Obvously, discoveries to come will show that things will get more and more complex; why are those RNA's sleeping?-http://phys.org/news/2012-08-cap-scientists-rna-phenomenon-dogma.html
Genome complexity
by David Turell , Wednesday, November 21, 2012, 15:02 (4386 days ago) @ David Turell
RNAzymes are non-coding RNA's that help with proper folding of newly made proteins.- http://phys.org/news/2012-11-rna-cooperation.html
Genome complexity
by David Turell , Friday, November 30, 2012, 04:41 (4378 days ago) @ David Turell
Long non-coding RNa seems to have function, but what? We will find out as research progresses.-http://www.biocompare.com/Editorial-Articles/122205-Long-Non-coding-RNAs/-Epigenetics marches on. goodbye neo-Darwiism.
Genome complexity
by David Turell , Sunday, December 09, 2012, 00:17 (4369 days ago) @ David Turell
it was obvious to me that the discovery of DNA and its coding for protein was just a tiny beginning of the complexity. We now have layers of codes upon codes and expression-of-genes systems galore. Just making protein doesn't tell us how the living cell really operates. Now in plants there are gene-expression non-transcription areas:- "Conserved noncoding sequences (CNSs) in DNA are reliable pointers to regulatory elements controlling gene expression. Using a comparative genomics approach with four dicotyledonous plant species (Arabidopsis thaliana, papaya [Carica papaya], poplar [Populus trichocarpa], and grape [Vitis vinifera]), we detected hundreds of CNSs upstream of Arabidopsis genes. Distinct positioning, length, and enrichment for transcription factor binding sites suggest these CNSs play a functional role in transcriptional regulation. The enrichment of transcription factors within the set of genes associated with CNS is consistent with the hypothesis that together they form part of a conserved transcriptional network whose function is to regulate other transcription factors and control development. We identified a set of promoters where regulatory mechanisms are likely to be shared between the model organism Arabidopsis and other dicots, providing areas of focus for further research."-http://www.plantcell.org/content/24/10/3949-And further commentary: -http://www2.warwick.ac.uk/newsandevents/pressreleases/discovery_of_100-The more complex, the less likely for chance, and the more likely a case for design.
Genome complexity
by hyjyljyj , Sunday, December 09, 2012, 13:57 (4369 days ago) @ David Turell
David: "The more complex, the less likely for chance, and the more likely a case for design."-That really is it in a nutshell, isn't it? -The more complex, the greater the number of bizarre coincidences occurring with flawless precision in type, location, magnitude and timing that we are expected to believe in, rather than believing in what's staring us in the face.-If it were only ONE single, giant, heaving coincidence bringing about life on Earth, for example, we MIGHT -- I say MIGHT -- be persuaded that it was just happenstance. When an unimaginable number of them are required just to make a single protein, and then another unimaginable number of them to get to the next level of organization, then another and another, at some point we get to ask, Are you kidding? Like the universe is just dying to create this insane level of order from chaos, against the gradient of entropy? Really? Then I guess I'll dump this box of spaghetti out of a helicopter and watch the noodles all fall to earth and stand vertically atop each other, end to end, stretching up into the sky. If the chance thing is true, then I ought to be able to get that comparatively simple, straightforward result in a ridiculously short time; it's not like I'm looking for the spontaneous generation of the first protein molecule or echidna. So once I stack them perfectly on my first or second try, then I'll go back up on my next flight, dump out another box and watch them spell out God Save the Queen. Because to those fully invested in Holy Random Chance as the Guiding Influence of the universe, there is, by definition, NO chain of events so unlikely that it would take more than 13.5 billion years to happen along.-(Wonder how much fuel I'd burn on repeat flights, as the noodles kept messing up and misspelling it: God Shave the Queen, then God Save the Queer, then Rod Gave Me Beer, then...)
