made it hard to convince many researchers that such intergenerational processes can occur in mammals, says Alexandra Weyrich of the German Centre for Integrative Biodiversity Research Halle-Jena-Leipzig. “The main problem is that we don’t know yet how [epigenetic changes are] transmitted to the next generation. If we solve that, then [the idea of epigenetic inheritance in mammals would be] more accepted [by] evolutionary biologists and geneticists.” ***

"To some scientists, the fact that cases of transgenerational epigenetic inheritance are often ephemeral—typically lasting only a handful of generations in C. elegans, for instance—argues against a significant evolutionary role. For simple traits controlled by single genetic loci, it would be hard for natural selection to produce a population where all individuals bear the same beneficial phenotype if that trait were unstable and reversed in some lineages, says Brian Charlesworth, an evolutionary geneticist at the University of Edinburgh. “That’s one problem, I think, for believing that this is an important evolutionary process—the apparent lack of stability in many of these cases where it does seem to be well-documented,” Charlesworth says.

"That’s why some scientists see epigenetic inheritance as no more than an adaptation in and of itself—perhaps a kind of bet-hedging strategy to transiently adapt to short-term environmental stressors without committing to stably transmitted, hard-wired changes.

***

"In humans, the evidence is even harder to interpret, with correlational studies so far failing to yield definitive answers about transgenerational epigenetic inheritance, Barau says. “I’m not a total [skeptic] of transgenerational epigenetic inheritance, it’s just that the burden of proof for this is quite high. And it hasn’t been achieved in many of the [claims], especially when you’re talking [about] humans.”

***

"Charlesworth, however, doesn’t see epigenetic inheritance as a challenge to fundamental rules of evolution laid out in the Modern Synthesis. Many documented cases involve subtle traits pertaining to stress responses and fertility, and not lineage-defining evolutionary innovations such as eyes or wings, for instance. In his view, it’s likely that the documented cases of epigenetic inheritance in worms, plants, and mammals are exceptions to the normal rules of heredity, he says. “The evidence from classical genetics, I should say, is pretty strongly against this being anything at all frequent. People have been working on genetics for over 120 years. There’s a huge body of evidence on . . . how [traits are] inherited.”

"Such discussions tap into a broader argument that has long raged over the EES, with frustration on both sides, researchers tell The Scientist. A recent article in The Guardian titled “Do we need a new theory of evolution?” generated rigorous debate among scientists on Twitter. “This all brings very heated discussions [at] the conferences and meetings,” Stajic says via email. “It is definitely very exciting times to be in the field.”

Comment: same result. Studies in simple organisms do not carry over to advanced complex forms. These are natural mechanisms. God, as designer, does not posse these problems, except belief.

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2724 views

Now definite:

https://www.the-scientist.com/news-opinion/bacteria-have-histones-after-all-study-70951

"With the exception of two known proteins, bacteria are generally thought to lack histones, having evolved an independent set of DNA-folding histonelike proteins instead. As evolutionary biologist Tobias Warnecke at the LMS London Institute of Medical Sciences explains, bacterial DNA-packaging proteins have 3D structures that are “clearly distinct.” Still, the general absence of histones in bacteria is puzzling given that bacteria exchange genes with archaea and eukaryotes—a process called horizontal gene transfer—and could have adopted more histones in this way.

"Now, Warnecke and colleagues are challenging the idea that these space-saving proteins are not commonplace in bacteria. In a preprint uploaded to bioRxiv this January that has yet to undergo peer review, the team describes hundreds of potential histone proteins in bacteria, including one that they predict interacts with DNA in an unusual way.

***

"The team detected a histone fold in an uncharacterized B. bacteriovorus’ protein called Bd0055 and wondered if this protein could help orchestrate DNA packaging. By observing that, in the presence of the protein, DNA moved much slower through pores in a gel, they confirmed that Bd0055 binds DNA. Deleting the gene turned out to be lethal in B. bacteriovorus cells both inside and outside prey bacteria, indicating that the protein is essential throughout the lifecycle.

"With all evidence thus far suggesting Bd0055 could be a typical histone protein, the team set out to determine if Bd0055 forms spools for DNA to wrap around. Computer simulations carried out by Shawn Laursen at the University of Colorado Boulder revealed that the protein-protein interactions that are needed to form spools would be unstable for this protein. Instead, the simulations revealed that Bd0055 might bind to the outer edges of DNA strands. Warnecke has never seen other histones behave this way. “There’s really nothing like the edge-on binding,” he says.

"Rather than packaging the DNA to occupy less space, the authors argue that the edge-on binding could straighten the strands and protect the DNA from over-compression during division into smaller cells. Indeed, straightened DNA spirals have been observed in this bacterium. Nessa Carey, a molecular biologist who works on histones and was not involved with the study, agrees, noting that “it’s a possible interpretation” but also wonders if the protein may have a shielding action against bacteriophages or arsenal in the prey bacterium. The protein could be “making DNA harder to get at and attack.”

"While Dame is intrigued by the findings, he notes that the function of the protein needs to be confirmed inside cells. Carey says that it’s “incredibly thorough structural work” but mentions that the lethal outcome of deleting the histone is unfortunate: “If all you get is a lethal phenotype, it tells you it’s important, but it doesn’t tell you why.” She proposes that more sophisticated genetic variants will be needed to build on these findings.

"B. bacteriovorus is known to have exchanged genes with a distant relative, Leptospira interrogans, in the past, and the researchers found a similar histone protein in this species. Laursen says he plans to investigate this histone next. His supervisor, Karolin Luger, tells The Scientist in an email that because Leptospira histones share many features with Bd0055, the team suspects they might bind DNA “in the same unorthodox manner,” but there are also “intriguing differences.”

Comment: histones are found but too early for a full story. Since bacteria don't store DNA in a nucleus it must be a different mechanism= for DNA control.

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2724 views

Germ cell mechanisms at work to protect the integrity of DNA sequences:

https://ecoevocommunity.nature.com/posts/genetic-instability-also-protects-genome-integ...

"Non-coding RNAs (ncRNAs) include small RNAs and long non-coding RNAs. They do not encode protein; however, they could be involved in the post-transcriptional regulation of genes. Among the classes of small ncRNAs, PIWI-interacting RNAs (piRNAs) are germ cell-specific and longer than other types of small RNAs, such as endogenous small interfering RNAs (siRNAs) and micro RNAs (miRNAs). Most piRNAs in mammalian testes are derived from long non-coding RNAs, which are fragmented into pre-piRNAs, and the pre-piRNAs loaded onto PIWI proteins at a 1:1 ratio undergo further trimming and 2’-O-methylation at the 3’end, which generates mature piRNAs (Sun et al., 2022). The primary function of mature piRNAs is to silence transposable elements (TEs) across bilateral animals.

"In mammalian testes, germ cells express a low amount of piRNAs during the pre-pachytene stages of germ cell development. In contrast, germ cells express highly abundant piRNAs during the pachytene stage of germ cell development. Because over 80 percent of pachytene piRNAs in adult mammalian testes lack obvious targets, earlier studies proposed that pachytene piRNAs regulate mRNAs or stabilize PIWI proteins essential for spermatogenesis. However, the exact function of pachytene piRNAs and the mechanism promoting rapid evolution and divergence of piRNAs and piRNA-producing loci still remains to be clearly understood.

"In our new paper, “Amniotes co-opt intrinsic genetic instability to protect germ-line genome integrity” (Sun et al., 2023), we revealed three fundamental evolutionary forces driving the rapid evolution of piRNA loci across amniotes. The first force is a high local mutation rate of structural variations (SVs), the second force is a positive selection to suppress young and actively mobilizing TEs (all identified TEs belong to retrotransposons) after meiosis, and the third force is a negative selection to eliminate deleterious SV hotspots. To reveal the above findings, we performed comprehensive comparative studies of amniotes, including six different chicken breeds, ducks (Pekin ducks), mice, and humans. Our new paper collectively indicates that genetic instability at the pachytene piRNA loci also protects germ-line genome integrity against TE mobilization by driving the formation of rapidly-evolving piRNA sequences."

Comment: An amazingly precise way germ cells protect DNA sequential integrity. Once again, not by chance but by precise design.

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2689 views

A strange relationship with older larger proteins:

https://phys.org/news/2023-02-evolution-mini-proteins-human.html

"Every biologist knows that small structures can sometimes have a big impact: Millions of signaling molecules, hormones, and other biomolecules are bustling around in our cells and tissues, playing a leading role in many of the key processes occurring in our bodies. Yet despite this knowledge, biologists and physicians long ignored a particular class of proteins—their assumption being that because the proteins were so small and only found in primates, they were insignificant and functionless.

The discoveries made by Professor Norbert Hübner at the Max Delbrück Center... "We were the first to prove the existence of thousands of new microproteins in human organs," says Hübner.

"In a new paper published in Molecular Cell, the team led by Hübner and van Heesch now describe how they systematically studied these mini-proteins, and what they learned from them. "We were able to show which genome sequences the proteins are encoded in, and when DNA mutations occurred in their evolution," explains Dr. Jorge Ruiz-Orera, ... bioinformatic gene analyses revealed that most human microproteins developed millions of years later in the evolutionary process than the larger proteins currently known to scientists.

"Yet the huge age gap doesn't appear to prevent the proteins from "talking" to each other. "Our lab experiments showed that the young and old proteins can bind to each other—and in doing so possibly influence each other," says lead author Dr. Jana Schulz, a researcher in Hübner's team and at the DZHK. She therefore suspects that contrary to long-held assumptions, the microproteins play a key role in a variety of cellular functions. The young proteins might also be heavily involved in evolutionary development thanks to comparatively rapid "innovations and adaptations."

***

"...the ability to bind does suggest the proteins might influence each other's functioning. Initial cellular experiments conducted at the Max Delbrück Center in collaboration with Professors Michael Gotthardt and Thomas Willnow confirm this assumption. This leads Ruiz-Orera to suspect that the microproteins "could influence cellular processes that are millions of years older than they are, because some old proteins were present in the very earliest life forms."

[/b]"Unlike the known, old proteins that are encoded in our genome, most microproteins emerged more or less "out of nowhere—in other words, out of DNA regions that weren't previously tasked with producing proteins," says Ruiz-Orera. Microproteins therefore didn't take the "conventional" and much easier route of being copied and derived from existing versions. And because these small proteins only emerged during human evolution, they are missing from the cells of most other animals, such as mice, fish and birds. These animals, however, have been found to possess their own collection of young, small proteins. [/b] (my bold)

"During their work, the researchers also discovered the smallest human proteins identified to date. "We found over 200 super-small proteins, all of which are smaller than 16 amino acids," says Dr. Clara Sandmann, the study's third lead author. Amino acids are the sole building blocks of proteins. Sandmann says this raises the question of how small a protein can be—or rather, how big it must be to be able to function. Usually, proteins consist of several hundred amino acids.

"The small proteins that were already known to scientists are known as peptides, and function as hormones or signal molecules. They are formed when they split off from larger precursor proteins. "Our work now shows that peptides of a similar size can develop in a different way," says Sandmann. These smallest-of-the-small proteins can also bind very specifically to larger proteins—but it remains unclear whether they can become hormones or similar: "We don't yet know what most of these microproteins do in our body," says Sandmann."

Comment: now we have a mini-protein gap along with a pyramidal neuron gap and the Cambrian gap. My bold is an amazing piece of discussion in a Darwinist article. Darwin based scientists don't like gaps. God, the designer is easily evoked. Steps in with new advances whenever He desires.

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2718 views

One specific molecule at work:

https://medicalxpress.com/news/2023-03-unveils-epigenetic-traffic-gene.html

"Scientists at The Institute of Cancer Research, London, reveal how a key epigenetic signal called H3K4me3—determines when and how DNA should be read and translated into proteins within our cells.

"The study shows that H3K4me3 ensures genes are transcribed and activated at the right time in a controlled manner, like a set of traffic lights regulating the flow of cars on a busy road. Understanding how it functions in normal cells can also shed new light on the development of cancer—and the role played by a breakdown in the regulation of gene activity.

"It has been known for more than 20 years that the enzymes placing H3K4me3, a chemical tag added to DNA, are crucial for normal cell development, as well as being linked to leukemia, breast, bowel and pancreatic cancers. But, until now, scientists lacked an understanding of what the chemical tag does, despite many years of research.

***

"Epigenetics affects gene activity, or expression, without changing the underlying genetic code—for example, by adding or removing chemical tags or modifications to DNA or proteins that the DNA is wrapped around, called histones. Chemical modifications such as H3K4me3 (tri-methylation of histone H3 lysine 4) can turn genes on or off, and are often altered in cancer.

"Using mouse stem cells and sophisticated genetic and biochemical experiments in the lab, researchers found that the H3K4me3 modification is essential for regulating how and when our genes are expressed.

"The team found that H3K4me3 acts like a traffic light at a busy intersection. By regulating the flow of RNA polymerase II—a protein complex that reads and decodes DNA—H3K4me3 determines when gene expression should start and the speed at which it runs.

"When it gives the green light, H3K4me3 allows RNA polymerase II to move along DNA, transcribing it into RNA as it moves. But without H3K4me3, RNA polymerase II gets stuck at specific points on the DNA, creating a hold-up and slowing down transcription.

***

"Study leader Professor Kristian Helin, Chief Executive of The Institute of Cancer Research, London, and a world leader in the study of epigenetics, said, "Our study offers a fundamental new understanding of epigenetics, a very exciting and still largely underexplored area of cancer research. We have solved a 20-year-old puzzle by discovering how a well-known epigenetic modification controls gene expression. Because the enzymes determining the level of H3K4me3 in the cell frequently are found mutated in cancer, our studies could have implications for understanding and treating cancer.'"

Comment: this is from research into how cancer develops. Natural processes must be understood first. Recognizing this is an automatic process, it is still not clear what influences the molecule into action.

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2730 views

New mechanism found:

https://phys.org/news/2023-03-dna-discovery-biotechnology.html

"...have uncovered a previously unknown aspect of how DNA double-stranded breaks are repaired.

"A large protein kinase called DNA-PK starts the DNA repair process; in their new report, two distinct DNA-PK protein complexes are characterized, each of which has a specific role in DNA repair that cannot be assumed by the other.

"It still gives me chills," says Meek. "I don't think anyone would have predicted this."

***

"Sometimes, only one of the two strands break. Because the DNA is still held together by the second strand, cells can repair the DNA fairly easily—the cells just copy the information from the second strand.

"It is more difficult for cells to repair DNA damage when both strands are broken. Information in the form of nucleotides can be lost and must be added back in before the DNA ends are rejoined. If a cell has multiple DNA double-stranded breaks, the DNA ends can be joined with the wrong partner. This type of mistake is often associated with many types of cancers.

"Double-stranded breaks also can be more difficult to repair if DNA-damaging agents cause chemical modifications at the DNA ends. Damaged DNA ends are often referred to as "dirty" ends.

"DNA-PK can help repair DNA double-stranded breaks in one of two ways. For breaks with missing information, it can target enzymes that can fill in missing nucleotides—sort of like a needle and thread stitching the DNA back together. For "dirty" ends, DNA-PK recruits enzymes that can cut off the damaged DNA so that the ends can be rejoined.

"Meek's team and their collaborators previously published structural studies that revealed two different DNA-PK complexes, called dimers. While many molecular geneticists already suspected that DNA-PK helps hold DNA ends together during the rejoining process, many wondered why there would be two dimers, instead of just one.

"In their new study, Meek and her collaborators discovered that the two distinct DNA-PK dimers have different functions; one complex recruits enzymes that fill in lost information, while the other activates cutting enzymes that remove "dirty" ends. The team also discovered that repair efficacy depends on equilibrium between the two dimers."

Comment: when DNA was first produced, this mechanism had to be present. No designer would build one without the other. Not by chance!

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2694 views

An unexpected finding:

https://www.the-scientist.com/news-opinion/micrornas-can-boost-gene-expression-study-70...

“'It changes the landscape of microRNA,” Lara Mahal, a chemist at the University of Alberta in Canada tells The Scientist. “There isn’t one mode of microRNA regulation: There are two.”

***

Comment: in studying the genome, it is like pealing an onion, one layer of control after another. Only a designer explains this.

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2588 views

A totally new finding, introns everywhere:

https://www.quantamagazine.org/how-a-dna-parasite-may-have-fragmented-our-genes-20230330/

"In their DNA, the information about how to make proteins isn’t laid out in long coherent strings of bases. Instead, genes are split into segments, with intervening sequences, or “introns,” spacing out the exons that encode bits of the protein. When eukaryotes express their genes, their cells have to splice out RNA from the introns and stitch together RNA from the exons to reconstruct the recipes for their proteins.

"The mystery of why eukaryotes rely on this baroque system deepened with the discovery that the different branches of the eukaryotic family tree varied widely in the abundance of their introns. The genes of yeast, for instance, have very few introns, but those of land plants have many. Introns make up almost 25% of human DNA. How this tremendous, enigmatic variation in intron frequency evolved has stirred debate among scientists for decades.

"Answers may finally be emerging, however, from recent studies of genetic elements called introners that some scientists regard as a kind of genomic parasite. These pieces of DNA can slip into genomes and multiply there, leaving profusions of introns behind them. Last November, researchers presented evidence that introners have been doing this in diverse eukaryotes throughout evolution. Moreover, they showed that introners could explain why explosive gains in introns seem to have been particularly common in aquatic forms of life.

***

"Because of the introns polka-dotting their DNA, if the genes of eukaryotes were translated directly into proteins, the resulting molecules would typically be nonfunctional garbage. For that reason, all eukaryotic cells are equipped with special genetic shears called spliceosomes. These protein complexes recognize the distinctive sequences that flank intron RNA and remove it from the preliminary RNA transcripts of active genes. Then they splice together the coding segments from exons to produce messenger RNA that can be translated into a working protein. (my bold)

***

"Why natural selection in eukaryotes favored introns that needed to be removed by spliceosomes is unknown. But the key might be that such introns allow for alternative splicing, a phenomenon that dramatically increases the diversity of products that can arise from a single gene. When the intron RNA is clipped out, the exon RNA sequences can be strung together in a new order to make slightly different proteins, Corbett-Detig explained. (my bold)

***

"The distinctive feature of introners is that they create introns. Introners copy and paste themselves into stretches of coding DNA that offer an appropriate splicing site. Then they move on, leaving behind a specific intron sequence flanked by splicing sites, which splits the coding DNA into two exons. This process can be repeated on a massive scale throughout a genome. In fungi, for example, introners appear to account for most of the intron gain during at least the last 100,000 years.