Genome complexity
by David Turell , Sunday, December 09, 2012, 15:04 (4368 days ago) @ hyjyljyj
David: "The more complex, the less likely for chance, and the more likely a case for design."-> hy: If it were only ONE single, giant, heaving coincidence bringing about life on Earth, for example, we MIGHT -- I say MIGHT -- be persuaded that it was just happenstance. When an unimaginable number of them are required just to make a single protein, and then another unimaginable number of them to get to the next level of organization, then another and another, at some point we get to ask, Are you kidding?-What I have always wondered is, did the Lords of Evolution, those University Ph.D.s ever take organic chemistry in college and then carry that knowledge over to look at the complexity of one organic enzyme made up of humdreds of amino acids, folded just so? And now finding that there are several layers of translation so that enzyme can be altered to do several jobs, not just one.-Darwin thought cells were simple blobs of protoplasm. I am quite sure Charlie would not have presented his theory so simply if he had the knowledge we have today. But you are right, it doesn't dissuade his stary-eyed atheist followers.
Genome complexity; another layer
by David Turell , Tuesday, December 11, 2012, 16:11 (4366 days ago) @ David Turell
A new study on the ciradian cycles shows the epigenetic controls of the mouse liver:-"In the case of humans and other vertebrates, a brain structure called the suprachiasmatic nucleus controls circadian responses. But there are also clocks throughout the body, including our visceral organs, that tell specific genes when to make the workhorse proteins that enable basic functions in our bodies, such as producing glucose for energy. In the liver, genes that control the metabolism of fat and cholesterol turn on and off in sync with these clocks. But genes do not switch on and off by themselves. Their activity is regulated by the "epigenome," a set of molecules that signal to the genes how many proteins they should make, and, most importantly from the circadian point of view, when they should be made."- Read more at: http://medicalxpress.com/news/2012-12-epigenetic-daily-liver.html#jCp
Genome complexity; another layer
by David Turell , Tuesday, December 11, 2012, 18:39 (4366 days ago) @ David Turell
More complexity:-http://www.genomeweb.com/arrays/copy-machines- "Such early CNV [copy number variations] work, though, generally presumed that such variants were rare, deleterious events, usually linked to disease. This understanding, Lee says, held until 2004, when a pair of papers — one by Lee and his collaborators in Nature Genetics and another in Science by Cold Spring Harbor Laboratory researcher Michael Wigler and colleagues — appeared a week apart, both demonstrating that CNVs were widespread throughout the human genome and likely a significant source of natural genetic variation. "Prior to 2004, [copy number] gains and losses were thought to be very rare and associated with highly penetrant genomic disorders," Lee says. "It wasn't until 2004 [that] our group and the group of Mike Wigler published papers back to back showing that there are a lot of gains and losses in the human genome in healthy individuals."-And found in genetic diseases
Genome complexity; quick DNA repair
by David Turell , Friday, December 14, 2012, 01:09 (4364 days ago) @ David Turell
Quick is necessary as mitosis is quick. More complexity, of course:-http://phys.org/news/2012-12-team-mystery-dna.html
Genome complexity;timing copies
by David Turell , Saturday, December 29, 2012, 15:19 (4348 days ago) @ David Turell
When transcribing from DNA bits of the code are gradually stuck together, but thre is a pause before final instructions are given. That pause mechanism is now found:-http://darwins-god.blogspot.com/2012/12/here-is-how-genes-are-exquisitely-timed.html-Look at the graphical abstract:-http://www.cell.com/cell-reports/retrieve/pii/S2211124712004214?_returnURL=http://linkinghub.elsevier.com/retrieve/pii/S2211124712004214?showall=true#Summary-The complexity continues to build with each new discovery. God the designer, anyone!
Genome complexity; another code
by David Turell , Monday, January 21, 2013, 14:53 (4325 days ago) @ David Turell
Varying production of amino acids under stress:-"What we found was that if the bacteria are in an environment where they can grow and thrive, each synonymous codon produces the same amount of protein," Subramaniam said. "But the moment we put them in an environment where they are starved of an amino acid, some codons produce a hundredfold more proteins than others." The difference, he said, lay with molecules called transfer RNA, or tRNA, which ferry amino acids to the cellular machinery that manufactures proteins. "What we found was that some of these tRNA molecules are much more efficient at being loaded with amino acids, while others are less so," Subramaniam said. "If these tRNA molecules can't deliver the amino acid to where it needs to be, the cell cannot manufacture the proteins it needs. In an environment where amino acids are in short supply, that ability to hold onto them becomes very important." While the system helps cells to make certain proteins efficiently under stressful conditions, it also acts as a biological failsafe, allowing the near-complete shutdown in the production of other proteins as a way to preserve limited resources.- Read more at: http://phys.org/news/2013-01-hidden-genetic-code-key-differences.html#jCp
Genome complexity; 4 stranded DNA
by David Turell , Tuesday, January 22, 2013, 21:00 (4324 days ago) @ David Turell
Another way DNA acts:-http://www.scientificamerican.com/article.cfm?id=four-strand-dna-structure-found-cells&WT.mc_id=SA_DD_20130122
Genome complexity; lncRNA
by David Turell , Friday, January 25, 2013, 14:41 (4322 days ago) @ David Turell
Learn about long non-coding RNA. Found in junk DNA they are important in embryology. Thre are so many layers of coding in the genome, but it all happened by chance?-http://medicalxpress.com/news/2013-01-non-coding-rna-molecules-differentiation-embryonic.html
Genome complexity; Transcription factors
by David Turell , Monday, January 28, 2013, 15:57 (4318 days ago) @ David Turell
The reason we have so few genes is the multiplicity of transcription factors so genes can do many jobs at once. The higher the animal on the evolution bush, the more factors:-http://www.sciencedaily.com/releases/2013/01/130117133356.htm
Genome complexity; Embryology
by David Turell , Tuesday, January 29, 2013, 15:37 (4317 days ago) @ David Turell
Long non-coding RNA helps build organs. Here the heart is described:-http://phys.org/news/2013-01-epigenetic-cardiogenesis-non-coding-rna-essential.html
Genome complexity; gene expression
by David Turell , Monday, February 04, 2013, 15:54 (4311 days ago) @ David Turell
Gene control is so complex we cannot imitate it in the lab, but we can do simple things:-http://www.sciencedaily.com/releases/2013/02/130203145558.htm
Genome complexity; epigenetic gene expression
by David Turell , Monday, February 04, 2013, 18:26 (4311 days ago) @ David Turell
You tube presentation of epigenetic markkers changing expression:-http://www.youtube.com/watch?feature=player_detailpage&v=nygyUMODV7Y
Genome complexity; garbage removal
by David Turell , Thursday, February 07, 2013, 14:48 (4308 days ago) @ David Turell
Cells make proteins that must be destroyed; cells also make RNA's that guide processes and then must be destroyed or the cell will become so stuffed it won't function. There is a proteosome for proteins and an exosome for RNAs:-"The structure of this complex allowed the scientists to understand how the exosome works. "It is quite an elaborate machine: the exosome complex forms a hollow barrel formed by nine different proteins through which RNA molecules are threaded to reach a tenth protein, the catalytic subunit that then shreds the RNA into pieces," says Debora Makino. The barrel is essential for this process because it helps to unwind the RNA and prepares it for shredding. "Cells lacking any of the ten proteins do not survive and this shows that not only the catalytic subunit but also the entire barrel is critical for the function of the exosome," Makino explains." (my bold)-http://www.sciencedaily.com/releases/2013/02/130204094606.htm-This fits Behe's definition of 'irreducable complexity', a structure that cannot have evolved one protein step at a time.-Further these processes are found in Archaea and other bacteria, again showing how complex the original living cells had to be.