***

"The work by Gozashti and his colleagues proved that introners are not distributed equally among eukaryotes. For example, introners are more than six times as likely to appear in the genomes of aquatic organisms as in those of terrestrial organisms. Moreover, nearly three-quarters of the genomes from aquatic species that contain introners host multiple introner families.

***

"Although horizontal gene transfer and introners share a connection to the aquatic environment, the findings don’t yet show definitively that this is where introners come from. But the discovery of introners’ widespread influence does challenge some theories about how genomes — particularly eukaryotic genomes — have evolved.

***

"The evolutionary arms race between invading genetic elements and the host may have a hand in generating a more complicated genome. The parasitic elements are in “constant conflict” with genetic elements that belong to the host, Gozashti explained, because they compete for genomic space. “All these moving pieces are constantly driving each other to evolve,” he said.

***

"Feschotte thinks that profusions of introns might help drive the evolution of families of genes that can change rapidly. Stuffed with new introns, those genes could co-opt the new variability enabled by alternative splicing. (my bold)

***

"Irina Arkhipova, a molecular evolutionary geneticist at the University of Chicago Marine Biological Laboratory, is interested in knowing more about how introners are spreading through the genome at such large scales. “It just leaves no trace of the enzyme that was responsible for this massive burst of mobility — that’s a mystery,” she said. “You basically have to catch it in the act while it’s still moving.”

Comment: my bolds show the increasing facility to make new proteins. A clever arrangement b y God, the designer.
Comment: my bolds show it is a neat trick to form more proteins.

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2371 views

A massive study across species and human:

https://www.quantamagazine.org/animal-mutation-rates-reveal-traits-that-speed-evolution...

"Bergeron and her team first gathered blood and tissue samples from family trios — a mother, a father and one of their offspring — from species in zoos, farms, research institutes and museums all over the world. They then compared the DNA of the parents and the offspring in each trio to pinpoint genetic differences between the generations.

***

"In the end, the researchers had 151 usable trios, representing species as physically, metabolically and behaviorally diverse as massive killer whales, tiny Siamese fighting fish, Texas banded geckos and humans.

***

"The study authors found that the higher the average effective population size for a species, the lower its mutation rate. That provided good evidence for the “drift-barrier hypothesis,” which Lynch devised a little over a decade ago. “Selection is relentlessly trying to reduce the mutation rate because most mutations are deleterious,” Lynch explained. But in species with smaller effective population sizes, natural selection gets weaker because genetic drift — the effect of pure chance on the spread of a mutation — gets stronger. That allows the mutation rate to rise.

"The findings also support another idea in the scientific literature, the male-driven evolution hypothesis, which proposes that males may contribute more mutations to the evolution of some species than females do. Bergeron and her colleagues found that germline mutation rates tended to be higher for males than for females — at least in mammals and birds, though not in reptiles and fish.

"The authors noted a possible reason for those differences: Because males in all species copy their DNA constantly to make sperm, they face endless opportunities for mutations to occur. Female fish and reptiles make eggs throughout their lifetimes too, so they run a similar risk of genetic error. But female mammals and birds are essentially born with all the egg cells they will ever produce, so their germlines are more protected.

***

"Factors like maturation time and numbers of offspring also played a role for some vertebrates, but contrary to expectations, the researchers didn’t find any effect related to body size. There’s a long-standing hypothesis that creatures with bigger body sizes should have more mutations because they have more cells and thus more opportunities for the DNA-copying machinery to make mistakes.

“.It was surprising to see that generation time seemed a lot more important than body size,” said Kelley Harris, an assistant professor of genome sciences at the University of Washington. “In the previous literature, those hypotheses are more on equal footing.'”

Comment: again the support for the thesis that mutations in genomes are dangerous. This is natural evolution as seen by Darwinists. Nit the way God does it, I assume.

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2338 views

Called sORFs for short open reading frames , they are functional:

https://www.the-scientist.com/news-opinion/humans-are-still-evolving-thanks-to-microgen...

"The genes described in the new study went undiscovered for so long because they’re teeny: They top out at about 300 nucleotides in length, while a typical human gene is 10 to 15,000 base pairs on average. Even though they possess start and stop codons that allow them to be read by cells’ transcriptional machinery just like traditional genes, these so-called microgenes—sometimes called short open reading frames (sORFs)—have long been assumed to be nonfunctional, Saghatelian explains.

"But recent studies found that knocking out sORFs stunts cell growth, indicating they’re important after all. One 2020 study, for example, found hundreds of functional sORFs in human cells, both in the coding and noncoding regions of the genome. The number was intriguing to Nikolaos Vakirlis, a computational evolutionary biologist at Biomedical Sciences Research Center Alexander Fleming in Vari, Greece, and he and his colleagues felt compelled to investigate these genetic oddities further, launching what became the newly published research. “We find species-specific genes everywhere,” Vakirlis says. “So there has to be an evolutionary route for them to originate.”

***

"Through this process, the team identified 155 microgenes that all vertebrates share. Forty-four of these are critical for cell growth, according to data from the previous study. Three have disease markers associated with ailments such as muscular dystrophy, retinitis pigmentosa, and Alazami syndrome. The team also found one microgene—associated with human heart tissue—that cropped up after chimps and humans split off from gorillas about 7 to 9 million years ago.

"Intriguingly, Vakirlis and his colleagues found that these new genes had emerged from the noncoding regions of DNA, rather than by mutation or duplication of existing genes. While gene duplication is thought to be the main source of new genes in all species, the appearance of microgenes might explain how humans developed some uniquely human characteristics, as well as how other animals gained uniquely species-specific phenotypes."

Comment: more junk DNA turns out to be useful. The real twist is how the reporter thinks humans are evolving, just because new genes were found. They are seven to nine million years old!!! The title of toe article is: "Humans Are Still Evolving Thanks to Microgenes". No they are not.

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2403 views

The structuring is called nucleosomes:

https://phys.org/news/2023-04-dna-packaging-cell-division.html

"The DNA molecule is located in the cell nucleus as a densely packed complex of DNA and protein, known as chromatin. Wrapped in sections around a core of special proteins known as histones, the DNA forms so-called nucleosomes, which are organized along the DNA like pearls on a string.

"For one of the fundamental processes of life, replication, the doubling of DNA, the standard textbook view tends to see this literally tangled structure as a hindrance that has to be loosened up and overcome with the expenditure of energy.

"A team led by molecular biologist Dr. Christoph F. Kurat from LMU's Biomedical Center (BMC) has now shown that this is not the whole truth: At certain places in the genome, the starting points of replication, a characteristic nucleosome structure is crucial for replication to get going in the first place, as the researchers report in the journal Nature.

"Before a cell can divide, its DNA has to double. This process does not initiate at one place only, rather the molecular machines of replication get to work simultaneously at many starting points along the chromosomes. Human cells possess around 30,000 of these so-called replication origins, while the single-celled baker's yeast with a small genome, which Kurat's team investigated as a model organism, possesses around 400 of them.

"Some time ago, researchers had discovered characteristic chromatin structures at these origins: The nucleosomes at these sites are arranged in very regular fashion, "in a much more orderly way than in the rest of the genome," says Kurat.

***

"...the researchers were able to demonstrate which factors generate the regular chromatin structure at the origins and how important this is for the replication machinery to get going at their starting points.

"'Mutated cells without this chromatin structure are not viable," says Erika Chacin, lead author of the study. A key factor for the start of replication is the protein complex ORC (Origin Recognition Complex), of which it has long been known that it recruits the necessary parts of the replication machines.

"To their surprise, the researchers discovered that this complex has a second function: It plays a crucial role in the genesis of the highly ordered chromatin structure at the origins, by arranging the nucleosomes accordingly in conjunction with so-called chromatin remodeler complexes."

Comment: such a complex set of coordinated reactions which must be created all at once to work. Another example of irreducible complexity requiring that it must be designed all at once.

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2426 views

So-called 'selfish genes' fight in the reproductive process:

https://www.the-scientist.com/features/probing-selfish-centromeres-unveils-an-evolution...

"The Portuguese island of Madeira is home to six different chromosomal races of mice, each with dramatically reduced diploid chromosome numbers compared to mice elsewhere. This striking diversity, first identified at the turn of the 21st century, can be explained by the repeated fusions of separate chromosomes. Each race has a different set of fusions, and a hybrid between two races would likely have reduced fertility or be sterile because of problems with chromosome pairing. Such reproductive isolation among populations is a key step on the road to speciation—and in the mice’s case, these chromosomal changes have all occurred within the 1,000 years.

***

"We usually think of the chromosome segregation machinery as ensuring unbiased, random segregation. As we learn in high school biology, if a diploid individual carries two different alleles of a gene (i.e., is heterozygous), then either allele is equally likely to end up in a haploid gamete. This law explains the 3:1 ratio of phenotypes that Mendel observed in his classic studies of heredity. Scientists have known for decades, however, that selfish genes can subvert Mendelian segregation to increase their frequency in the next generation, a phenomenon known as meiotic drive. The Madeira mice suggest that fusion chromosomes can also drive unequal inheritance.

"Because Rb fusions are easy to identify morphologically, and because mouse oocytes are an established model system, studying these fusions in mice provided an entry for my lab at the University of Pennsylvania to investigate the cell biology of meiotic drive, starting in 2010. Focusing on the centromere—the part of each chromosome that interacts with spindle microtubules to direct segregation in mitosis or meiosis—we found that the structure’s size determines the direction of biased segregation, with bigger centromeres preferentially segregating into the egg.

***

"As a readout for functional asymmetry, we measured the position of the paired homologous chromosomes on the meiotic spindle. Chromosomes are positioned at the spindle equator when centromeres are functionally similar, as in a typical metaphase configuration, and off center when centromeres are functionally different. We found that chromosomes are positioned closer to the spindle equator when the kinetochore pathway is weakened, consistent with our prediction that the centromeres become functionally more similar. Conversely, when we weakened the heterochromatin pathway by knocking out the centromere protein CENP-B, which contributes to formation of heterochromatin near the centromere, we found that centromeres became functionally more different (i.e., more off center).

***

"Thus, there appear to be competing parallel pathways: the kinetochore pathway exploited by selfish centromeres, and the heterochromatin pathway that promotes equal segregation. This means that proteins in both pathways can evolve to suppress drive by either weakening the kinetochore pathway or strengthening the heterochromatin pathway. Consistent with this prediction, by comparing rodent genomes in our study, we found signatures of adaptive evolution in components of both pathways, suggesting that changes in multiple centromere proteins can suppress the costs of drive.

"Our and other groups’ analyses are just beginning to probe the genetic conflict between selfish centromere DNA and rapidly evolving centromere proteins. We have experimental mouse model systems and a conceptual framework for drive and suppression, and we know which amino acid changes in centromere proteins have signatures of positive selection. We now face the challenge of designing experiments to dissect the functional consequences of these changes, which may be subtle."

Comment: to call competing molecular pathway 'selfish' returns to the stupidity of Dawkin's selfish gene mantra. What we are seeing is competing automatic molecular pathways, not competing human football teams! An interesting thought about possible speciation method.

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2362 views

How bacteria constantly repair DNA mistakes in copying, etc.:

https://phys.org/news/2023-05-reveal-dna-mechanism.html

"The report describes the molecular mechanism behind a DNA repair pathway that counters the mistaken inclusion of a certain type of molecular building block, ribonucleotides, into genetic codes. Such mistakes are frequent in code-copying process in bacteria and other organisms. Given that ribonucleotide misincorporation can result in detrimental DNA code changes (mutations) and DNA breaks, all organisms have evolved to have a DNA repair pathway called ribonucleotide excision repair (RER) that quickly fixes such errors.

"Last year a team led by Evgeny Nudler, Ph.D., the Julie Wilson Anderson Professor in the Department of Biochemistry and Molecular Pharmacology at NYU Langone Health, published two analyses of DNA repair in living E. coli cells. They found that most of the repair of certain types of DNA damage (bulky lesions), such as those caused by UV irradiation, can occur because damaged code sections have first been identified by a protein machine called RNA polymerase. RNA polymerase motors down the DNA chain, reading the code of DNA "letters" as it transcribes instructions into RNA molecules, which then direct protein building.

"Nudler and coworkers found that during this transcription process, RNA polymerase also finds DNA lesions, and then serves as a platform for the assembly of a DNA repair machine called nucleotide excision repair (NER) complex. NER then snips out faulty DNA found and replaces it with an accurate copy. Without the action of RNA polymerase, little NER, if any, occurs in living bacteria.

"Now the new study in Cell provides the first evidence that, like in the NER pathway, RER is tightly coupled to transcription. The study authors found evidence that the key enzyme involved in RER, RNaseHII, also cooperates with RNA polymerase as it scans for misincorporated ribonucleotides in the DNA chains of living bacterial cells.

***

"Ribonucleotides (the building blocks of RNA) and deoxyribonucleotides (DNA components) are related compounds. As cells copy and build DNA chains in bacterial cells, they often mistakenly incorporate ribonucleotides into DNA chains in place of deoxyribonucleotides because they differ by only a single oxygen atom, say the study authors. In bacterial cells, DNA polymerase III is known to make about 2,000 of these mistakes every time it copies a cell's genetic material. To maintain genome integrity, the bulk of misplaced ribonucleotides are removed by the RER pathway, but a key question had been about how RNaseHII finds relatively rare ribonucleotide lesions amidst an "ocean" of intact cellular DNA codes so quickly.

"As they did in their 2022 studies, the researchers used quantitative mass spectrometry and in vivo protein-protein crosslinking to map the distances between chemically linked proteins, and so determined the key surfaces of RNaseHII and RNA polymerase as they interact in living bacterial cells. In this way they determined that most RNaseHII molecules couple with RNA polymerase.

"In addition, they used cryogenic electron microscopy (CryoEM) to capture the high-resolution structures of RNaseHII bound to RNA polymerase to reveal the protein-protein interactions that define the RER complex. Further, structure-guided genetic experiments that weakened the RNA polymerase/RNaseHII interaction compromised RER.

"'This work supports a model where RNaseHII scans DNA for misplaced ribonucleotides by riding on RNA polymerase while it moves along DNA," says first study author Zhitai Hao, a post-doctoral scholar in Nudler's lab."

Comment: replication works at such high speeds, mistakes must happen, and this mechanism is in place to correct them. This cannot have evolved by chance, as complex as it is.

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2191 views

All chromosomes have them:

https://phys.org/news/2023-05-exploring-centromere-role-formation-species.html

"Centromeres, the DNA sections often found at the center of the chromosomes, display enormous interspecies diversity, despite having the same vital role during cell division across almost the entire tree of life. An international team of researchers has discovered that the variation in centromere DNA regions can be strikingly large even within a single species.

***

"There is a special region in each chromosome, often found at its center: its centromere. During cell division, it ensures that new cells—from sperm and eggs to skin and neurons—end up with the correct number of each chromosome. Despite their role in cell division staying the same across almost all plants and animals, centromeres of different species surprisingly vary radically in size and structure. Biologists have termed this contrast between extreme diversity and ultra-conserved function the "centromere paradox."

***

"The researchers considered two alternative hypotheses: The large diversity could be shared by all species and passed down from a common ancestor. Alternatively, it could be recent, emerging only after the species began to diverge from one another.

"To find out, the team analyzed a large number of individuals from Arabidopsis thaliana, a common roadside weed and a favorite model organism of plant scientists, as well as material from the sister species Arabidopsis lyrata. The team was surprised that centromeres from very closely related individuals could have substantial structural differences.

"'In a way, our analysis proved both our alternative hypotheses true," Weigel says. "There is striking diversity within the species; but comparing the two species with each other, the differences look even more extreme."

"The large centromere variety raises the question how the rapid diversification came about. The team found that Arabidopsis centromeres have recently been invaded by a mobile genetic element called ATHILA. This "selfish gene" is a distant relative of retroviruses such as HIV, yet lacks the ability to escape the cell.

"The invasion is countered by the clean-up machinery that continuously polices the genome for foreign elements: to ensure continued centromere function, the cell frequently overwrites parts of it, thereby often eliminating the new ATHILA elements. This is how small building blocks of DNA may be eliminated or copied over and over again, causing the centromeres to grow or shrink and diversify from one another.

"'It seems as if these repeated cycles of invasion and purging are the main drivers of rapid centromere evolution," says Fernando Rabanal from Weigel's lab. These mechanisms might be paralleled in other species, including humans.

"'It is amazing to think that the hide and seek between centromeres and their mobile invaders may be repeated across species," Bousios says. "The game remains the same, yet the actors change.'"

Comment: we know species differ, but even with seeing these genome differences, we don't know how or why speciation happens.

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2190 views

Like bacteria edit DNA:

https://www.sciencenews.org/article/octopus-squid-rna-editing-dna-cephalopods

"Octopuses are like aliens living among us — they do a lot of things differently from land animals, or even other sea creatures...Andd to a greater extent than most creatures, octopuses squirt the molecular equivalent of red ink over their genetic instructions with astounding abandon, like a copy editor run amok.

"These edits modify RNA, the molecule used to translate information from the genetic blueprint stored in DNA, while leaving the DNA unaltered.

"Scientists don’t yet know for sure why octopuses, and other shell-less cephalopods including squid and cuttlefish, are such prolific editors. Researchers are debating whether this form of genetic editing gave cephalopods an evolutionary leg (or tentacle) up or whether the editing is just a sometimes useful accident.

***

"RNA editing can cause divergences from the DNA instructions, creating some proteins that have different amino acids than specified by the DNA.

"Editing chemically modifies one of RNA’s four building blocks, or bases. Those bases are often referred to by the first letters of their names: A, C, G and U, for adenine, cytosine, guanine and uracil (RNA’s version of the DNA base thymine). In an RNA molecule, the bases are linked to sugars; the adenine-sugar unit, for instance, is referred to as adenosine.

"There are many ways to edit RNA letters. Cephalopods excel at a type of editing known as adenosine to inosine, or A-to-I, editing. This happens when an enzyme called ADAR2 strips a nitrogen and two hydrogen atoms off adenosine (the A). That chemical peel turns adenosine into inosine (I).

***

"Cephalopods take RNA recoding to a whole new level, Albertin says. Longfin squid (Doryteuthis pealeii) have 57,108 recoding sites, Rosenthal, Eisenberg and colleagues reported in 2015 in eLife. Since then, the researchers have examined multiple species of octopus, squid and cuttlefish, each time finding tens of thousands of recoding sites.

"Soft-bodied, or coleoid, cephalopods may have more opportunities for editing than other animals because of where at least one of the ADAR enzymes, ADAR2, is located in the cell. Most animals edit RNAs in the nucleus — the compartment where DNA is stored and copied into RNA — before sending the messages out to meet up with ribosomes. But cephalopods also have the enzymes in the cytoplasm, the cells’ jellylike guts, Rosenthal and colleagues discovered.