Genome complexity; chromosome protection
by David Turell , Thursday, February 07, 2013, 15:24 (4308 days ago) @ David Turell
:TRF2 is a complex protein with four functional domains (regions). Okamoto probed the specific functions of these four domains by creating artificial TRF2-like proteins—in which one or more functional domains were replaced with non-functional "dummy" domains. By studying how these artificial TRF2s functioned in cells, he could determine the separate functions of each individual domain."- Read more at: http://medicalxpress.com/news/2013-02-chromosomes-loose.html#jCp-Not a very simple protein. It keeps chromosomes separated.
Genome complexity; new study techniques
by David Turell , Friday, February 08, 2013, 15:46 (4307 days ago) @ David Turell
From electron microscopy with dyes and fluoressing molecules to holography!-http://www.sciencedaily.com/releases/2013/02/130207172205.htm
Genome complexity; epigenetics
by David Turell , Tuesday, February 12, 2013, 21:09 (4303 days ago) @ David Turell
A You tube video of the complexity involved in epigenetic adaptational controls which can lead to inheritable changes. This removes a major tenet of Darwinism that evolution is entirely at random and a chance mechanism that never implies purpose. Organisms can adapt and it may be purposeful most of the time. However, chance mutations do occur and must have some effect although most chance mutationsd have been found to be deleterious:-http://www.youtube.com/watch?feature=player_detailpage&v=52d5jWK1vdc-Science progress seems to be on God's side.
Genome complexity; epigenetics
by dhw, Thursday, February 14, 2013, 15:09 (4301 days ago) @ David Turell
DAVID: A You tube video of the complexity involved in epigenetic adaptational controls which can lead to inheritable changes. This removes a major tenet of Darwinism that evolution is entirely at random and a chance mechanism that never implies purpose. Organisms can adapt and it may be purposeful most of the time. However, chance mutations do occur and must have some effect although most chance mutations have been found to be deleterious:-http://www.youtube.com/watch?feature=player_detailpage&v=52d5jWK1vdc-Science progress seems to be on God's side.-If the speaker's monotone doesn't send you to sleep, this is stirring stuff! He seems to lay emphasis, though, on environmental stress as a major factor, and in your very helpful summary, David, you also emphasize adaptation. What interests me far more is innovation, and although we have no idea to what extent the two overlap, it seems to me that adaptation is more likely to preserve existing species, whereas innovation obviously leads to new ones. (By species, I don't mean varieties of, say, finch, but different organisms like elephants, eagles, ants, sharks, humans.) The speaker does mention macroevolution, but still talks of it being induced by the environment, which again suggests adaptation. That is why, in my amateur way, I keep pushing the idea that the mechanism for change ... whether adaptation or innovation ... has a built-in inventiveness which enables organisms not only to respond to stress for the sake of survival, but also to invent new organs that will take advantage of new environments. Without innovation, there can be no evolution!-You and I have agreed, David, that random mutations and gradualism are major weaknesses in Darwin's theory, and so I like the speaker's conclusion ... that we now need a theory that will combine Darwinian, Lamarckian and saltational processes. He also mentioned the vitally important element of "cooperation" (so he could have added Margulisian to his list). Well, how about "the intelligent genome"? It fits in with all that we know about evolution, and it appears to fit in with all the latest discoveries concerning genetics and epigenetics. You will quite rightly ask where the intelligence comes from (you always do!), but the focus here is on how evolution works, and that for me is an end in itself.