***

"In most of a cephalopod’s body, RNA editing doesn’t often affect the makeup of proteins. But in the nervous system, it’s a different story. In longfin squids’ nervous systems, 70 percent of edits in protein-producing RNAs recode proteins. And RNAs in the nervous system of the California two-spot octopus (Octopus bimaculoides) are recoded three to six times as often as in other organs or tissues.

***

"Evidence for and against RNA recoding’s evolutionary value has come mainly from examining the total genetic makeup, or genomes, of various cephalopod species. But scientists would like to directly test whether recoded RNAs have an effect on cephalopod biology. Doing that will require some new tools and creative thinking.

***

"Albertin, Rosenthal and colleagues have developed ways to change the genes of squid with the gene editor CRISPR/Cas9. The team created an albino squid by using CRISPR/Cas9 to knock out, or disable, a gene that produces pigment. The researchers may be able to change editing sites in DNA or in RNA and test their function, Albertin says.

"This science is still in its early stages, and the story may lead somewhere unexpected. Still, with cephalopods’ skillful editing, it’s bound to be a good read."

Comment: enormous article I chopped short. Basically, they know what is happening, but as yet do not understand why. If evolution produced it there must be a reason. We'll have to wait for results. As with bacteria who edit DNA these are free-living organisms who must have survival protection. Perhaps this is it.

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2158 views

Newly discovered coding in supposedly silent telomeres:

https://phys.org/news/2023-02-scientists-stunning-discovery-protein-telomeres.html

"Once thought incapable of encoding proteins due to their simple monotonous repetitions of DNA, tiny telomeres at the tips of our chromosomes seem to hold a potent biological function that's potentially relevant to our understanding of cancer and aging.

"Reporting in the Proceedings of the National Academy of Sciences, UNC School of Medicine researchers Taghreed Al-Turki, Ph.D., and Jack Griffith, Ph.D., made the stunning discovery that telomeres contain genetic information to produce two small proteins, one of which they found is elevated in some human cancer cells, as well as cells from patients suffering from telomere-related defects.

"'Based on our research, we think simple blood tests for these proteins could provide a valuable screen for certain cancers and other human diseases," said Griffith, the Kenan Distinguished Professor of Microbiology and Immunology and member of the UNC Lineberger Comprehensive Cancer Center. "These tests also could provide a measure of 'telomere health,' because we know telomeres shorten with age."

"Telomeres contain a unique DNA sequence consisting of endless repeats of TTAGGG bases that somehow inhibit chromosomes from sticking to each other. Two decades ago, the Griffith laboratory showed that the end of a telomere's DNA loops back on itself to form a tiny circle, thus hiding the end and blocking chromosome-to-chromosome fusions. When cells divide, telomeres shorten, eventually becoming so short that the cell can no longer divide properly, leading to cell death.

***

"They conducted experiments—as described in the PNAS paper—to show how telomeric DNA can instruct the cell to produce signaling proteins they termed VR (valine-arginine) and GL (glycine-leucine). Signaling proteins are essentially chemicals that trigger a chain reaction of other proteins inside cells that then lead to a biological function important for health or disease.

"Al-Turki and Griffith then chemically synthesized VR and GL to examine their properties using powerful electron and confocal microscopes along with state-of-the-art biological methods, revealing that the VR protein is present in elevated amounts in some human cancer cells, as well as cells from patients suffering from diseases resulting from defective telomeres.

"'We think it's possible that as we age, the amount of VR and GL in our blood will steadily rise, potentially providing a new biomarker for biological age as contrasted to chronological age," said Al-Turki, a postdoctoral researcher in the Griffith lab. "We think inflammation may also trigger the production of these proteins.'"

Comment: Telomeres seemed to passively protect chromosome ends but they are active in the process of cell health and cell death. Therev is more to be discovered here.

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2159 views

From shark to skate:

https://www.quantamagazine.org/how-3d-changes-in-the-genome-turned-sharks-into-skates-2...

"Now researchers have discovered how skates evolved their distinctive profile: Rearrangements in the skate’s DNA sequence altered the 3D structure of its genome and disrupted ancient connections between key developmental genes and the regulatory sequences that governed them. Those changes in turn redrafted the animal’s body plan.

***

"By comparing the genome of the little skate to the genomes of other vertebrates, the researchers determined that the skate genome has generally remained very similar to that of their vertebrate ancestors at the sequence level. However, there were a few notable rearrangements that would have affected the genome’s 3D structure. In the DNA of individuals, such rearrangements can cause diseases by throwing off gene regulation. The discovery led the researchers to wonder whether the rearrangements in skates might have similarly disrupted the original genetic instructions for their body plan.

***

"In vertebrates, sets of functionally related genes and their enhancers are physically grouped together in three dimensions in units called topologically associating domains, or TADs. Boundary regions help to ensure that enhancers only act on genes in the same TAD.

"However, when major genome rearrangements occur — like the ones that the team was seeing in the skate’s DNA — boundaries can be lost, and the relative positions of genes on chromosomes can change. As a result, “some enhancers can provide instructions to the wrong gene,” explained Dario Lupiáñez, an evolutionary biologist at the Max Delbrück Center in Berlin and one of the senior authors of the study.

"It seemed possible that the changes in the 3D architecture of the skate genome might have disrupted the ancient blocks of genes the skates inherited from their sharklike ancestors, affecting the genes’ function.

***

"It suggested that the disruption of the ancestral TAD had produced the skate’s distinctive fins by activating PCP genes in a new part of the body.

“'This rearrangement of the TAD basically changes the entire environment of the gene and brings new enhancers into the vicinity of the gene,” Lupiáñez said.

***

"In the picture of skate evolution that the researchers have reconstructed, at some point after the skate lineage diverged from sharks, they acquired a mutation in an enhancer that made their hoxa genes active in both the front and the back of their pectoral fins. And within the new tissues growing along the anterior of the fin, genome rearrangements caused the PCP pathway to be activated by enhancers in a different TAD, which had the further effect of making the fin extend forward and fuse with the animal’s head.

“'By forming the winglike structure, [the skates] are able now to inhabit a whole different ecological niche, the bottom of the ocean,” Amemiya explained.

***

“'This is a completely new way to think about evolution,” he said. Structural rearrangements “can cause a gene to be activated in a place where it should not be.” He added: “This can be a mechanism of disease, but it can also serve as a driver of evolution.'”

Comment: the 3-D arrangement of DNA is very important since the same genes can be driven into new actions. It may help explain our small genome.

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2129 views

The brain to eye connections in octopus described.

https://www.biorxiv.org/content/10.1101/2023.02.16.528734v1

" summary:

"Cephalopods are highly visual animals with camera-type eyes, large brains, and a rich repertoire of visually guided behaviors. However, the cephalopod brain evolved independently from that of other highly visual species, such as vertebrates, and therefore the neural circuits that process sensory information are profoundly different. It is largely unknown how their powerful but unique visual system functions, since there have been no direct neural measurements of visual responses in the cephalopod brain. In this study, we used two-photon calcium imaging to record visually evoked responses in the primary visual processing center of the octopus central brain, the optic lobe, to determine how basic features of the visual scene are represented and organized. We found spatially localized receptive fields for light (ON) and dark (OFF) stimuli, which were retinotopically organized across the optic lobe, demonstrating a hallmark of visual system organization shared across many species. Examination of these responses revealed transformations of the visual representation across the layers of the optic lobe, including the emergence of the OFF pathway and increased size selectivity. We also identified asymmetries in the spatial processing of ON and OFF stimuli, which suggest unique circuit mechanisms for form processing that may have evolved to suit the specific demands of processing an underwater visual scene. This study provides insight into the neural processing and functional organization of the octopus visual system, highlighting both shared and unique aspects, and lays a foundation for future studies of the neural circuits that mediate visual processing and behavior in cephalopods."

Comment: the octopus has a camera eye just like ours, so evolution is convergent here. But the brain connections are very different. Considering the way the octopus is primarily under water, that alters the way light waves impinge in the retina requiring a different way for the brain interpreting vision.

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2110 views

DNA is constantly in motion:

https://www.sciencedaily.com/releases/2023/06/230629193228.htm

"They highlight the stochastic (random) motion of two specific gene elements on a chromosome, which have to come into contact for the gene to become active in 3D space.

***

"'Despite being heavily condensed, chromosomes are not static; they are jiggling around all the time," the physicist continues. These dynamics are very important. Whenever a specific gene has to be activated, two regions on the polymer called "enhancer" and "promoter" need to come into close contact and bind to each other. Only when this happens, a cellular machinery reads off the gene's information and forms the RNA molecule, which eventually gives rise to proteins that are essential for all the processes a living organism requires.

"Depending on the organism, the enhancer and promoter can be quite far from each other on the chromosome. "With previously used methods, you could get a static view of the distance between these elements, but not how the system evolves over time," Brückner explains. Intrigued by this missing information, the scientists set out to get a dynamic look at how these elements are organized and how they move in 3D space in real time.

"To achieve this goal, the experimental scientists from Princeton established a method to track those two DNA elements over a certain time period in a fly embryo. Through genetic manipulation, the DNA elements were fluorescently labeled, with the enhancer region illuminating in green and the promoter in blue. Using live imaging (time-lapse microscopy of living cells) the scientists were able to visualize the fluorescent spots in fly embryos to see how they were moving around to find each other.

"Once the two spots came into proximity, the gene was activated and an additional red light turned on as the RNA was also tagged with red fluorophores. Brückner excitedly adds, "We got a visual readout of when the enhancer and promoter got in contact. That gave us a lot of information about their trajectories."

***

"Due to the combination of dense packing and fast motion, the binding of these two gene regions depends much less on their distance along the chromosome than previously anticipated. "If such a system is in a fluid and dynamic state all the time, long-distance communication is much better than we might have thought," Brückner adds."

Comment: it is not distance along the chromosome, but the 3-D relationship from the movements of DNA.

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2072 views

DNA has to be copied perfectly:

https://knowablemagazine.org/article/living-world/2023/how-dna-is-copied?utm_source=Kno...

"The cell controls the start of DNA replication in a two-step process. The whole goal of the process is to control the actions of a crucial enzyme — called a helicase — that unwinds the DNA double helix in preparation for copying it. In the first step, inactive helicases are loaded onto the DNA at the origins, where replication starts. During the second step, the helicases are activated, to unwind the DNA.

"Kicking off the process is a cluster of six proteins that sit down at the origins. Called ORC, this cluster is shaped like a double-layer ring with a handy notch that allows it to slide onto the DNA strands, Berger’s team has found.

"In baker’s yeast, which is a favorite for scientists studying DNA replication, these start sites are easy to spot: They have a specific, 11- to 17-letter core DNA sequence, rich in adenine and thymine chemical bases. Scientists have watched as ORC grabs onto the DNA and then slides along, scanning for the origin sequence until it finds the right spot.

"But in humans and other complex life forms, the start sites aren’t so clearly demarcated, and it’s not quite clear what makes the ORC settle down and grab on, says Alessandro Costa, a structural biologist...Replication seems more likely to start in places where the genome — normally tightly spooled around proteins called histones — has loosened up.

"Once ORC has settled onto the DNA, it attracts a second protein complex: one that includes the helicase that will eventually unwind the DNA. Costa and colleagues used electron microscopy to work out how ORC lures in first one helicase, and then another. The helicases are also ring-shaped, and each one opens up to wrap around the double-stranded DNA. Then the two helicases close up again, facing toward each other on the DNA strands, like two beads on a string.

***

"Things kick into high gear when a crucial molecule called CDK waves the green flag, jump-starting chemical steps that lure in even more proteins. One of them is DNA polymerase — what Costa calls the “typewriter” that will build new DNA strands — which hitches onto each helicase. Others activate the helicases, which can now burn energy to chug along the DNA.

"As this occurs, the helicases change shape, pushing on one DNA strand and pulling on the other. This creates strain on the weak hydrogen bonds that normally hold the two strands together by the bases — the As, Cs, Ts and Gs that make up the rungs of the DNA ladder. The two strands get ripped apart. Costa and colleagues have observed how the two helicases untwist the DNA between them, and they’ve seen how the helicases keep the unbound bases stable and out of the way.

"At first, both helicases are wrapped around both strands of DNA, and they can’t get very far like this, because they are facing each other and will just run into each other. But next, they each undergo a change in position, spitting one DNA strand or the other out of the ring. Now separated, they can jostle past each other, and replication proceeds apace.

"Each helicase motors along its single strand, in the opposite direction from the other. They leave the origin behind and yank apart those hydrogen-bonded base pairs as they travel. The DNA polymerase is right behind, copying the DNA letters as they’re freed from their partners.

"CDK’s second job is to stop any more helicases from hopping on the origins. Thus, there is one start of replication per origin, ensuring proper copying of the genome — although copying doesn’t begin at the same time at each site. The whole process of DNA replication, in human cells, takes about eight hours.

"There is still plenty to be worked out. For one thing, the DNA that’s being copied is not a naked double helix. It’s wrapped around histones and attached to lots of other proteins that are busy turning genes on or off or making RNA copies of the genes. How do those jostling proteins affect each other and avoid getting in each other’s way?"

Comment: This happens trillions of times a day. The rare mistakes add up over time to give the false impression that mistakes are common. This process, with all its parts acting in concert, is irreducibly complex and must be designed all at once.

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2102 views

They have to be designed:

https://evolutionnews.org/2023/06/on-the-irreducible-complexity-of-sperm-cells/

"The head carries densely coiled chromatin fibers, containing the haploid genome — totaling half of the genetic material that will be inherited by the next generation (the other half will come from the mother’s egg cell). The tight packaging of the DNA serves to minimize its volume for transport.

"On the tip of the sperm head is a membranous organelle, called the acrosome, that contains various hydrolytic enzymes. When these are secreted, they digest the egg cell membrane, thereby facilitating penetration of the ovum. Without the acrosome, the sperm cell will be unable to penetrate the egg cell membrane to fertilize the ovum.

"When a sperm reaches the vicinity of the egg, it undergoes a series of molecular interactions with the zona pellucida, which is a specialized extracellular matrix surrounding the egg. Specific receptors on the sperm’s plasma membrane, such as spermadhesins or integrins, recognize and bind to corresponding ligands on the zona pellucida. This binding triggers the activation of signaling pathways in the sperm. Binding of the sperm receptors to the zona pellucida ligands leads to an influx of calcium ions (Ca2+) into the sperm cell. This calcium influx is typically mediated by ion channels or receptors on the sperm’s plasma membrane, which are activated upon ligand-receptor binding. The increase in intracellular calcium levels initiates a signaling cascade within the sperm cell. Calcium ions act as second messengers and trigger the activation of various downstream signaling molecules and enzymes, including protein kinases. As a result of the calcium-mediated signaling cascade, the acrosome undergoes exocytosis. The membrane surrounding the acrosome fuses with the sperm’s plasma membrane, causing the release of the acrosomal contents, including enzymes such as hyaluronidase and acrosin. The enzymes released from the acrosome help degrade the glycoprotein matrix of the zona pellucida, allowing the sperm to penetrate and reach the egg’s plasma membrane. The acrosomal contents aid in the breakdown of the protective layers surrounding the egg, facilitating the fusion of the sperm and egg membranes.

"The formation of the acrosome itself is divided into four stages. The first stage, the “Golgi phase,” is dependent upon the Golgi apparatus, which produces and packages the proteins and enzymes needed for acrosome formation. These proteins are then transported into the developing acrosome vesicle. In the second phase, the “cap phase,” the Golgi-derived vesicle (known as the proacrosomal vesicle) fuses with the anterior portion of the nucleus, forming a cap-like structure over the nucleus. The fusion of the vesicle with the nucleus is mediated by membrane trafficking processes... In the final phase, the “maturation phase,” the acrosome undergoes further modifications and maturation. Enzymes within the acrosome become fully activated and the acrosomal matrix undergoes changes, becoming more condensed. The acrosomal granule, which is the central region of the acrosome, becomes highly electron-dense due to the accumulation of enzymes and proteins. The mature acrosome is now ready for its role in fertilization.

***

"The middle piece consists of a central filamentous core, around which are many strategically placed mitochondria that synthesize the energy molecule adenosine triphosphate (ATP). The complexity and design of energy generation within the mitochondria — including the processes of glycolysis, the citric acid (or, Krebs) cycle, the electron transport chain, and oxidative phosphorylation — could be its own series of articles.

"The ATP generated by the mitochondria energizes the power strokes of the flagellum, driving its journey through the female cervix, uterus, and uterine tubes. As such, the middle piece of the sperm cell is absolutely essential to its function of swimming through the female uterus and fallopian tube to fertilize her egg. Without the middle piece and its mitochondria, the sperm cells are completely immobile.

"Unlike a bacterial flagellum (which rotates like a motor), a sperm flagellum beats with a whip-like motion to produce motility. How does the flagellum work? In 2018, Jianfeng Lin and Daniela Nicastro elucidated the mechanism of flagellar motility.3 Their data indicated that “bending was generated by the asymmetric distribution of dynein activity on opposite sides of the flagellum”4 (dyneins are ATP-powered molecular motors that “walk” along microtubules towards their minus end). Their results also revealed that alternating flagellar bending occurs due to “a ‘switch-inhibition’ mechanism in which force imbalance is generated by inhibiting…dyneins on alternating sides of the flagellum. In other words, regulatory signals lead to the inhibition of dynein motors on one side of the flagellum. Meanwhile, on the other side, the dyneins walk along the microtubules. The flagellum bends in one direction due to molecular linkers that resist this sliding. The flagellar bending alternates by repeatedly switching the side of dynein inhibition."

Comment: the design of sexual reproduction is irreducibly complex. Much more so than simple cell splitting. Only a designing mind can create this.

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2052 views

Both protect and stimulate sperm:

https://evolutionnews.org/2023/07/the-design-of-the-seminal-fluid-and-sperm-capacitation/

"...Only a small handful of the original sperm cells will make it as far as the egg. Thus, it is necessary that hundreds of millions of sperm cells are released in order to have a reasonable chance of the egg cell being fertilized.

"Seminal fluid also provides essential nutrients to support the survival and motility of the sperm. These include fructose — which serves as a source of energy for the sperm, fueling the mitochondrial production of ATP — as well as other sugars, amino acids, and enzymes. If the seminal fluid did not contain fructose, to power the mitochondria, this would have drastic implications for sperm cell motility and viability.

"The seminal fluid is also alkaline. This is important because the vagina has an acidic pH, produced by the normal flora (bacterial populations) of the vagina. This environment would be unfavorable to sperm cells. But the alkalinity of the seminal fluid helps to neutralize the vagina’s acidic pH, assisting the survival of the sperm.

"Following ejaculation, the seminal fluid initially coagulates to form a gel-like consistency. This coagulation helps to keep the semen in the vagina and cervix, preventing it from immediately leaking out and thereby greatly increasing the odds of a successful fertilization. This occurs upon exposure to the air or the alkaline environment of the female reproductive tract, activating clotting factors present in the seminal fluid, including tissue transglutaminase. The transglutaminase converts semenogelin (a major protein in seminal fluid secreted by the seminal vesicles) into a sticky protein called fibrin. Fibrin forms a network-like structure that entraps sperm and other components of the semen.

"If the semen remained in this state, the sperm would be permanently immobile and unable to fertilize the egg. Over time, however, the coagulated semen liquefies due to enzymes present in the fluid that slowly break down the fibrin network, allowing the sperm to move more freely. Anamthathmakula and Winuthayanon note that “The liquefaction process is crucial for the sperm to gain their motility and successful transport to the fertilization site in Fallopian tubes (or oviducts in animals). Hyperviscous semen or failure in liquefaction is one of the causes of male infertility.”1 In fact, targeting these serine proteases has been suggested as a target for novel non-hormonal contraceptives.

"From an evolutionary perspective, it is difficult to envision a scenario where semen coagulation evolved, without simultaneously having a mechanism for liquefaction. This is a prime example of a non-adaptive intermediate that is prohibitive to evolution by natural selection. (my bold)

"In order for a sperm cell to fertilize an egg, it has to undergo capacitation. This takes place in the female reproductive tract. The process of capacitation involves a series of biochemical and physiological changes that prepare the sperm for successful interaction with the egg and is crucial in order for the sperm cell to acquire the ability to fertilize.

"When sperm are initially ejaculated, they possess certain molecules and proteins on their surface that inhibit their ability to fertilize an egg. During capacitation, these surface molecules, such as cholesterol and glycoproteins, are removed or modified, allowing the sperm to become more receptive to the egg. As capacitation progresses, the motility pattern of sperm also changes. They undergo hyperactivation, which is characterized by increased amplitude and asymmetrical beating of the tail. Hyperactivated sperm exhibit vigorous movements, which help them to navigate through the female reproductive tract and reach the egg. Capacitation also involves changes in the composition and fluidity of the sperm cell membrane. These changes allow the sperm to better interact with the egg’s zona pellucida. The acrosome becomes primed for the acrosome reaction, which releases these enzymes to allow penetration of the egg membrane.

"Capacitation is associated with an increase in calcium ion influx into the sperm. Calcium plays a crucial role in various intracellular signaling processes that are necessary for sperm function and fertilization."

Comment from the article:

"In summary, various features of the head, middle piece, and flagellum, together with the properties of the seminal fluid, are critical to the sperm cell’s function of reaching and fertilizing an egg. If any one of these parts is not present or fails to function properly, the sperm cell is rendered completely impotent, and reproduction cannot occur. The phenomenon of human reproduction points to a cause with foresight — one that can visualize a foreordained outcome and bring together everything needed to realize that end goal. There is no cause in the universe that is known to have such a capacity of foresight other than intelligent design."

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2110 views

Bind DNA, protein and RNA:

https://phys.org/news/2023-07-tango-reveals-transcription-factors-dna.html

"Transcription factors help to regulate gene expression—turning genes on or off and dialing up or down their level of activity—often in partnership with the proteins that they bind. They anchor themselves and their partner proteins to DNA at binding sites in genetic regulatory sequences, bringing together the components that are needed to make gene expression happen.

"Transcription factors are a well-known family of proteins, but new research from Whitehead Institute Member Richard Young and colleagues shows that the picture we have had of them is incomplete. In a paper published in Molecular Cell on July 3, Young and postdocs Ozgur Oksuz and Jonathan Henninger reveal that along with DNA and protein, many transcription factors can also bind RNA.

"The researchers found that RNA binding keeps transcription factors near their DNA binding sites for longer, helping to fine tune gene expression. This rethinking of how transcription factors work may lead to a better understanding of gene regulation, and may provide new targets for RNA-based therapeutics.

***

"'We show that RNA binding by transcription factors is a general phenomenon," Oksuz says. "Individual examples in the past were thought to be exceptions to the rule. Other studies dismissed signs of RNA binding in transcription factors as an artifact—an accident of the experiment rather than a real finding. The clues have been there all along, but I think earlier work was so focused on the DNA and protein interactions that they didn't consider RNA."

"The reason that researchers had not recognized transcription factors' RNA binding region as such is because it is not a typical RNA binding domain. Typical RNA binding domains form stable structures that researchers can detect or predict with current technologies. Transcription factors do not contain such structures, and so standard searches for RNA binding domains had not identified them in transcription factors.

***

"Next, the researchers tested to see if RNA binding affected the transcription factors' function. When transcription factors had their ARMs mutated so they couldn't bind RNA, those transcription factors were less effective in finding their target sites, remaining at those sites and regulating genes. The mutations did not prevent transcription factors from functioning altogether, suggesting that RNA binding contributes to fine-tuning of gene regulation.

"Further experiments confirmed the importance of RNA binding to transcription factor function. The researchers mutated the ARM of a transcription factor important to embryonic development, and found that this led to developmental defects in zebrafish. Additionally, they looked through a list of genetic mutations known to contribute to cancer and heritable diseases, and found that a number of these occur in the RNA binding regions of transcription factors. All of these findings point to RNA binding playing an important role in transcription factors' regulation of gene expression.

"They may also provide therapeutic opportunities. The transcription factors studied by the researchers were found to bind RNA molecules that are produced in the regulatory regions of the genome where the transcription factors bind DNA. This set of transcription factors includes factors that can increase or decrease gene expression."

Comment: another layer of genome controls uncovered. Continuing evidence of purposeful design.

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2120 views

From competition in the genome:

https://www.sciencealert.com/long-lived-fungi-have-evolved-a-way-to-cheat-death-for-cen...

"The filaments of mushroom-forming fungi spend much of their long lives with two, separate nuclei, each containing one-half of a full set of chromosomes. Only in the gills of mushrooms moments before forming spores do the two haploid nuclei mesh together in a brief union to reproduce asexually.

"Mutations in either nucleus rob the affected mycelium of its ability to fuse its spindly filament to another, forcing other mycelia to pay the cost in spore formation. Given enough time, mutated mycelia will dominate the fungus, reducing its ability to make spores at all.

"First discovered in fast growing Neurospora crassa mold in 2016, the mutated nuclei were dubbed 'cheaters' for the way mutated mycelia can't begin asexual fusion with their own filaments to form spores, but can piggyback off other fully functioning mycelia they may encounter.

***

" 'Because these [fungal] mutations are selected within the mycelium, but reduce the fitness of the mycelium as a whole, you can think of them as a kind of 'nucleus cancers'," explains evolutionary biologist and lead author Duur Aanen, of Wageningen University.

"Aanen and colleagues compared fast-growing molds and long-lived mushroom mycelia that can live for hundreds of years. They suggest the latter use a special type of cell division called a 'clamp connection' to screen against selfish mutants, enabling them to live long lives without amassing too many genetic faults.

"In this form of cell division, one of the filament's haploid nuclei is interned in a holding bay until the cell can check its quality – and that filament fusion is possible.

"'Both nuclei [are] continuously testing each other for the ability to fuse, a test that nuclei with mutations in fusion genes fail," explains Aanen. "If the cell cannot fuse, it means a dead-end for the cell and thus the end of its nucleus."

***

"Though there are some parallels in this new study, fungi are strange beings, comprising a whole other kingdom of life to us animals. So there may be less chance of scientists finding some cellular machinery in fungi capable of quashing cancer that could be relevant to humans."

Comment: fungi and molds are basic constituents of good soils. Perhaps God designed them to last so long to provide that necessary support for soils.

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2078 views

The unexpected when genes combine effects:

https://www.quantamagazine.org/how-genetic-surprises-complicate-the-old-doctrine-of-dna...

"Does an unseen force lurk within genetics? Biologists have made enormous strides over the past 100 years in understanding the role of the millions of parcels that convey our genetic information — DNA, RNA and proteins. But they have also learned about undetectable interactions between these biochemical agents, hiding in their midst like ghosts in the machine, complicating our quest to learn the secrets of life, one gene at a time. These interactions all fit under the umbrella of “epistasis” — not exactly a new idea in biology, but one whose influence and importance are only now being fully appreciated. (my bold)

"Geneticist Daniel Weinreich and colleagues suggested that epistasis is akin to the “surprise” at the effects of mutations when they combine, given what we know about them individually. Whenever a life form’s observable attributes differ from what the DNA would lead you to expect, epistasis may be to blame. Imagine that you know of two hypothetical mutations associated with a flower stem that’s ordinarily 40 centimeters long: Mutation A is associated with a long stem (say, 50 centimeters), and mutation B confers a short stem (30 centimeters). You might expect the mutations to cancel each other out, leaving a flower with a normal-length stem. Or perhaps the combination of mutations adds their independent lengths together, resulting in an extra-long stem (80 centimeters). But instead they end up producing an extra-short stem (10 centimeters). Geneticists would say that there is a nonlinear relationship between the effects of mutations A and B, which gives you the surprising outcome. This is a signature of epistasis.

***

"Predicting how genes will work might be tricky, but we can’t set the bar so high that it requires knowing everything about every gene (and mutation). Such a reality would make many of our efforts hopelessly messy. Alas, the only reasonable response to this objection is a common one in science: It is not nature’s job to make itself easy to study, or to submit to our assumptions. Life is complex. We must let it be.

***

"...a new idea called global epistasis suggests that the ghost might not be so ghostly. With our hypothetical flower-stem mutations A and B, a global epistasis approach would suggest that the effects of adding mutation B to any genome (whether or not it contains mutation A) will follow a set pattern. Perhaps mutation B acts like a negative amplifier of other mutations, and when in the presence of a mutation that confers a long stem, it reverses the effect. These kinds of patterns have already been observed in several systems independently. How widespread this global epistasis is, and to which systems it applies, is still the object of current research. But it is exciting to know that there might be a way to predict the surprise.

"The “ghost in the machine” metaphor was originally used to discuss the mind-body duality problem, the distinction between the nonphysical mind and the mechanical body it controls. It has often been invoked to describe the fear that we might not be building what we think we are — whether it’s increasingly intelligent machines or our understanding of subtly interacting genetic codes. And indeed, bioengineering is where epistasis might cause us the most trouble. Anyone who wants to engineer new livestock (or designer babies) with desirable traits, one mutation at a time, will need to contend with the constant specter of unforeseen consequences — to say nothing of the enormous ethical issues.

"These ghosts make the work of geneticists that much more challenging, true. But they also make the biological world that much more fantastic."

Comment: Mendelian genetics was very simplistic, dominant or recessive like adding two plus two and getting four. The study of the genome doesn't offer simplicity. We may know the relationship of a gene to a characteristic, but we do not know how the gene exerts its influence. Until we do epistaxis will frustrate us. The 'ghost in the machine' is the mind of teh designer.

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1990 views

In horizontal transfer:

https://www.quantamagazine.org/selfish-virus-like-dna-can-carry-genes-between-species-2...

"In new research published in Science, researchers have identified a unique class of genetic elements as the agents responsible for shuttling certain genes between multiple species of simple invertebrates called roundworms. A jump from one worm to another may not sound like much, but the worms in question diverged many millions of years ago, making them as different at the molecular level as fish and humans. The genetic elements, called Mavericks, have been detected in a wide range of animals, both invertebrates and vertebrates, and they display many features found in the genomes of viruses. Given those properties, researchers suspect that Mavericks — and similar elements, including some not yet discovered — may have mediated horizontal gene transfers throughout the history of life.

***

"The complete picture of the genome revealed that the shuttled gene was embedded within a set of virus-like genes and a transposon, all of which Burga recognized as making up a Maverick.

"Mavericks are an ancient and fragmented class of jumping genes prevalent in the genomes of protists, fungi and animals, including humans. These massive mobile elements were initially assumed to be inactive, mutated relics of obsolete genes. But later research revealed that Mavericks can be reactivated, and that they can mediate horizontal gene transfer between some species of protists. Complete, intact Mavericks had never been characterized in a multicellular organism. The roundworms therefore presented a rare opportunity to study them.

"The Maverick in one of these roundworms, however, had an additional gene — one encoding a protein called a fusogen that enables a virus to fuse with a cell and transfer its genome into it. “Without fusogen, there would be no way for the virus to transfer its genes,” said Sonya Angeline Widen, a postdoctoral researcher in Burga’s laboratory and co-lead author with Bes of the new study. The discovery of the protein strongly suggested that this Maverick had the ability to form a virus-like particle and invade different cell types.

***

"There is reason to believe that gene transfer using massive transposons may be more common in nature. Recent research led by Aaron Vogan of Uppsala University in Sweden has found massive mobile genetic elements called Starships that shuttle genes around in multiple species of fungi. Vogan suspects that Starships transferring key genes between fungal pathogens may have created the new strains that cause rolling epidemics of wheat diseases, such as tan spot (yellow leaf spot). (my bold)

***

Researchers have come to appreciate that transposon-like genetic elements are “key drivers of genome evolution,” Zanders said. To really understand genomes, we must understand these “selfish elements” that can jump between species, she added. (my bold)

Comment: the bolds above are perhaps the way a designer would have managed recoding genomes.

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1921 views

There is a mathematical pattern:

https://www.livescience.com/physics-mathematics/mathematics/scientists-uncover-hidden-m...

"Scientists have discovered that a key function from a "pure" branch of mathematics can predict how often genetic mutations lead to changes in function.

"These rules, laid out by the so-called sum-of-digits function, also govern some aspects of protein folding, computer coding and certain magnetic states in physics.

"'Part of what we're trying to do is find a universal explanation for a lot of these trends which have been observed in nature," said lead study author Vaibhav Mohanty, a theoretical physicist

***

"For every genotype — letters of DNA for a given gene — there is a phenotype, or end result: a new protein, or even a behavior in the case of a gene that regulates another set of genes. A given genotype can accrue a number of mutations before its phenotype changes; this accumulation of neutral mutations is a major way evolution proceeds.

***

"Adding up the digits used to represent these five sequences gives you the average number of mutations those genotypes can take on before their phenotypes shift, the researchers found.

"This led to the second intriguing discovery: These sums of digits, plotted out on a graph, formed what's called a blancmange curve, a fractal curve named after a French dessert (which looks like a fancy molded pudding).

"In a fractal curve, "if you zoom into the curve it looks exactly the same as if you were zoomed out, and you can continue to zoom in infinitely and infinitely and infinitely and it would be the same," Mohanty said.

"These findings revealed some interesting secrets about error correction, Mohanty said. For instance, the natural systems the researchers studied tended to handle errors differently than humans do when setting up data storage, like in digital messages or on CDs or DVDs. In these technological examples, all errors are treated equally, while biological systems tend to protect certain sequences more than others. (my bold)

"That's not surprising for genetic sequences, where there might be several linchpin sequences and then others that are more peripheral to the main gene function, Mohanty said. "

Comment: more evidence that God is a mathematician as He conducts evolution.

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1730 views

Some new description:

https://www.sciencenews.org/article/new-dna-telomere-chromosomes-pangenome

"The Y chromosome is the smallest of the human chromosomes. “In the old time, people thought that it’s just a junkyard for human genomic material, and it only serves one purpose … to determine male sex,” says Yun-Fai Chris Lau, a human geneticist at the University of California, San Francisco, who was not involved in the work. Like comedian Rodney Dangerfield, the Y chromosome gets no respect, he says.

"But it’s clear that the Y does more than determining male sex, Lau says. Some males lose the Y chromosome from some of their cells. The loss puts them at risk for cancer, Alzheimer’s disease and other illnesses. (My bold)

***

"There are repeated sequences of DNA letters, or bases — the information-carrying building blocks of DNA — laid end to end and stretching for millions of bases like seemingly endless rows of identical puzzle pieces. Some parts of the chromosome have the puzzle pieces inverted. And some stretches of DNA contain palindromes; the DNA letters read the same in both directions. Then there are multiple copies of individual genes.

"Having a truly complete reference Y chromosome will allow researchers to better understand the role the chromosome plays in the body, he says. “When you’re putting your puzzle back together again you always save the repetitive bits, like the grass or the trees or the sky, for the end.”

"A separate study, also published online August 23 in Nature, sequenced the entire Y chromosome from 43 people, including 21 of African descent. That study found that the male sex chromosome can vary in length from person to person by millions of DNA bases, meaning that in some people, the chromosome has extra copies of some genes or other bits of DNA. For instance, males may have between 23 to 39 copies of TSPY genes, involved in sperm production, the researchers found.

"Having complete Y chromosomes from multiple people helped Phillippy and colleagues clear up a mystery. The old reference chromosome had the TSPY2 gene located near one tip of the chromosome. But the telomere-to-telomere version showed it close to the centromere — the pinched-in part of the chromosome — and backward compared with the reference.

“'We confirmed that it was correct in our assembly, so then we were just assuming that it was an error in the old assembly,” Phillippy says. But the second study showed that both versions were right. TSPY2 has jumped around on the chromosome. Some people have it at one location, while others have it at the other."

Comment: there is worry that the Y chromosome is disappearing in evolution. This article does not mention it.

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1707 views

Definitive study:

https://phys.org/news/2023-09-downstream-rna-hairpins-orchestrating-mrna.html

"Any genome is constructed with instructions that inform when to start and stop the transcription of RNA segments. These segments can contain multiple start codons, which can then be selectively used as beginning points for the ribosome to start translating them into proteins. The current study has identified a mechanism by which the selection process between potential starting points takes place.

"Ribosomal subunits assemble on an mRNA molecule and scan it for the AUG start codon to initiate protein synthesis. Sometimes, the first start codon encountered is used as initiation, and sometimes, it is not recognized. If it is not recognized, the scanning continues down the mRNA, where it may find an alternative starting point or a more easily recognized starting point (the main AUG).

"The study discovered that if the mRNA has a hairpin loop located between two starting codons, the scanning process will be slowed down, providing more time for recognition of the upstream start codon (uAUG), leading to a higher translation rate from this starting point.

***

"The study identified RNA helicases, specifically RH37-like helicases, as enzymes involved in unwinding hairpin structures near uAUGs during the immune response in Arabidopsis. Elevated levels of these helicases under immune response eliminated the traffic jam caused by the hairpin, which then increased translation from the alternative start codon and thus produced a different protein.