Genome complexity; epigenetics: Lamarck is back
by David Turell , Wednesday, June 01, 2016, 01:34 (3099 days ago) @ dhw
This essay makes some interesting remarks about Lamarck and epigenetics, and the problems Darwin adherents and atheists are having:-http://www.abc.net.au/radionational/programs/ockhamsrazor/descartes-to-dawkins-history-of-machine-living-things/7438002-"One important person to describe living things self-transforming machines was 18th century French naturalist, Jean-Baptiste Lamarck.-"You might have heard of Lamarck as a crackpot: the man who said that giraffes' long necks are due to reaching high-up fruit. You may also have heard that Darwin got rid of Lamarck's idea of the inheritance of acquired characteristics. But in fact that's not true at all. Darwin was very much influenced by Lamarck.-"In particular, Charles Darwin believed in the inheritance of acquired characteristics, or what he generally called the effects of use and disuse—for example, that moles eventually evolved to be blind on account of not using their eyes.-"In that sense, Darwin was very much a Lamarckian. So why did we all learn in high school biology class that Lamarck was crazy and Darwin got rid of all his crazy ideas?-"Lamarck's description of evolution as resulting from living organisms' own agency threatened God's monopoly on creation. In the wake of the French Revolution, this made Lamarck seemed like a very dangerous sort of Frenchman.-"Around the turn of the 20th century, Darwinists wanting to promote a strong and viable Darwinism started trying to eradicate every trace of Lamarckism.-***-"Weismann cut the tails off mice in order to show that their offspring had perfectly normal tails. He presented his findings as a definitive refutation of Lamarck. His mice continue to appear in biology textbooks as just that. -"But of course, they had no bearing on Lamarck's theory at all—since Lamarck believed, as I've said, that organisms transformed themselves by acts of will, by habits and behaviours.-"You could hardly call having your tail lopped off an act of will, a habit or a behaviour. -***-"Today's neo-Darwinists—people such as Richard Dawkins and Daniel Dennett—are really Weismannians (in fact, Dawkins has called himself an ‘extreme Weismannian').-"Even outside of evolutionary biology, some of the most influential thinkers and writers in biology and cognitive science today have adopted the Weismannian view that living organisms are essentially passive, made of dumb and inert mechanical parts.-"Cognitive scientist Steven Pinker is an example: he has written that the human mind can be reduced to ‘armies of idiots'—mindless sub-routines in the brain that merely do what they are programmed to.-"The idea that mind can be reduced to mindlessness and living agency to passive mechanical parts is a central tenet of the New Atheism movement.-***-"The engineering or design model of living nature, which they have all adopted, implies a designer. If you truly want to eliminate the designer, you need to naturalise his agency: allow the possibility that living nature has the agency to create and transform itself. (my bold)-***-"What's especially fascinating to me is that Lamarckism has been making a comeback in the last 10 or 15 years: biologists have been finding various ways in which changes in an individual organism can be inherited.-"The field of epigenetics is largely devoted to this. Epigenetics studies all the ways in which factors outside the DNA shape the way an organism is formed, and many of these epigenetic factors can change in heritable ways.-"In this sense, an organism might have agency with regard to its evolutionary destiny, just as Lamarck thought."-Comment: Note my bold. This is the crux of my discussion with dhw. We still don't know exactly how the epigenetic adaptations we see can lead to new species, if at all.
Genome complexity; epigenetics: Lamarck is back
by dhw, Wednesday, June 01, 2016, 13:22 (3099 days ago) @ David Turell
DAVID: This essay makes some interesting remarks about Lamarck and epigenetics, and the problems Darwin adherents and atheists are having:-http://www.abc.net.au/radionational/programs/ockhamsrazor/descartes-to-dawkins-history-...-Thank you for this revealing contribution to our debate. The quotes below make it very clear that so-called Darwin adherents have deliberately twisted Darwin's beliefs to fit in with their own. Shame on them. -QUOTES: "You might have heard of Lamarck as a crackpot: the man who said that giraffes' long necks are due to reaching high-up fruit. You may also have heard that Darwin got rid of Lamarck's idea of the inheritance of acquired characteristics. But in fact that's not true at all. Darwin was very much influenced by Lamarck. "In particular, Charles Darwin believed in the inheritance of acquired characteristics, or what he generally called the effects of use and disuse—for example, that moles eventually evolved to be blind on account of not using their eyes. "In that sense, Darwin was very much a Lamarckian. So why did we all learn in high school biology class that Lamarck was crazy and Darwin got rid of all his crazy ideas? "Lamarck's description of evolution as resulting from living organisms' own agency threatened God's monopoly on creation.”