"The "if this, then that" mechanism functions much like a logic gate, allowing the same mRNA segment to produce an alternative protein when the situation dictates.

"The researchers introduced a hairpin structure downstream of a start codon in ATF4, a well-known mammalian stress-responsive gene with higher expression levels under cellular stress conditions. This condition inhibited the translation of ATF4 through enhanced translation initiation of a less recognized start codon.

***

"The experimental results demonstrate that upstream start codons and downstream hairpin structure-mediated translation initiation mechanisms are not limited to plants but are also present and functional in human cells. This suggests a universal logic gate mechanism for start-codon selection in translation initiation across different organisms with both conserved evolutionary insights and future therapeutic targeting implications.

Comment: just another complex system sowing tight controls, and more evidence for design. Also more evidence protein shape determines function.

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1658 views

Duplicated genomes newly recognized as good for organisms:

https://www.science.org/content/article/cells-extra-genomes-may-help-tissues-respond-in...

"As polyploid cells emerge as common and seemingly crucial, this once obscure topic is now bringing together cancer researchers, developmental biologists, evolutionary biologists, cell biologists, and agricultural scientists. About 150 researchers gathered in Florida in May for a meeting Losick helped organize, Polyploidy Across the Tree of Life, trading information from their normally siloed fields.

***

"Polyploidy may be a coping method not just for individual organisms, but for entire species. About 30% of plants are fully polyploid, meaning all their cells have double or more the number of chromosomes found in their ancestors. The same is true for a small number of animals—several salamanders, for example. Evolutionary biologists have found that polyploid organisms are often at a competitive disadvantage compared with diploid counterparts, raising questions about why the trait persists. By pinpointing when genome duplications occurred millions of years ago, researchers are glimpsing a potential answer: Polyploidy may help species weather catastrophic environmental changes. At all sorts of spatial and temporal scales, polyploidy is a “damage response,” suggests Douglas Soltis, a plant evolutionary biologist at the University of Florida. “It’s the single most important evolutionary thing that nobody talks about.”

***

"Fox, Losick, and others also documented how the cells contribute to healing. In fruit flies, some of the mammoth cells quickly plug the space left by puncture wounds, and because they have multiple copies of various genes, they can make extra proteins that speed healing. For example, where the needle poke destroys muscle, these cells make a lot of myosin protein, which helps muscles contract. The extra DNA of polyploid cells, Losick suggests, may also make them resistant to injury-induced DNA damage from inflammation that would cause a normal diploid cell to die, bogging down recovery.

***

"Losick has identified a protein that helps control polyploidy in fruit flies: the fly equivalent of a mammalian molecule called YAP1, for yes1 associated transcriptional regulator. YAP1 was known to help regulate genes that control organ size. It also turns out to stimulate polyploidy in insect wound healing, and to curb the process when its activity falls. The Florence team found YAP1 has the same role in mouse kidneys. “It was amazing that we were seeing very similar things, in the Drosophila [abdomen] and in the mammalian kidney,” Romagnani says.

***

"Sometimes these joined genomes duplicated yet again—wheat has six sets of chromosomes; strawberries have eight. The multiple copies of key genes for growth and nutrients can result in denser heads of grain, bigger fruit, and taller, sweeter stalks.

"Those traits may delight human consumers, but for plants, “many, if not most, whole genome duplications are actually maladaptive,” says Yves Van de Peer, an evolutionary biologist at Ghent University. Polyploid plants need more nutrients, for example, and seem to grow slower than their diploid counterparts. Yet the trait persists, and Van de Peer believes the answer, again, comes down to coping with stress.

***

"Tia-Lynn Ashman and Martin Turcotte, evolutionary ecologists at the University of Pittsburgh, have also studied polyploidy in duckweed populations. The polyploid plants tended to grow more slowly and reached smaller population sizes than their diploid counterparts. But they supported a more diverse ecosystem of microbes, Ashman reported at the meeting.

"That could be another beneficial consequence of polyploidy. Increasingly, researchers are recognizing that an organism’s microbiome helps it survive, so a more diverse roster of microbial guests may enable the host to digest more kinds of food or enhance resilience in other ways. The increased diversity “could provide a mechanism for the broader ecological range of polyploids seen at the global scale,” Ashman suggests.

"What is certain is the polyploid cells, far from being abnormal, are one of life’s major mechanisms for coping with the stresses of injury, disease, and a hostile environment. At the meeting, “There was the increasing realization that whole-genome doubling does not simply double everything in the cell—rather we are seeing unique biology,” says Pamela Soltis, a plant evolutionary biologist at the Florida Museum of Natural History."

Comment: a whole new research field is opening up. Genetics in just becoming even more complex. Excess sets of chromosomes are helpful.

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1627 views

There are many:

https://phys.org/news/2023-09-transposons-selfish-genes-key-elements.html

"In 2001 the sequencing of the human genome revealed a surprising fact: over 45% of our genome comes from sequences called transposons, "jumping" genes that can move within the genome, generating new copies of themselves through molecular mechanisms of cut-and-paste or copy-and-paste.

***

"Most of the copies generated by transposons are inactive today, but in the human genome and that of other mammals there are about a hundred copies of transposons belonging to the so-called LINE (Long Interspersed Nuclear Elements) family that are still potentially active. This means they can be transcribed, producing messenger RNAs that, when translated into proteins, can also contribute to a copy and paste process of genetic sequences.

"This ability of LINE transposons poses a potential risk to genome integrity: the random insertion of a new gene copy could interfere with important genetic functions. To protect against this danger, over the course of evolution, organisms have developed cellular defense mechanisms capable of blocking or limiting the activity of transposons, thus helping to preserve genome stability.

***

"The key discovery is that LINE elements are recognized by protein complexes that initiate transcription processes essential for proper embryonic development.

"Federico Ansaloni, the study's lead author and former SISSA Ph.D. student, now a researcher at the Karolinska Institute in Stockholm, remarks, "Studying the very early stages of embryonic development allows us to outline the biological processes underlying the formation of a new individual. I find it fascinating that transposons, long considered junk DNA, are actually key elements in such a delicate process."

"Finally, the article "Exploratory analysis of L1 retrotransposons expression in autism," published in Molecular Autism, examines how LINE transposons behave in the brains of people with autism spectrum disorders. What the researchers discovered is that the transcription regulation of these sequences is different only in a small group of individuals with autism.

"The data analysis also identified a group of genes containing LINE copies that, when activated, suppress the transcription of the host genes, suggesting that these sequences contain specific signals recognized by cell regulatory mechanisms.

***

"Remo Sanges, coordinator of the Ph.D. in Functional and Structural Genomics at SISSA and co-coordinator of the research, states, "It is fascinating to observe that, once the ability to identify transposon sequences evolved, our genome developed the ability to exploit these selfish elements to its advantage, using them as signals that can turn on or off entire transcriptional programs, making them indispensable for normal embryonic and brain development."

***

"'With our research, it turns out that the most important functionality of these elements is at the RNA level and therefore independent of creating new copies. This discovery could explain why many copies of these elements are kept active and finely regulated in the genome of all living beings.'"

Comment: DNA is intrinsically packed with coded information and transposons are not jumping at random but in a controlled fashion. This cannot develop by chance. They are also related to aging:

https://phys.org/news/2023-09-transposable-elements-reveals-potential-methods.html

"The scientists have identified a specific process, called the Piwi-piRNA pathway, that helps control these TEs. They've seen this pathway at work in certain cells that don't age, like cancer stem cells, and notably, the enigmatic Turritopsis dohrnii, commonly known as the "immortal jellyfish." By strengthening this pathway in a worm called Caenorhabditis elegans, the worm lived significantly longer.[30%]

***

"Additionally, the team found epigenetic changes in the DNA of these worms as they aged, specifically in the TEs. These changes, known as DNA N6-adenine methylation, was observed to increase TE transcription an jumping as the animal aged.

"Dr. Vellai emphasized the potential implications of this discovery: "This epigenetic modification may pave the way for a method to determine age from DNA, providing an accurate biological clock.'"

Comment: More functions will be found.

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1632 views

Using markers;

https://www.sciencedaily.com/releases/2023/11/231116150849.htm

"A new theoretical model helps explain how epigenetic memories, encoded in chemical modifications of chromatin, are passed from generation to generation. Within each cell's nucleus, researchers suggest, the 3D folding patterns of its genome determines which parts of the genome will be marked by these chemical modifications.

***

"The research team suggests that within each cell's nucleus, the 3D folding pattern of its genome determines which parts of the genome will be marked by these chemical modifications. After a cell copies its DNA, the marks are partially lost, but the 3D folding allows each daughter cell to easily restore the chemical marks needed to maintain its identity. And each time a cell divides, chemical marks allow a cell to restore its 3D folding of its genome. This way, by juggling the memory between 3D folding and the marks, the memory can be preserved over hundreds of cell divisions.

"'A key aspect of how cell types differ is that different genes are turned on or off. It's very difficult to transform one cell type to another because these states are very committed," says Jeremy Owen PhD '22, the lead author of the study. "What we have done in this work is develop a simple model that highlights qualitative features of the chemical systems inside cells and how they need to work in order to make memories of gene expression stable."

***

"In their new study, Mirny and his colleagues wanted to answer the question of how those epigenetic marks are maintained from generation to generation. They developed a computational model of a polymer with a few marked regions, and saw that these marked regions collapse into each other, forming a dense clump. Then they studied how these marks are lost and gained.

"When a cell copies its DNA to divide it between two daughter cells, each copy gets about half of the epigenetic marks. The cell then needs to restore the lost marks before the DNA is passed to the daughter cells, and the way chromosomes were folded serves as a blueprint for where these remaining marks should go."

Comment: cell division must have these complex controls which are irreducibly complex and must be designed

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1494 views

From a virus protein that has balanced charges in its coat:

https://www.the-scientist.com/news/a-virus-that-generates-electricity-71501?utm_campaig...

"...researchers reported that a bioengineered virus generated electricity when exposed to heat, a phenomenon known as pyroelectricity.1 By working with viruses, the researchers hope to better understand bioelectricity in the human body and apply this knowledge to power novel biomaterials.

"The M13 bacteriophage, a rod-shaped virus that infects bacteria, is adorned in a molecular coat, woven from nearly 3,000 copies of a helical protein. The protein is positively charged on the inside and negatively charged on the outside, but the arrangement of the thick protein coat balances out the charges.

"Over a decade ago, Lee’s research team put the squeeze on the coat proteins, which caused the bacteriophage to exhibit piezoelectricity—the ability to transform mechanical force into electricity.3 When the researchers applied pressure to the viruses, the coat proteins changed shape, breaking the charge symmetry and becoming polarized, which generated an electric field and induced a current.

"In their new study, the researchers addressed whether they could similarly use heat to shift the charge and generate electricity. They edited the genetic code of the viruses to include a specific protein sequence that is attracted to nickel. This way, the viruses would bind to and stand straight up on a thin nickel-coated plate, like a city block of skyscrapers. Then, they blasted these viral cities with heat, either with fire or a laser. As the proteins melted and unfolded, the proteins’ charges became unbalanced, generating voltage. “The heat induced a polarization change, and the polarization change induced the electric potential,” Lee said.

"Although the naturally occurring helical protein produces some pyroelectricity, the researchers wanted to see if they could give the molecule some added spark. To do this, they genetically altered the bacteriophage to add a string of glutamate, a negatively charged building block of proteins, into the outside of the coat protein.1,4 When the researchers turned up the heat, the added glutamate amplified the polarization change, more than doubling the pyroelectricity of the normal protein."

“'The very fact that they can genetically mutate the virus and make them pyroelectric—it's fascinating work,” said Syed Tofail, a physicist at the University of Limerick who wasn’t involved in the study. (my bold)

***

"While the voltage that the researchers detected by heating the viruses was small, they plan to boost the virus to power more complex electronics. Since M13 viruses self-replicate, scientists can scale up the total number of viruses, and “we can amplify the electricity in a similar way,” Lee said. “It’s a big motivation.'”

Comment: the major point to me is the ease with which humans are editing DNA. God must do it easily. All living organisms make some electricity so taht is not new news.

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1481 views

By mutations in copying:

https://phys.org/news/2023-12-genes.html

"The complexity of living organisms is encoded within their genes, but where do these genes come from? Researchers at the University of Helsinki resolved outstanding questions around the origin of small regulatory genes, and described a mechanism that creates their DNA palindromes. Under suitable circumstances, these palindromes evolve into microRNA genes.

"The human genome contains ca. 20,000 genes that are used for the construction of proteins. Actions of these classical genes are coordinated by thousands of regulatory genes, the smallest of which encode microRNA molecules that are 22 base pairs in length. While the number of genes remains relatively constant, occasionally, new genes emerge during evolution. Similar to the genesis of biological life, the origin of new genes has continued to fascinate scientists.

***

"In their project, the researchers studied errors in DNA replication. Ari Löytynoja, the project leader, compares DNA replication to typing of text.

"'DNA is copied one base at a time, and typically mutations are erroneous single bases, like mis-punches on a laptop keyboard. We studied a mechanism creating larger errors, like copy-pasting text from another context. We were especially interested in cases that copied the text backward so that it creates a palindrome."

"Researchers recognized that DNA replication errors could sometimes be beneficial. They described these findings to Mikko Frilander, an expert in RNA biology. He immediately saw the connection to the structure of RNA molecules.

""In an RNA molecule, the bases of adjacent palindromes can pair and form structures resembling a hairpin. Such structures are crucial for the function of the RNA molecules," he explains.

***

"By focusing on humans and other primates, researchers in Helsinki demonstrated that the newly found mechanism can explain at least a quarter of the novel microRNA genes. As similar cases were found in other evolutionary lineages, the origin mechanism appears universal.

"In principle, the rise of microRNA genes is so easy that novel genes could affect human health. Heli Mönttinen sees the significance of the work more broadly, for example, in understanding the basic principles of biological life.

"'The emergence of new genes from nothing has fascinated researchers. We now have an elegant model for the evolution of RNA genes," she highlights.

Comment: copying backwards is a mutation mechanism which has given beneficial RNA genes. Most mutations are bad so this finding is unusual. Perhaps God at work in a dabble programming.

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1440 views

Widespread controls:

https://phys.org/news/2023-12-sex-chromosomes-responsible.html

"Human sex chromosomes originated from a pair of autosomes, the ordinary or non-sex chromosomes that contain the majority of our genome and come in identical pairs. That ancestral pair of autosomes diverged to become two different chromosomes, X and Y. Even though X and Y have grown apart from each other and taken on unique functions—namely, determining sex and driving sex differences in males and females—they also retain shared functions inherited from their common ancestor.

***

"The research, published in Cell Genomics on December 13, shows that genes expressed from the X and Y chromosomes impact cells throughout the body—not just in the reproductive system—by dialing up or down the expression of thousands of genes found on other chromosomes.

"Furthermore, the researchers found that the gene pair responsible for around half of this regulatory behavior, ZFX and ZFY, found on the X and Y chromosome respectively, have essentially the same regulatory effects as each other. This suggests that ZFX and ZFY inherited their role as influential gene regulators from their shared ancestor and have independently maintained it, even as their respective chromosomes diverged, because that regulatory role is critical for human growth and development. The genes regulated by ZFX and ZFY are involved in all sorts of important biological processes, showing that the sex chromosomes contribute widely to functions beyond those related to sex characteristics.

***

"'By using the natural variation of sex chromosome composition in the human population, we were able to mathematically model how the number of X and Y chromosomes impacts expression of genes in a way that's never been done before. By taking this approach, we gained new insights into the massive impact that X and Y genes have broadly throughout the genome," San Roman says.

***

"They found that thousands of genes changed their expression levels in response to changes in the number of X and/or Y chromosomes present. The effects scaled linearly, meaning that each additional X or Y chromosome changed gene expression by the same amount. Which genes were affected, and by how much, were different for each of the cell types, suggesting that each type of cell in the body may have a unique response to gene regulation by X and Y chromosome genes.

***

"A subtlety thus far not discussed is that when Page and San Roman think about the sex chromosomes, they no longer think of X as most people think of it. Their work has convinced them that our current understanding of the sex chromosomes is imprecise. Although the human sex chromosomes are defined as X and Y, in fact there are two types of X chromosomes, and only one of them differs between typical males and females. Every human in the world has one "active X" chromosome. This chromosome is, like an autosome, universally present and so its presence has no bearing on sex.

***

"'These chromosomes have historically been known as the 'inactive' X and the 'gene-poor' Y chromosomes, and given little attention beyond how they contribute to sex differentiation, so it was stunning to us to see how wide their network of influence was," Page says. "These chromosomes contain genes like ZFX and ZFY that are global gene regulators, and I think as we learn more about them, it's going to completely change how we think about the genetics of the human X and Y chromosomes.'"

Comment: it is always surprising to me that researchers are so surprised at the complexity they unearth. We don't know what we don't know, and genetic controls are purposeful and precise.

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1419 views

The unknome refers to the massive gap in our knowledge about all genes:

https://www.the-scientist.com/stepping-into-the-unknome-71706

"To encourage research on these many mystery genes, a team of scientists have created a new publicly available database that ranks genes based on how little is known about them.3 Using this new directory, they selected more than 200 neglected genes that are evolutionarily conserved between fruit flies and humans. The systematic silencing of these genes in fruit flies revealed that many are essential for survival and other important biological functions, demonstrating that there is still much to be explored in the vast unknowns in the genome.

***

“'There's still a couple thousand genes in the human genome, at least, for which essentially nothing is known, and then there are some where a little is known, but not very much,” said Munro.

***

“'Quite often we'd turn out proteins, or other people would find proteins, which are very well conserved in evolution, but absolutely nothing is known about them,” said Munro.

***

"An initial screen revealed that nearly 25 percent of the unknown genes were essential for survival. “The Drosophila geneticists found that quite surprising as they sort of assumed that everything important had been found by conventional genetic screens in flies,” said Munro.

***

"They found that many of these genes contributed to male and female fertility, wing growth, aberrant protein removal, locomotion, and resilience to stress. One gene, CG11103—called TM2 domain containing 2 (TM2D2) in humans—surprised Munro and his team. When they deleted the gene in female flies, any eggs they laid failed to develop. They linked this failure to launch to an overproduction of cells in the offsprings’ nervous systems, a phenotype that indicates defects in the conserved and highly studied Notch signaling pathway. “Despite all the work that's been done on [the Notch signaling pathway], this gene had not been found,” said Munro.

***

"Previous research by Stoeger revealed that scientists continue to focus their research on a minority of known genes identified before the Human Genome Project. In a recent study, Stoeger and his team examined where in the -omics analysis pipeline these understudied genes leak out and found that scientists tend to abandon them while writing up the results, instead drawing attention to known, popular genes.

"The availability and reliability of reagents is another rate-limiting step, as is convincing researchers to step into the unknome. “It is risky,” said Munro. “It's something where you have to have a very good reason or a good clue to take on something like this, because it is very challenging.” Additionally, funding bodies tend to be risk averse when doling out the dough for research, but Munro said that he has spoken with a couple of organizations that are considering funding research into the unknome to address this problem.

***

"Beyond its potential value in guiding scientists towards neglected proteins, the Unknome database also highlights just how much of biology remains to be explored. Looking to the future, Munro is excited to see what new tools, like the Unknome database, help reveal. “There might be things out there which are like the unknowns,” said Munro. “No one's looking for the components because no one knows the biological process exists yet. That may sound a bit fanciful, but there are a few examples.” CRISPR was hiding in plain sight in Escherichia coli, leaving scientists like Munro to wonder what else is out there."

Comment: everything in the genome must mean something. There is/was purpose at work in creating it. This paper outlines the difficulties research groups face. But the rewards like CRISPR are worth the new efforts. We can code DNA for a number of genetic diseases now with more undoubtedly coming. Please remember we are using living material while not knowing the big black box, which is how genes accomplish their business. God remains one step ahead of us.

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1330 views

Special epigenetic marks are part of the process:

https://www.sciencedaily.com/releases/2024/03/240306150553.htm

"The Burga Lab at the Institute of Molecular Biotechnology...uncovered a novel gene regulation process, associated with the silencing of selfish genes, that could represent the first step in the evolution of imprinting. Their discovery, reported in Nature, could begin to solve the mystery of how and why imprinting first evolved. 

***

"In diploid organisms, one set of chromosomes is inherited from each parent. However, not all of the genes contained within will be expressed equally; instead, some may be silenced depending on whether they were inherited from the mother or the father. This phenomenon, known as genomic imprinting, depends on DNA methylation, an epigenetic signal that is erased and rewritten in every generation. Genomic imprinting arose independently in mammals and plants over 100 million years ago. However, how this mechanism evolved has, so far, remained largely a mystery.

***

"Pliota was investigating toxin-antidote elements (TAs), a type of selfish element that has evolved a fascinating mechanism to ensure its own inheritance: When a mother carries the TA, it will "poison" its eggs with a toxin that can only be countered by an antidote which is also present in the TA," she explains, "this way, all descendants that don't inherit the TA will either die or be developmentally delayed. 

***

"To figure out the mechanism of the observed parent-of-origin effect, the Burga group decided to study the main germline defense mechanism against selfish genetic elements, known as the piRNA pathway. In the piRNA pathway, a coordinated effort of different small RNA molecules and proteins silences the expression of selfish elements during germline development to ensure genome stability in reproduction. 

***

"They proved that, in maternal inheritance, the TA is accompanied by the toxin mRNA, which is expressed in the germline of the mother and loaded into the egg. The Burga group showed that this mRNA marks the TA as "own," avoiding its silencing by the piRNA pathway. This process is called epigenetic licensing, and its balance with the piRNA pathway determines whether a gene is expressed or not. 

"On the other hand, when the TA is inherited paternally, the lack of maternal mRNA means there is no licensing, leading to a strong repression of the toxin gene and very low levels of toxin being expressed. By default, the piRNA pathway will silence the toxin gene explains Burga. Unless there's maternal mRNA that licenses it by repressing the piRNA pathway. This inhibition of the inhibitor is what causes the toxin gene to be active, and the eggs to be poisoned. 

"Interestingly, this silencing pattern was observed to last for several generations, meaning that lack of licensing in one generation can even affect their great-grand-daughters. This is not the case in genomic imprinting, which gets reset in each generation. 

"The results from the Burga group cement the evolutionary link between parent-specific gene expression and host defence mechanisms, tracing the origins back to organisms that lack DNA methylation and canonical imprinting. Despite the differences between these processes in worms and mammals, the Burga group believes that the mechanism they described could represent an evolutionary first step for more advanced forms of inherited silencing. These more advanced forms of silencing ended up regulating the expression of the cell's endogenous genes, leading to the evolution of genomic imprinting."

Comment: this genome process is highly complex requiring very exact proteins to act in the rles they do. How did a chance evolutionary process find them among the morass of possible protein forms that might exist or be made to esist? Not by chance!

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1264 views

Specific protein chaperones are used:

https://phys.org/news/2024-03-protein-multicellular-evolution.html

"Researchers have discovered a mechanism steering the evolution of multicellular life. They identify how altered protein folding drives multicellular evolution.

***

"The study, published in Science Advances, puts the spotlight on the regulation of proteins in understanding evolution.

"'By demonstrating the effect of protein-level changes in facilitating evolutionary change, this work highlights why knowledge of the genetic code in itself does not provide a full understanding of how organisms acquire adaptive behaviors. Achieving such understanding requires mapping the entire flow of genetic information, extending all the way to the actionable states of proteins that ultimately control the behavior of cells," says Associate Professor Juha Saarikangas from the Helsinki Institute of Life...

***

"Researchers identified a non-genetic mechanism at the base of this new multicellular trait, which acts at the level of protein folding. The authors found that the expression of the chaperone protein Hsp90, which helps other proteins acquire their functional shape, was gradually turned down as snowflake yeast evolved larger, tougher bodies.

"It turns out Hsp90 acted as a critically-important tuning knob, destabilizing a central molecule that regulates the progression of the cell cycle, causing cells to become elongated. This elongated shape, in turn, allows cells to wrap around one another, forming larger, more mechanically tough multicellular groups.

"'Hsp90 has long been known to stabilize proteins and help them fold properly," explains lead author Kristopher Montrose, from the Helsinki Institute of Life Science, Finland. "What we've found is that slight alterations in how Hsp90 operates can have profound effects not just on single cells, but on the very nature of multicellular organisms."

"From an evolutionary perspective, this work highlights the power of non-genetic mechanisms in rapid evolutionary change.

"'We tend to focus on genetic change and were quite surprised to find such large changes in the behavior of chaperone proteins. This underscores how creative and unpredictable evolution can be when finding solutions to new problems, like building a tough body," says Professor Will Ratcliff from the Georgia Institute of Technology."

Comment: the fact that genes work through influencing protein folding, which changes the proteins' function, add to the layers of control in the genomes sphere of influences. Again, the article assumes evolution operates with purpose. This is not Darwinist theory, is it?

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1308 views

Old genes used in a different way:

https://mail.google.com/mail/u/0/#inbox/FMfcgzGxSHgkzbptQmvlbsKKRccQvqzp

"...when researchers propagated only the biggest yeast cells for thousands of generations, these single-celled fungi went from making snowflake-esque clusters “weaker than gelatin” to clumps “as strong as wood” and 20,000 times the size of initial flakes (see above). Partly to thank for this impressive transformation is the chaperone protein Hsp90, which helps fold other proteins into their proper shapes, they report.

***

"Georgia Institute of Technology evolutionary biologist William Ratcliff and colleagues originally set out to recreate the evolutionary origins of multicellular organisms in the lab. To do this, they cultured brewer’s yeast in tubes for some 3000 generations...
selecting only the largest ones. Within two months, their single-celled starters had become ‘snowflakes’: conjoined clusters of elongated cells. And these flakes got bigger and bigger until their branches began to tangle with one another, creating dense clumps that withstood mechanical testing as well as some varieties of wood.

***

"They found that the tougher yeasts—which evolved in five separate runs of the experiment—had dialed down the gene for Hsp90, making about 40% less of it. That had knock-on effects: Because Hsp90 stabilizes a protein called Csc28, 40% less Hsp90 resulted in 25% less Cdc28. And Cdc28 happens to be involved in telling the cell when to progress through certain stages of the cell cycle.

"All of this ultimately means that the yeast cells take longer to complete the process of budding into new cells—and during that delay, they grow, leading to the elongated shape. Intriguingly, neither the gene for Hsp90 nor the one for Cdc28 were mutated. Instead, the altered activity of a transcription factor was responsible for the morphological change. “We tend to focus on genetic change and were quite surprised to find such large changes in the behavior of chaperone proteins,” Ratcliff says . “This underscores how creative and unpredictable evolution can be when finding solutions to new problems, like building a tough body.” (my bold)

From the original paper:

https://www.science.org/doi/10.1126/sciadv.adn2706?utm_source=sfmc&utm_medium=email...

"Abstract
The evolution of multicellularity paved the way for the origin of complex life on Earth, but little is known about the mechanistic basis of early multicellular evolution. Here, we examine the molecular basis of multicellular adaptation in the multicellularity long-term evolution experiment (MuLTEE). We demonstrate that cellular elongation, a key adaptation underpinning increased biophysical toughness and organismal size, is convergently driven by down-regulation of the chaperone Hsp90. Mechanistically, Hsp90-mediated morphogenesis operates by destabilizing the cyclin-dependent kinase Cdc28, resulting in delayed mitosis and prolonged polarized growth. Reinstatement of Hsp90 or Cdc28 expression resulted in shortened cells that formed smaller groups with reduced multicellular fitness. Together, our results show how ancient protein folding systems can be tuned to drive rapid evolution at a new level of biological individuality by revealing novel developmental phenotypes." (my bold)

Comment: the complexity of the various levels of genetic controls is shown in this study. A simple change in controls of folding in chaperone proteins caused major phenotypical changes. No new mutations needed. We do not know how often this type of transcription alteration is used in creating new modified forms. What it does infer is how human are formed with only a catalog of 20,000+ genes by the possible interplay of varying gene expressions, by modification of transcription factors.

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1334 views

Molecular forks direct the action:

https://www.sciencemagazinedigital.org/sciencemagazine/library/item/15_march_2024/41803...

"DNA replication is initiated at multiple loci to ensure timely duplication of eukaryotic genomes. Sister replication forks progress bidirectionally, and replication terminates when two convergent forks encounter one another. To investigate the coordination of replication forks, we developed a replication associated in situ HiC method to capture chromatin interactions involving nascent DNA. We identify more than 2000 fountain-like structures of chromatin contacts in human and mouse genomes, indicative of coupling of DNA replication forks. Replication fork interaction not only occurs between sister forks but also involves forks from two distinct origins to predetermine replication termination. Termination associated chromatin fountains are sensitive to replication stress and lead to coupled forks–associated genomic deletions in cancers. These findings reveal the spatial organization of DNA replication forks within the chromatin context."

Comment: a highly technical article, impossible to edit. They discuss their findings in DNA repair of lesions. An example:

"'The human genome harbors numerous DNA-template lesions or replication barriers that stall replication forks. Moreover, in E. coli, blocking one fork causes a substantial reduction in the replication speed of the other fork. Therefore, it is possible that in mammalian cells, both coupled forks stall when either is impaired. In this context, we observed similar replication speeds for coupled forks. Upon DNA-template lesions, the replisome at the damaged strand may or may not disassemble from chromatin to create more space for DNA repair, whereas the other replisome can mark stalled replication forks and facilitate fork restart at the right position. However, upon global replication stress such as aphidicolin, it becomes more challenging for two failed coupled forks to restart DNA replication. In this context, the two ends of genomic deletions in cancers are distributed similarly around the centers of both types of fountains, implying that the coupled forks may collapse to induce DNA breaks simultaneously. Alternatively, it is also possible that incomplete DNA replication under global replication stress is induced by the disruption of fork coupling. The dual failure of coupled sister forks may be rescued by the firing of neighbor dormant origins, but origin-poor type-II fountains might lead to incomplete DNA replication under global replication stress. This feature is similar to CFSs and RDC genes. Of note, the overlap of type-II fountains and CFSs may also be attributable to the possibility that origin-poor regions support long stretches of type-II fountains and favor fountain detection."

Comment: Skim this and denying design in impossible.

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1264 views

New RNA functional forms found:

https://www.sciencemagazinedigital.org/sciencemagazine/library/item/05_april_2024/41859...

"A plethora of new types of noncoding RNAs have been discovered, including thousands of long noncoding RNAs (lncRNAs), many of which have no identified functions. Throughout this “RNA revolution,” one property of RNA has been thought to be constant: RNAs are shortlived molecules that turn over, unlike DNA, which is much more stable. On page 53 of this issue, Zocher et al. challenge that paradigm by showing that newly synthesized RNA labeled with 5-ethynyl uridine (EU) in early postnatal mice was still present in many brain cells 2 years later. The complex pattern of when and which cells are labeled suggests that EU that is incorporated into RNA in neural progenitor cells (NPCs) frequently remains in adult neurons. This suggests that a diversity of long and repeat-rich RNAs, collectively called long-lived RNAs (LL-RNAs), can be stable fixtures in postmitotic and quiescent neural cells.

"There have been decades of studies that demonstrate that the half-lives of mRNA range from minutes to hours, with relatively “stable” ribosomal RNA persisting for days. So how could LL-RNAs not have been found before? A key difference is that Zocher et al. examined RNA in mouse brains filled with postmitotic neurons, whereas most studies have examined proliferative cells. The prior studies show that RNA turnover is dynamically regulated to meet cellular demands. Thus, because RNAs are not subject to unrestrained ribonucleases (RNases), if they are structurally protected in nuclei, perhaps they can persist indefinitely.

"An important point is that the persistent EU label observed by Zocher et al. is distinctly nuclear. Why would this be, particularly because RNAs for protein production are in the cytoplasm? Answers to this question will require future research, but the authors provide one possibility focused on satellite RNAs, which are expressed from small tandem satellite repeats that form peri- and centromeric heterochromatin. Several studies have shown that brief transient satellite RNA expression in cycling cells plays a role in peri- and centromere structure in chromosomes. Zocher et al. report that satellite RNA is enriched in LL-RNAs and further suggest that it continually serves to maintain repressive chromatin modifications, particularly histone H3 lysine 27 (H3K27) methylation, on centromeric heterochromatin.

***

"Stable RNAs, potentially analogous to LL-RNAs, may have been found before. Evidence of long-lived structural RNAs in the nuclei of human cells was reported in 2014. The highly repetitive “junk” RNA of the genome, called CoT-1 RNA, was detected in human cells by in situ hybridization. CoT-1 RNA labeled euchromatin, not heterochromatin, and had unusual properties. CoT-1 RNA tightly localized in cis to the chromosome territory (unlike mRNAs), and the bright RNA territory remained unperturbed for 16 to 32 hours after transcriptional inhibition. Although there are caveats to the use of transcriptional inhibitors, the results suggested that CoT-1 RNA may be part of a protein-RNA nuclear scaffold (also known as the matrix), the existence of which was reported in earlier studies, although these results were debated.

"Recently, a more-selective procedure was developed to isolate highly insoluble nuclear RNAs that remain after robust extraction and deoxyribonuclease (DNAse) digestion and that cofractionate with architectural RNAs [X-inactive specific transcript (XIST) and nuclear paraspeckle assembly transcript 1 (NEAT1)], which have established roles in forming nuclear structures. The 15% of insoluble scaffold RNAs (scaffRNAs) that remained with XIST and NEAT1 RNAs were CoT-1 RNAs. Sequencing showed that scaffRNAs were largely long and repeatrich, primarily intron-rich pre-mRNAs, lncRNAs, and intergenic transcripts. There are strong similarities between these scaffRNAs and the EU-labeled LL-RNAs found by Zocher et al. Potentially relevant to LLRNA functions, the removal of scaffRNAs, by numerous different means, rapidly resulted in condensation of euchromatin and delocalized specific nuclear matrix proteins, which other studies further support regulate chromatin packaging."

Comment: sorry for the density of this summary article, which points out that RNA's are the workhorses of the genome. The known population of RNA's is now enormous. Which leads to the next obvious point: such complexity demands design.

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1266 views

Avoid making new telomeres:

https://www.the-scientist.com/keeping-telomeres-in-their-places-71791?utm_campaign=TS_N...

"Luckily, cells have developed a complex set of repair mechanisms to protect vulnerable DNA and fix damage so that the cell’s genomic instruction manual remains intact. Cells use homologous recombination to stitch double-stranded breaks (DSB) back together and the enzyme telomerase to cap exposed ends of a DNA strand with a repetitive DNA sequence called a telomere.

"However, if cells use the wrong repair mechanism for a given situation, it can be disastrous. For example, if telomerase tries to seal up a DSB, it can sever the chromosome, causing the cell to lose key genes. “The whole system falls apart,” said Titia de Lange, a cell biologist at Rockefeller University.

"Scientists have observed that this can happen in yeast and corn, but whether it occurred in humans remained a mystery until now. de Lange’s team has finally figured out just how rare this catastrophic event is in humans and how cells keep it in check. In a study published in Science, they revealed that while telomerase occasionally acts at DSB, the ataxia telangiectasia and Rad3-related (ATR) protein typically runs interference to give the cell a chance to repair these breaks.

***

"To figure out how the cells blocked telomerase from acting at DSB, de Lange’s team genetically inactivated many different enzymes and repair pathways to see if any of them repressed telomere formation. Eventually, they discovered the genomic guardian: ATR, a protein that senses DNA damage and triggers homologous recombination. When they inhibited ATR, the number of new telomeres nearly tripled.

***

"Much remains for de Lange and her team to reveal about ATR. Although they found that ATR represses telomerase, they don’t know how this happens. Arnoult said that she wonders whether there are other redundant pathways that can also influence telomere formation at DSB in other contexts. She pointed to other species where telomeres that form at DSB are a normal part of development.4,5 “Studying those species may give us clues of how they can do that very efficiently and why it's prevented in humans,” Arnoult said.

Comment: A view into how processes are controlled from making accidents. Making a telomere and thus putting an end on broken DNA at the wrong place destroys genes. ATR is the guiding force here. Now is a point to ponder. Did this defense develop because breaks happened early on, or was it designed from the beginning to avoid early loss of genes from brakes? Darwin-type unguided chance evolution could not have achieved this degree of controls. God's design of life requires this degree of freedom for active molecules creating a function. It must allow for mistake control. If this is how living biochemistry works, it must be the only way it can work.

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1209 views

Just posted:

https://evolutionnews.org/2024/05/are-guppies-examples-of-darwinian-macroevolution/

"...a series of beautiful experiments led by professor David N. Reznick, who captured guppies from the downstream pools (where predators are prevalent) and moved them upstream (where predators are rare). The experiments were designed to answer the following question: “How, why, and how fast does adaptive evolution happen in the real world?” (Reznick and Travis 2019) What Reznick’s team observed is that the guppies from the downstream pools underwent rapid transformations when placed into the new upstream environment. The transplants took longer to reach sexual maturity and got larger. But the rate at which this happened was surprisingly fast. When the team calculated the rate of evolution for these genetic changes, using a unit called the Darwin, they reported the guppies changed at a rate of 3,700 to 45,000 Darwins while most of the rates found in fossils are only 0.1 to 1.0 Darwins.