-Please note “own agency” - the active role organisms may play in their own evolution. The next quote provides a problem for your own theory: QUOTE: "Even outside of evolutionary biology, some of the most influential thinkers and writers in biology and cognitive science today have adopted the Weismannian view that living organisms are essentially passive, made of dumb and inert mechanical parts.”-This is also your own theistic view when you revert to your theory of divine preprogramming. According to that, all the “parts” can do is passively obey the instructions laid down for them by your God 3.8 billion years ago, or let themselves be dabbled with.-QUOTE: "The engineering or design model of living nature, which they have all adopted, implies a designer. If you truly want to eliminate the designer, you need to naturalise his agency: allow the possibility that living nature has the agency to create and transform itself." (David's bold) David's comment: Note my bold. This is the crux of my discussion with dhw. We still don't know exactly how the epigenetic adaptations we see can lead to new species, if at all.-Your bold is certainly true: if you want to eliminate the designer, you have to eliminate the designer. But allowing the possibility that organisms have the “agency” to transform themselves does not by any means eliminate the designer, since this still leaves wide open the question of how life began, and how organisms came to possess the “agency” to transform themselves. Your bold is not the crux of our discussion, because my hypothesis that evolution develops through the “agency” of the organisms themselves is NOT a means of eliminating the designer. It explains the higgledy-piggledy bush, and is an alternative to your hypothesis that your God preprogrammed or dabbled every innovation (and natural wonder) in the course of life's history for the purpose of “balancing nature” in order to produce and feed humans.
Genome complexity; epigenetics: Lamarck is back
by David Turell , Wednesday, June 01, 2016, 22:48 (3098 days ago) @ dhw
dhw: "Lamarck's description of evolution as resulting from living organisms' own agency threatened God's monopoly on creation.”[/i] > > Please note “own agency” - the active role organisms may play in their own evolution. The next quote provides a problem for your own theory: > > QUOTE: "Even outside of evolutionary biology, some of the most influential thinkers and writers in biology and cognitive science today have adopted the Weismannian view that living organisms are essentially passive, made of dumb and inert mechanical parts.” > > This is also your own theistic view when you revert to your theory of divine preprogramming. According to that, all the “parts” can do is passively obey the instructions laid down for them by your God 3.8 billion years ago, or let themselves be dabbled with.-That is not a problem for me, but it is for you. My problem with that assumption is I can't discern how God controls evolution whether by pre-programming, or dabbling or both, but I'm content that He is in control. > > QUOTE: "The engineering or design model of living nature, which they have all adopted, implies a designer. If you truly want to eliminate the designer, you need to naturalise his agency: allow the possibility that living nature has the agency to create and transform itself." (David's bold) > David's comment: Note my bold. This is the crux of my discussion with dhw. We still don't know exactly how the epigenetic adaptations we see can lead to new species, if at all. > > dhw: Your bold is certainly true: if you want to eliminate the designer, you have to eliminate the designer. But allowing the possibility that organisms have the “agency” to transform themselves does not by any means eliminate the designer, since this still leaves wide open the question of how life began, and how organisms came to possess the “agency” to transform themselves. Your bold is not the crux of our discussion, because my hypothesis that evolution develops through the “agency” of the organisms themselves is NOT a means of eliminating the designer. It explains the higgledy-piggledy bush, and is an alternative to your hypothesis that your God preprogrammed or dabbled every innovation (and natural wonder) in the course of life's history for the purpose of “balancing nature” in order to produce and feed humans.-Of course, your analysis is excellent, IF organisms can develop the evolutionary agency on their own. In my view they can't as in the essay. But my complexification theory explains the bush also, because it is a variation on your theme.