***

"According to the predation-driven selection hypothesis, the guppies grew larger when predation was relaxed. This suggests that in the downstream pools where predation is higher, the larger adults must be more at risk of being eaten than the smaller guppies. They came up with a way to mark individual guppies that would allow them to be recaptured, which facilitated Reznick’s team being able to calculate the death rates for adult and juvenile guppies. However, after collecting this data, they found that death rates were similar for these different sizes of guppies. This discovery showed that the cause of change could not be direct predation. So, what was causing the changes?

***

"Instead of direct predation affecting the guppies’ life history, the guppies exhibited density dependent selection which means the population density was affecting life history traits. In the upstream pools where there was lower predation, the populations grew larger which meant population density increased. This might also have a selection effect. To directly quote from their abstract: “We have shown that the agent of selection on the life history, behavior, and physiology in low-predation communities is high population density and the cascade of ecological effects that stems from it.” (Reznick and Travis 2019) In other words the purported mechanism is that when the population of guppies is dense, certain individuals harboring specific alleles have a reproductive advantage, leading to allele frequency changes in the population.

***

"This means the same allele frequency changes from one group of guppies from stream A were observed in a different group of guppies from stream B. This is not expected if such changes are due to random mutation (RM). (van der Zee et al. 2022) After all, what are the chances that RM would make the exact same changes over and over again?

"No new mutations were observed. Instead, the pre-existing allele frequency in the population shifted and this is hypothesized to be due to natural selection (NS) based on standing genetic variation. They say, “the rapid and repeatable evolution of life histories in six introduced populations means that this evolution was fueled by standing genetic variation rather than by new mutations.” This means the adaptive capacity was built into the population of the organism itself. There was no RM that did something new and helpful, that was then picked by the “agent” of NS.

***

"Reznick’s work shows that standing genetic variation was already baked in within the guppy population, leaving no role for random mutation. Because the variation was baked in, this places novelty-generation farther back in history, into a setting where there is less direct access to the environmental pressures that the variation is responding to. But wait, aren’t RM/NS both required for something to be considered evolution and an example of macroevolution?

"Identifying the origin of novelty-generation as random mutation is pivotal to providing an authentic instance of Darwinian macroevolution. Instead, what we have here is an example of how populations rapidly adapt using preexisting genetic variation. Thus, these results do not provide favorable evidence for Darwinian macroevolution. Instead, they demonstrate that a previously touted example of “evolution happening before our eyes” is merely an example of population dynamics. This is where preservation of genetic diversity amongst the population means that individuals within the population represent different optimizations for unique environments.

***

"This leaves us at a place where some questions have been resolved, but the most important persist. Random mutation (RM) has been eliminated as the cause for the rapid parallel changes in the guppies. Predatory-driven selection, a form of natural selection, has also been eliminated as a possibility. However, the outstanding question of where the standing genetic variation ultimately came from remains."

Comment: this paper shows us that the ability to make large variations is built into the DNA of a species. Certainly not macroevolution, but a reasonable explanation as to how species accomplish necessary changes without using new mutations

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1183 views

Next paper;

https://evolutionnews.org/2024/05/predictions-for-the-guppy-from-the-engineering-design...

"One hypothesis involves preservation of genetic diversity amongst the population, where diversity means that individuals within a population represent different optimizations for unique environments. Think of this scenario as a normal distribution where certain individuals in the population, who are not well suited for one environment (i.e., downstream), could thrive if placed in a different location (i.e., upstream) and gradually their alleles would become dominant in that environment.

***

"A second hypothesis is that there is a sensing mechanism, which in response to detected environmental inputs would trigger germline reprogramming. This relies on organisms sensing changes in the environment and triggering internal programming of allele frequency in the next generation, rather than natural selection (NS) based on standing genetic variation being the source of change. While a fully described mechanism of this nature has yet to be identified in living systems, there is some evidence supporting this hypothesis.

***

"Additionally, a recent study found substantial differences in germline mutation rates among three separate guppy families. These de novo mutations were shared among many siblings, indicating they occurred early in embryonic development. These findings are consistent with certain individuals within a population being programmed for adaptation, while others are not.

***

"What Separates Design/Engineering from Darwinian Macroevolution?
Some unique aspects which separate the design/engineering model from the evolutionary one are:

"Adaption is expected to be tightly regulated, targeted, and sometimes reversible, just like human-engineered tracking systems. Because of these features, adaptation is expected to be predictable.

"The organism, not the environment, exerts control over its adaptation.
The design of the organism determines what environmental stimuli the organism tracks and responds to.

"Environments do not possess agent-like capabilities of “selecting” which organisms will breed. The traits of organisms themselves are responsible.

"Organisms are problem-solving entities not passive objects being shaped by the environment.
Organism operational parameters have a limited range.

"Expanding that last point, for the guppy and all the other listed examples, the main design architecture of the organism remains unchanged despite the fact that a trait’s variability can be adjusted for optimum performance. The guppy can change and adapt like a well-engineered system, but at the end of the day, it is still a guppy."

Comment: a very different view of adaptability controlled by specific mechanisms in the DNA. It follows Shapiro's thinking. A designer could well have arranged this system. It is still within the species, not speciation.

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1222 views

Waiting to be fertilized, should not change:

https://www.quantamagazine.org/how-idle-egg-cells-defend-their-dna-from-damage-20240513/

"Out of all the cells in the body, oocytes are the most patient. The immature egg cells form inside a female’s body when she’s still a fetus in her mother’s womb, and then they wait in a quiescent state for years, if not decades. Cocooned inside ovaries, they pause, neither dividing nor replicating their DNA, so that one day they may pass along pristinely preserved genetic information to the next generation.

"Yet sitting quietly for year upon year without degrading is immensely challenging for cells. Dormancy may reduce the wear and tear on oocytes, but it also reduces their ability to repair the inevitable damage they sustain at the molecular level. Recently, in a study published in Cell, researchers discovered how mouse oocytes keep DNA safe from damaging proteins. The cells construct special compartments within themselves to temporarily sequester the proteins. Then, heeding a molecular signal, the storage units disperse all at once, practically vanishing along with their dangerous cargo. Thus cleaned, the oocyte is left to mature safely.

***

"Oocytes are long-lived, an uncommon trait among cells. A female human baby is typically born with 1 million to 2 million of them. Early in life, the cells are tiny and generally don’t do much — researchers often call them “idle.” But over time they get much bigger: During the first decade of life, human oocytes grow 64-fold — a “massive expansion” that demands a lot from the energy-producing cellular organelles called mitochondria, said Elvan Böke, a cell biologist at the Center for Genomic Regulation in Barcelona, Spain. The number of mitochondria in oocytes balloons from just a few thousand to hundreds of thousands.

"Having lots of mitochondria is normally risky for cells because their chemical activity generates toxic byproducts known as free radicals. But when Böke peered inside dormant human and frog oocytes, they weren’t overloaded with free radicals at all. As she reported in a Nature paper published in 2022, the oocytes’ mitochondria were doing something surprising: They were skipping the step in their energy-generating process that produces these dangerous molecules. This meant that they produced less energy overall; Böke speculated that they direct all the energy they do produce for growth. No other cell had been observed to do this.

***

"Because oocytes expand so massively and produce proteins so intensively during their growth period, Böke expected to see high protein activity in the two major pathways responsible for clearing aggregates. Instead, she saw less activity in immature oocytes than in mature egg cells.

“'It doesn’t make much sense,” she said. “Why would you put your degradative activity down if you’re going to grow and make lots of things?”

"It was because the oocytes weren’t degrading the damaging proteins — they were storing them to destroy later.

"When Böke and her team infused oocytes with a dye that illuminates protein aggregates, she saw the proteins clustered in large compartments. Probing further, she used electron microscopy to reveal these distinct storage units as super-organelles, which she named ELVAs, or endolysosomal vesicular assemblies. These pouchlike objects are composed of lysosomes — the cell’s waste-disposal organelles — and other protein-degrading machinery.

"In young oocytes, they are situated throughout the cytoplasm. Later, as oocytes mature, ELVAs fuse together, relocate and ramp up their degradative machinery. By the time an oocyte is fully mature, harmful protein aggregates are undetectable, and the ELVAs vanish, revealing a clean cytoplasm.

***

"For example, researchers have found that some long-lived stem cells also have ELVA-like components, which capture and store aggregates until the cells are ready to divide. Neurons, too, can develop triage centers, called aggresomes, for organizing misfolded proteins. However, neurons destroy their cellular detritus throughout their life spans, while oocytes store them and then wipe them out all at once. Böke speculated that the oocytes’ method is more energy-efficient: Since their mitochondria produce less energy overall, they need all of it for necessary growth to reach reproductive maturity."

Comment: we all see the concept here, protect myself until I am needed later. These cells show purposeful activity to fuel the concept. Chance mutations cannot do this. Only purposeful design fits.

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1162 views

Demonstrates importance:

https://www.wsj.com/public/resources/documents/jklT7uqz6jGqeF5D3CZe-WSJNewsPaper-6-28-2...

"Vertical descent from common ancestry is fundamental to our understanding of evolution.
Charles Darwin analogized the panoply of life to a tree with a thick, basilar trunk branching
out into numerous limbs, all connected through shared descent. Here is the master himself: “The affinities of all the beings of the same class have sometimes been represented by a
great tree. I believe this simile largely speaks the truth.”

"Phylogeny—the tracing of evolutionary relationships—relies on the tree metaphor, though Mr. Mindell is correct to draw attention to the simultaneous reality of horizontal networks. What animates “The Network of Life” is not a radical revision of our current understanding of biological interconnection or the mechanism of evolutionary change. The book instead offers an updated, more sophisticated appreciation of how some living things, some of the time,
exchange genes with members of the same generation. The most familiar example of horizontal gene exchange occurs when individuals of closely related species interbreed, producing hybrids and thereby introducing genes from one lineage into another. “Researchers are finding
hybridization among species to be much more common than previously thought,” Mr. Mindell writes. “Recent estimates are that roughly 25 percent of the world’s flowering plant species and 10 percent of animals have arisen through hybridization.”

"Introgression—the mixing of genes between species—has been revealed in human ancestry by the presence, in modern populations, of Neanderthal and Denisovan DNA. Mr. Mindell points to other cases of introgression, including between coyotes and gray wolves and between brown and polar bears. “All hybridization phenomena, including introgression,” he writes, “qualify as horizontal evolution, because genetic material is exchanged between different species, rather than between parents and offspring, the path of vertical evolution. They denote networking rather than branching.” Birds of a feather may flock together, but they do not literally give genes to one other—the actual exchange manifests in offspring. Thus inter-species hybridization still has a vertical component. A notable exception is recombination, a process that is widespread in bacteria, archaea and certain viruses. Among these opulations, individuals will occasionally connect, exchange genetic material and then go their separate ways: the equivalent of a one-night stand, with important consequences for human health.

***

"Mr. Mindell pays special attention to endosymbiosis, in which one tiny organism comes to
reside inside another, sometimes creating a merger. “Some of the most consequential innovations in life’s 3.8-billion-year history,” he writes, “stem from a joining of previously distinct lineages by endosymbiosis.” The process gave rise to mitochondria, the “energy owerhouses” of our cells, and to chloroplasts, the intracellular denizens that enable
plants to conduct photosynthesis.

"Mr. Mindell recognizes that the horizontal perspective does not supersede its vertical counterpart: “Horizontal evolution is often most reliably identified against abackdrop of vertical evolution. The two are complementary in revealing the complex patterns of relationships among lifeforms.” He argues that, compared with the conventional narrative, life should be envisioned “as a vast tangled system of streams, variously dividing, joining, meandering, and dividing again, as it carries and integrates species and their genes through time, with succeeding generations linked by
currents and networks of heritability.'”

Comment: we have seen all of this through the years. These mechanisms are part of the engine of evolution in its advances into increasing complexity.

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578 views

These are glycoRNA's:

https://phys.org/news/2024-08-unveiling-glycornas.html

"In a groundbreaking exploration of cell surface biology, Ryan Flynn has uncovered a surprising role for RNA outside the confines of the cell. Flynn's research, which focuses on the biology of cell surface RNA, led to the discovery that certain RNAs are chemically linked to glycans—complex carbohydrate polymers found on the cell surface.

***

"That discovery challenged the long-held notion that nucleic acids are restricted to the intracellular environment, revealing a previously unrecognized layer of complexity in cell surface biology.

"In new research published in Cell, Flynn and colleagues have discovered the mechanism of how RNA is chemically linked to N-glycans. Before this research, only proteins and lipids were known to be conjugated to glycans. Flynn's team has now added RNA to this list, a finding with important implications for understanding cellular biology.

***

"'In the 2021 paper, we found evidence that glycoRNAs can interact with immune receptors," he says. This suggests that glycoRNAs could be a crucial component in how the immune system recognizes and responds to cells, potentially influencing everything from pathogen detection to autoimmune responses.

"The presence of glycoRNAs on the cell surface could also have broader implications for cell-cell communication and signaling. As Flynn elaborated, "If you're trying to develop a mechanism understanding of why someone has autoimmunity, if you don't think about the RNA on the cell surface, you'll necessarily be missing something."

***

"'The goal of this is to stimulate more interest in glycoRNA biology and cell surface RNA biology," Flynn emphasizes. "This paper not only expands the understanding of RNA biology but has also opened up new possibilities for research into cell surface interactions and immune system function."

"As the scientific community begins to explore this uncharted territory, the impact of Flynn's research will likely drive new discoveries and potentially lead to novel therapeutic strategies."

Comment: The immune system becomes more and more complex.

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379 views

These structures seem very important:

https://www.sciencedaily.com/releases/2024/08/240829132437.htm

"Researchers map 50,000 of DNA's mysterious 'knots' in the human genome

"DNA is well-known for its double helix shape. But the human genome also contains more than 50,000 unusual 'knot'-like DNA structures called i-motifs, researchers at the Garvan Institute of Medical Research have discovered.

***

"'In this study, we mapped more than 50,000 i-motif sites in the human genome that occur in all three of the cell types we examined," says senior author Professor Daniel Christ, Head of the Antibody Therapeutics Lab and Director of the Centre for Targeted Therapy at Garvan. "That's a remarkably high number for a DNA structure whose existence in cells was once considered controversial. Our findings confirm that i-motifs are not just laboratory curiosities but widespread -- and likely to play key roles in genomic function."

"I-motifs are DNA structures that differ from the iconic double helix shape. They form when stretches of cytosine letters on the same DNA strand pair with each other, creating a four-stranded, twisted structure protruding from the double helix.

"The researchers found that i-motifs are not randomly scattered but concentrated in key functional areas of the genome, including regions that control gene activity.

"We discovered that i-motifs are associated with genes that are highly active during specific times in the cell cycle. This suggests they play a dynamic role in regulating gene activity," says Cristian David Peña Martinez, a research officer in the Antibody Therapeutics Lab and first author of the study.

***

"'The widespread presence of i-motifs near these 'holy grail' sequences involved in hard-to-treat cancers opens up new possibilities for new diagnostic and therapeutic approaches. It might be possible to design drugs that target i-motifs to influence gene expression, which could expand current treatment options," says Associate Professor Sarah Kummerfeld, Chief Scientific Officer at Garvan and co-author of the study."

Comment: our DNA with only 20,000 genes makes very complex humans. Only complexity like these forms can achieve the result. Nothing is unused or meaningless.

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342 views

Latest findings:

https://www.quantamagazine.org/cells-across-the-tree-of-life-exchange-text-messages-usi...

"For a molecule of RNA, the world is a dangerous place. Unlike DNA, which can persist for millions of years in its remarkably stable, double-stranded form, RNA isn’t built to last — not even within the cell that made it. Unless it’s protectively tethered to a larger molecule, RNA can degrade in minutes or less. And outside a cell? Forget about it. Voracious, RNA-destroying enzymes are everywhere, secreted by all forms of life as a defense against viruses that spell out their genetic identity in RNA code. (my bold)

"There is one way RNA can survive outside a cell unscathed: in a tiny, protective bubble. For
decades, researchers have noticed cells releasing these bubbles of cell membrane, called extracellular vesicles (EVs), packed with degraded RNA, proteins and other molecules.
But these sacs were considered little more than trash bags that whisk broken-down molecular
junk out of a cell during routine decluttering.

"Since then, a wealth of evidence has emerged supporting this theory, enabled by improvements in sequencing technology that allow scientists to detect and decode increasingly small RNA segments. Since Valadi published his experiments, other researchers have also seen EVs filled with complex RNA combinations. These RNA sequences can contain detailed information about the cell that authored them and trigger specific effects in recipient cells. The findings have led some researchers to suggest that RNA may be a molecular lingua franca that transcends traditional taxonomic boundaries and can therefore encode messages that remain intelligible across the tree of life.

"In 2024, new studies have exposed additional layers of this story, showing, for example, that
along with bacteria and eukaryotic cells, archaea also exchange vesicle-bound RNA, which confirms that the phenomenon is universal to all three domains of life. Another study has expanded our understanding of cross-kingdom cellular communication by showing that plants and infecting fungi can use packets of havoc-wreaking RNA as a form of coevolutionary information warfare: Ann enemy cell reads the RNA and builds self-harming protein with its own molecular
machinery.

***

"The microbiologist Susanne Erdmann recently found archaea enclosing RNA in life, which features cells built differently from bacteria or eukaryotes like us.n Because EVs are the same size and density as the virus particles Erdmann’s team studies at the Max Planck Institute for Marine nMicrobiology in Germany, they “always pop up nwhen you isolate and purify viruses, ” she said. Eventually, her group got curious and decided to peek at what’s inside. ncellular bubbles and dispatching it into the environment. Her discovery extended our
knowledge of this messaging ability to all three domains of life.

***

"That suggested to her that the RNA wasn’t ending up in the EVs by chance, and that the
process wasn’t just waste disposal. “It’s very unlikely that [archaea] use them for cell-to-cell communication, ” she said. “Why else would you invest so much energy in throwing out
random RNA in vesicles?”

***

"As a message, RNA is transient. This is a feature, not a bug: It can have only short-term
effects on other cells before it degrades. And since the RNA inside a cell is constantly
changing, n“the message that you can send to your neighboring cell” can also change very
quickly, Erdmann said. In that sense, it’s more like a quick text message or email meant to
communicate timely information than, say, runes etched in stone or a formal memo on
letterhead.