Genome complexity; epigenetics: Lamarck is back
by dhw, Thursday, June 02, 2016, 12:49 (3098 days ago) @ David Turell
QUOTE: "Even outside of evolutionary biology, some of the most influential thinkers and writers in biology and cognitive science today have adopted the Weismannian view that living organisms are essentially passive, made of dumb and inert mechanical parts.” Dhw: This is also your own theistic view when you revert to your theory of divine preprogramming. According to that, all the “parts” can do is passively obey the instructions laid down for them by your God 3.8 billion years ago, or let themselves be dabbled with.-DAVID: That is not a problem for me, but it is for you. My problem with that assumption is I can't discern how God controls evolution whether by pre-programming, or dabbling or both, but I'm content that He is in control.-Once again you are turning your back on the “free mechanism” you had accepted on Monday 30 May. However, all this highlights a basic contradiction in the essay you quoted: the author stated that Lamarck was dangerous in his time because his “description of evolution as resulting from living organism's own agency threatened God's monopoly on creation.” And yet he goes on to say that Darwinists and now neo-Darwinists (atheists) like Dawkins have tried to eradicate Lamarckism! As I see it, Lamarckism would actually help the atheist cause by adding purposeful change to random mutations, and so I can only assume that the opposition is purely scientific (lack of evidence) rather than agenda-driven. But since you say the subject creates problems for atheists, perhaps you can tell us their other objections. On the other hand, Lamarckism does not exclude the existence of God as the maker of the inventive mechanism, but it does create a challenge to your preprogramming theory. Epigenetics seems to be the new form of Lamarckism, and even you admit you don't know how far the process might extend - but that doesn't matter to you, because you are content that God either preprogrammed or dabbled every single innovation. dhw: Your bold is not the crux of our discussion, because my hypothesis that evolution develops through the “agency” of the organisms themselves is NOT a means of eliminating the designer. It explains the higgledy-piggledy bush, and is an alternative to your hypothesis […]. DAVID: Of course, your analysis is excellent, IF organisms can develop the evolutionary agency on their own. In my view they can't as in the essay. But my complexification theory explains the bush also, because it is a variation on your theme.-Your swift reversion to your God programming every complexity is not a variation on my theme at all. It is the exact opposite. All you are now saying is that the bush is higgledy-piggledy because God deliberately preprogrammed or dabbled every twig (just for the sake of complexity). I am saying it is higgledy-piggledy because (theistic version) God gave organisms the freedom to create their own complexities.
Genome complexity; epigenetics: Lamarck is back
by David Turell , Friday, June 03, 2016, 02:03 (3097 days ago) @ dhw
QUOTE: "Even outside of evolutionary biology, some of the most influential thinkers and writers in biology and cognitive science today have adopted the Weismannian view that living organisms are essentially passive, made of dumb and inert mechanical parts.” > Dhw: This is also your own theistic view when you revert to your theory of divine preprogramming. According to that, all the “parts” can do is passively obey the instructions laid down for them by your God 3.8 billion years ago, or let themselves be dabbled with. > > DAVID: That is not a problem for me, but it is for you. My problem with that assumption is I can't discern how God controls evolution whether by pre-programming, or dabbling or both, but I'm content that He is in control. > > dhw: Once again you are turning your back on the “free mechanism” you had accepted on Monday 30 May.... Epigenetics seems to be the new form of Lamarckism, and even you admit you don't know how far the process might extend - but that doesn't matter to you, because you are content that God either preprogrammed or dabbled every single innovation.-My mind is still mulling. I'm back on the complexity track today, as you will see. > > dhw: Your swift reversion to your God programming every complexity is not a variation on my theme at all. It is the exact opposite. All you are now saying is that the bush is higgledy-piggledy because God deliberately preprogrammed or dabbled every twig (just for the sake of complexity). I am saying it is higgledy-piggledy because (theistic version) God gave organisms the freedom to create their own complexities.-I'm agreeing with you. I like the idea of complexity for complexity's sake, with God's dabbling after the complexity appears, as He sees necessary.
Genome complexity; epigenetics: Lamarck is back
by David Turell , Thursday, August 17, 2017, 15:32 (2657 days ago) @ David Turell
Another essay on how important epigenetics is:
https://aeon.co/essays/on-epigenetics-we-need-both-darwin-s-and-lamarck-s-theories?utm_...