***

"However, its flexible backbone lets RNA fold into a number of shapes that can impact cell
biology. It can act as an enzyme to accelerate chemical reactions within cells. It can bind to DNA to activate or silence the expression of genes. And competing strands of RNA can
tangle up mRNA instructions in a process called RNA interference that prevents the production of new proteins.

***

"How can RNA from one branch of the tree of life be understood by organisms on another? It’s a common language, Buck said. RNA has most likely been around since the very beginning of life. While organisms have evolved and diversified, their RNA-reading machinery has largely stayed the same. “RNA already has a meaning in every cell, ” Buck said. “And it’s a pretty simple code.”

***

"To her knowledge, Jin said, this is the first time she’s seen evidence of organisms across
kingdoms exchanging mRNA messages and reading them into proteins. But she thinks it’s
likely to be seen in lots of other systems, once people start looking for it."

Comment: note my bold. This fragility of RNA makes it a very unlikely candidate to start life. On the other hand, it is amazing how useful it is. Another example for design.

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299 views

A new one described:

https://www.sciencedaily.com/releases/2024/10/241004121853.htm

"DNA damage response, or DDR for short, is the technical term for this. Specific signaling pathways usually initiate the immediate recognition and repair of DNA damage, thus ensuring the survival of the cell.

***

"The group has identified a new mechanism of the DNA damage response that is mediated via an RNA transcript. Their results help to broaden the conceptual view on the DNA damage response and to link it more closely with RNA metabolism.

***

"'In our study, we focused on so-called long non-coding RNA transcripts. Previous data suggest that some of these transcripts act as regulators of genome stability," says Kaspar Burger, explaining the background to the work. The study focused on the nuclear enriched abundant transcript 1 -- also known as NEAT1 -- which is found in high concentrations in many tumor cells. NEAT1 is also known to react to DNA damage and to cellular stress. However, its exact role in the DNA damage response was previously unclear.

"'Our hypothesis was that RNA metabolism involves NEAT1 in the DNA damage response in order to ensure the stability of the genome," says Burger. To test this hypothesis, the research group experimentally investigated how NEAT1 reacts to serious damage to the genome -- so-called DNA double-strand breaks -- in human bone cancer cells. The result: "We were able to show that DNA double-strand breaks increase both the number of NEAT1 transcripts and the amount of N6-methyladenosine marks on NEAT1," says the scientist.

***

"The experiments conducted by Kaspar Burger and his team show that the frequent occurrence of DNA double-strand breaks causes excessive methylation of NEAT1, which leads to changes in the NEAT1 secondary structure. As a result, highly methylated NEAT1 accumulates at some of these lesions to drive the recognition of broken DNA. In turn, experimentally induced suppression of NEAT1 levels delayed the DNA damage response, resulting in increased amounts of DNA damage.

"NEAT1 itself does not repair DNA damage. However, as the Würzburg team discovered, it enables the controlled release and activation of an RNA-binding DNA repair factor. In this way, the cell can recognize and repair DNA damage highly efficiently."

Comment: another very precise mechanism to aid in DNA repair. In separating chromosomes during cell splitting forces are acting and can cause tears. This is unlike a mistake in folding, thus another form of mistake as is the joining improperly of molecules. Living mistakes are or was the result of all these free-floating actions, upon which operational life begins.

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284 views

The real way it happens:

https://www.the-scientist.com/dna-polymerase-works-in-short-bursts-rather-than-one-long...

"...suggesting that DNA replication and proofreading involves multiple polymerases. Now, in a publication in Nature Communications, a team at Vrije University Amsterdam provided additional evidence that DNA polymerase does not replicate DNA as continuously as once believed.

***

"The researchers observed that, on average, a single DNA polymerase molecule remained bound to the nucleic acid at the junction for slightly more than one second—far from the continuous binding that most textbooks describe. Further contrasting from the dogma, during this time, a single enzyme only performed either extension or proofreading, occasionally also pausing on the DNA; rather than backing up to fix an error, the enzyme detached from the nucleic acid to let another bind.

“'The idea of having a motor that you put in reverse sounds very appealing to us, but it's much more efficient to throw the motor out,” Wuite explained. Unlike cars, a cell has multiple DNA polymerase motors, so an enzyme that is already in the configuration needed to bind the DNA and correct the error can take over. This exchange takes less energy than the same protein changing conformation to fulfill a different function.

"However, DNA polymerase’s activity appeared seamless and uniform, so the team considered that a process existed to help one enzyme pick up where another left off, acting like a memory. They analyzed one extension event and observed that polymerases unbound and rebound multiple times, but each time, they resumed the same function.

"To study this further, the team assessed the activity state—enzymatic or paused—before, during, and after a fluorescent polymerase bound the DNA over the course of several experiments. They found that the most common pattern was for the activity to be the same at all three observational points, whether the enzymatic period was during exonuclease repair or DNA extension.

“'This experiment is really the nail in the coffin of this model where everything is sitting stably on the DNA,” van Oijen said. He added that structural studies will be important for adding additional context to these mechanisms."

Comment: this adds much more complexity to the process of DNA copying with many more moving parts. Recognizing mistakes means the molecules carry a copy of what is expected as they read the new copy. As all of this is highly repetitive and exacting only design could produce it.

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250 views

Reduces repeated copying:

https://www.the-scientist.com/ovarian-proteins-that-last-a-lifetime-help-maintain-egg-c...

"In a recent study, Schuh and her team showed that cells in the mammalian ovary contain proteins with extremely long lives.1 The findings, published in Nature Cell Biology, shed light on the adaptations that help maintain oocytes with minimal damage throughout a female animal’s reproductive life and offer clues about fertility decline in aging ovaries.

“'Although the biology of extremely long-lived proteins in aging has been known for a while, this is the first paper to carefully characterize the nature and identity of those proteins in the ovary,” said Lei Lei, a reproductive biologist at the University of Missouri School of Medicine, who was not associated with the study. Making new proteins comes with the risk of making mistakes, which oocytes cannot afford to do, she added. “Because after all, you’re going to support a new life.”

***

"The long-lived proteins belonged to different cell components like mitochondria, ribosomes, and chromatin, and were involved in functions like metabolism and DNA repair.

"The ovary consists of cells other than oocytes, like stromal and thecal cells, that play essential roles in fertility. The team wondered whether these cells also housed long-lived proteins. They analyzed proteins from the ovaries of mice up to 15 months old, an advanced age for mice. Mathematical modeling showed that more than 10 percent of the proteins had a half-life of more than 100 days, with many persisting in the ovaries for most of the animals’ lives. In comparison, less than one percent of proteins in the cartilage, brain, and muscle had such long lives. These long-lived ovarian proteins have essential functions in structures like the mitochondria and cytoskeleton, and processes like protein homeostasis and chromatin maintenance. RNA sequencing revealed that aside from oocytes, a subset of somatic cells in the ovary also carried such long-lived proteins.

"The researchers next wondered how these proteins were able to persist for such a long time. To determine if altered protein homeostasis played a role, they tested whether aged oocytes contained aggregates of misfolded proteins. Microscopy revealed no such aggregates in aged oocytes. The researchers further confirmed that age did not reduce the activity of proteasomes—complexes that degrade misfolded proteins to maintain protein homeostasis in cells.

"Analyzing protein abundance in the ovaries showed enrichment of antioxidants and chaperones that help in protein folding, suggesting that proteins are maintained over long periods by preventing protein misfolding and protecting against oxidative damage.

***

"Mass spectrometry revealed that ovarian aging is associated with a reduction of many long-lived proteins. This causes an extensive remodeling of the ovarian protein landscape, which eventually leads to gradual fertility decline after the age of three months in mice.

"Finding long-lived proteins in the ovary was not entirely unexpected, said Schuh. “But that so many proteins persist for a very long time period, that was surprising,” she said. Her team has started looking into some of these long-lived proteins to understand why they do not degrade more often, and what the functional implications of their longevity are.

***

“'How [these results] relate directly to humans, we do not know yet,” agreed Schuh. However, she expects that human ovarian proteins would also be long-lived. Although it’s difficult to study this in people at the moment, she noted that, “expanding this to humans one day would be absolutely exciting.'”

Comment: this arrangement requires conceptual thought. It must be recognized that repeated copying results in errors. Darwin style evolution can't do that. Design can.

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211 views

Three proteins involved in the process:

https://www.sciencemagazinedigital.org/sciencemagazine/library/item/25_october_2024/422...

"Guided by its predictions, both have independently identified a complex of three proteins that sits on the head of a sperm and locks onto the surface of an egg cell during fertilization.

***

"In 2005, a team in Japan showed that deleting a particular gene in mice caused the animals to make healthy looking, motile sperm that nevertheless failed to fuse with egg cells. They named the gene Izumo1, after a Shinto shrine to marriage. Nearly a decade later, another group discovered a protein receptor on egg cells that bound to Izumo1, and named it Juno, after the Roman goddess of fertility. Others have found additional proteins: In 2020, for example, a team showed mice that had had their Spaca6 gene knocked out produced sperm with the same defects as rodents lacking Izumo1.

***

"In both teams’ studies, the AI program predicted the formation of a three-protein complex, or trimer, on sperm between Izumo1, Spaca6, and another known protein, Tmem81, which had not previously been associated with fertilization. In the eLife study, the team including Wright and led by structural biologist Luca Jovine at the Karolinska Institute analyzed mouse and human protein structures with the program and found the trimer could form a larger complex with Juno and another protein on egg cells called CD9.

"The other team, led by molecular biologist Andrea Pauli at the Research Institute of Molecular Pathology (IMP) at the Vienna Biocenter, went further and carried out experiments to see whether their AI-identified complex existed in the real world. They found that deleting the gene for Tmem81 in zebrafish and mice caused the same sperm defects as did deletions of Izumo1 or Spaca6, confirming this third protein was also critical for fertilization.

"The researchers also found that adding antibodies for Izumo1, Spaca6, or Tmem81 to samples of zebrafish sperm always pulled out all three proteins together, confirming they formed a trimer, as AI had predicted. “I think that was probably one of the happiest days in lab,” says Victoria Deneke, an IMP molecular biologist and co-author of the Cell paper. “It’s not a prediction … it’s actual experimental data.”

"Surprisingly, AlphaFold-Multimer also predicted—and experiments with zebrafish proteins subsequently supported— that different parts of this sperm trimer are responsible for binding to the distinctive receptors of mammalian versus zebrafish eggs. It’s remarkable that the sperm complex has stayed the same across vertebrate evolution whereas egg receptors have changed, Pauli says. The findings might reflect how eggs adapted to different environments—fish eggs are typically fertilized outside the animal, whereas mammalian eggs are fertilized within."

Comment: A complex of three proteins must be found by chance or the process is designed. Logically it is designed. especially considering the necesary eggv receptors.

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151 views

They make blood cells until you die:

https://www.the-scientist.com/how-stem-cells-stay-young-72321

"Aging is inevitable for most cell types in the human body, but hematopoietic stem cells (HSCs) seem to defy the process. They retain their self-renewing ability almost throughout an organism’s lifetime and exhibit a delayed onset of typical hallmarks of aging like DNA damage or protein aggregation. “Stem cells are really remarkable in their longevity,” said Andre Catic, a researcher working on aging at the Baylor College of Medicine.

"Previously, scientists found that one reason contributing to HSC longevity was that they could exist in a functionally inactive state for prolonged periods.1 Now, Catic and his team found another clue as to how these cells maintain their youth. In a study published recently in Nature Cell Biology, they reported that HSCs contain high levels of a protein cyclophilin A which prevents these cells from rapid aging.2 Understanding mechanisms of how HSCs avoid the wear and tear of senescence has wide-ranging implications, from figuring out cells’ fundamental anti-aging secrets to determining how these mechanisms breaking down could lead to leukemia.

***

"Curious as to why that’s the case, Catic and his team isolated stem and progenitor cells from the bone marrow of mice to see if there was something in their proteome. As aging in other cells is driven by proteins clumping together, they combed the proteome for mechanisms that could cause less protein aggregation or clear up existing protein clumps.

"That’s how they came across cyclophilin A, a chaperone that was highly expressed in these HSCs. The scientists found that aged HSCs had lower levels of cyclophilin A, and that genetically removing it from young HSCs accelerated their aging. They also showed that re-introducing cyclophilin A to older HSCs rejuvenated them and improved their functions. All the evidence pointed towards this chaperone playing a key role in the longevity of these stem cells.

“'What is interesting is that it's not one of those chaperones that is active at the back end of proteins’ lives,” said Catic. “Many chaperones, they help misfolded proteins, [they] refold them again, and get them back into solution, or they're involved in their degradation. Cyclophilin A is involved in the first step of protein synthesis.”

"Next, the team further investigated cyclophilin A to better understand its role in translation. When they checked what kinds of proteins it bound to, they found many RNA-binding proteins involved in ribosome assembly. Based on their findings, the scientists hypothesized that cyclophilin A was associated with ribosomes and inferred that it could be helping proteins fold as they come out of the ribosome.

"The team also found that this chaperone aided the synthesis of proteins filled with intrinsically disordered regions (IDRs). These indetermined structures within the proteins are also called floppy domains. As they don’t have a very fixed structure, such proteins can adopt whatever conformation is needed, according to Catic.

"An advantage of this flexibility is that these proteins can have multiple binding partners; they can act as scaffolding proteins that can bring together other proteins, RNA, and DNA to form complexes in the cell. “They help entire pathways come together, and that is why we believe they're important for so many basic processes such as splicing and translation,” said Catic.

"Catic believes that these intrinsically disordered proteins could be involved in many important cellular functions which help keep the stem cells healthy, which is why cyclophilin A promoting their translation is helpful for the stem cells’ longevity."

Comment: careful research has shown how these stem cells survive. How did this evolve? Not by chance. How does chance know in advance how long animals might live and need new blood cells? Obvoiusly it doesn't. Only chance can create this.

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37 views

A new study:

https://phys.org/news/2024-11-gene-results-extensive-regions-dna.html

"Some sequences in the genome cause genes to be switched on or off. Until now, each of these gene switches, or so-called enhancers, was thought to have its own place on the DNA. Different enhancers are therefore separated from each other, even if they control the same gene, and switch it on in different parts of the body.

"A recent study from the University of Bonn and the LMU Munich challenges this idea. The findings are also important because gene switches are thought to play a central role in evolution. The study has been published in the journal Science Advances.

"The blueprint of plant and animal forms is encoded in their DNA. But only a small part of the genome—about two percent in mammals—contains genes, the instructions for making proteins. The rest largely controls when and where these genes are active: how many of their transcripts are produced, and thus how many proteins are made from these transcripts.

"Some of these regulatory sequences, called "enhancers," work like dimmer switches used to modulate the light in our living room. Indeed, they specifically increase the expression of a particular gene, where and when this gene is required. Genes controlling morphology often respond to several independent enhancers, each determining the expression of the gene in a different body part.

***

"'We have taken a closer look at two of these enhancers," says Museridze.

"The first controls the formation of a color pattern on the wings, while the second controls the coloring of the head, thorax and abdomen. Both are active at the same time during the fly's metamorphosis. The team discovered that the body enhancer is not, as expected, located in a different region of DNA from the wing enhancer.

"Instead, there are extensive regions of DNA that belong to both gene switches, i.e. they influence the pigmentation of both the wing and the body.

"The results suggest that the architecture of regulatory sequences in the genome is much more complex than previously thought. This has far-reaching implications for how traits change during evolution. According to current knowledge, enhancers play a key role in this process.

"This is because many proteins are so important to an organism that a mutation in their gene (i.e., the DNA sequence that contains the instructions for building the protein) would cause serious problems or even certain death. As a result, genes that control body shape, such as the number of wings or legs, rarely change over the course of evolution. Enhancers offer a way out of this dilemma: when they mutate, the activity of the corresponding gene changes, but only in a specific tissue and at a specific time.

"'The cost of mutating an enhancer is therefore often lower than the cost of mutating the gene directly," says Mariam Museridze.

"This makes it easier for new traits to emerge during evolution. It is like baking a cake: If you mix eggs, flour, milk and sugar, you can get completely different types of dough, depending on the mixing ratio. In this metaphor, the enhancers would be responsible for the quantity of ingredients, not the type of ingredients.

"A genetic mutation is like accidentally replacing one ingredient with something completely different—for example, using sawdust instead of flour. The result will certainly not taste very good. A mutation in an enhancer, on the other hand, would change the amount of flour.

"'If enhancers are not as modular as we thought, this means that mutations in them can have much broader effects," says Museridze.

"This means that such a mutation could affect the amount of several ingredients at the same time. However, it is also possible that the enhancers retain their independence and continue to control the amount of a single ingredient, even though their sequences are interwoven and shared."

Comment: this is a clever way to control change, to modulate it through the enhancers. A mutation can have a variety of effects,

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Genome complexity: epigenetics (Introduction)

Genome complexity: epigenetics in plants

Genome complexity: epigenetics

Genome complexity: Shapiro on epigenetics

Genome complexity: Diet changes DNA

Genome complexity: Diet changes morphology

Genome complexity: alternative splicing

Genome complexity: alternative splicing

Genome complexity: Shapiro on epigenetics

Genome complexity: precise body plan

Genome complexity: rapid adaptation

Genome complexity: passing modifications

Genome complexity: passing modifications

Genome complexity: cells know what to do

Genome complexity: cells reading DNA

Genome complexity: gene expression

Genome complexity: gene expression

Genome complexity: squid epigenetics

Genome complexity: squid epigenetics

Genome complexity: squid epigenetics

Genome complexity: cells reading DNA

Genome complexity: DNA repair

Genome complexity: rapid functional recovery

Genome complexity: human epigenetics

Genome complexity: telomere function

Genome complexity: quantum jitters

Genome complexity: horizontal gene transfers

Genome complexity: how DNA coils and uncoils

Genome complexity: small RNA silences genes

Genome complexity: importance of epigenetics

Genome complexity: importance of epigenetics

Genome complexity: histones

Genome complexity: cells dump garbage

Genome complexity: educating T cells

Genome complexity: RNA polymerase

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Genome complexity: lesser species; Hunter questions

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Genome complexity: A code within a code?

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Genome complexity: A code within a code?

Genome complexity: A code within a code?

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Genome complexity: Mechanisms of DNA repair

Genome complexity: Controlling gene expression

Genome complexity: Repairing double-stranded DNA breaks

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Genome complexity: importance of epigenetics

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Genome complexity: epigenetics in action

Genome complexity: epigenetics in action

Genome complexity: epigenetics in action

Genome complexity: epigenetics in action

Genome complexity: epigenetics in action

Genome complexity: epigenetics in action

Genome complexity: epigenetics in action

Genome complexity: epigenetics in action

Genome complexity: epigenetics in action