"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. Environmental factors such as temperature or emotional stress have been shown to alter DNA methylation, and these changes can be permanently programmed and inherited over generations – a process known as epigenetic transgenerational inheritance.
"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. The combination of DNA and histone together has been called ‘chromatin structures’ – and the coils, loops and twists in chromatin structures in response to environmental stress can permanently alter gene expression as well.
"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.
"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.
***
"In another recent study, we examined evolution on the macro-evolutionary scale – speciation. One of the classic examples of speciation involves Darwin’s finches in the Galapagos Islands. A group of finches radiated out from a single species to become 16 different species of varying size and with different traits such as altered beak structure. Our team and collaborators set out to examine the DNA from five of those distinct species. We observed DNA sequence mutations from one species to the next, but the epigenetic changes in DNA methylation (epimutations) were higher in number and more correlated with the phylogenetic (family tree) distance between the species. 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.
***
"Nearly all types of genetic mutations are known to have a precursor epigenetic change that increases the susceptibility to develop that mutation. We observed that direct environmental exposure in the first generation had epigenetic changes and no genetic mutations but, transgenerationally, an increase in genetic mutations was identified. Since environmental epigenetics can promote both trait variation and mutations, it accelerates the engine of evolution in a way that Darwinian mechanisms alone cannot.
***
"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,
***
"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: Lamarck lives. The author is an active research scientist in the field of epigenetics.
Genome complexity; epigenetics: Lamarck is back
by dhw, Friday, August 18, 2017, 13:36 (2656 days ago) @ David Turell
DAVID: Another essay on how important epigenetics is:
https://aeon.co/essays/on-epigenetics-we-need-both-darwin-s-and-lamarck-s-theories?utm_...
QUOTE: In another recent study, we examined evolution on the macro-evolutionary scale – speciation. One of the classic examples of speciation involves Darwin’s finches in the Galapagos Islands.
I am a convinced evolutionist, but I find this kind of vocabulary irritating because it glosses over the problem of the very word “speciation”. Darwin’s finches were variations, and the explanation for those variations is wonderfully logical. But it offers no explanation for the innovations necessary to make single cells develop into elephants, eagles, sharks and humans.
QUOTE: A unified theory of evolution should combine both neo-Lamarckian and neo-Darwinian aspects to expand our understanding of how environment impacts evolution.
I agree 100%, and the major question is what is the mechanism that enables organisms to respond to the environment not just by adaptation but also by innovation.
Genome complexity; epigenetics: Lamarck is back
by David Turell , Friday, August 18, 2017, 15:38 (2656 days ago) @ dhw
DAVID: Another essay on how important epigenetics is:
https://aeon.co/essays/on-epigenetics-we-need-both-darwin-s-and-lamarck-s-theories?utm_...
QUOTE: In another recent study, we examined evolution on the macro-evolutionary scale – speciation. One of the classic examples of speciation involves Darwin’s finches in the Galapagos Islands.
dhw: I am a convinced evolutionist, but I find this kind of vocabulary irritating because it glosses over the problem of the very word “speciation”. Darwin’s finches were variations, and the explanation for those variations is wonderfully logical. But it offers no explanation for the innovations necessary to make single cells develop into elephants, eagles, sharks and humans.
QUOTE: A unified theory of evolution should combine both neo-Lamarckian and neo-Darwinian aspects to expand our understanding of how environment impacts evolution.
dhw: I agree 100%, and the major question is what is the mechanism that enables organisms to respond to the environment not just by adaptation but also by innovation.
Yes, speciation is not explained. Epigenetics does not explain the big gaps in the fossil record.
Genome complexity; epigenetics: Lamarck is back
by David Turell , Wednesday, August 29, 2018, 20:04 (2279 days ago) @ David Turell
Peter Ward in a new book:
http://nautil.us/issue/63/horizons/why-the-earth-has-fewer-species-than-we-think
"More and more, biologists are discovering that organisms thought to be different species are, in fact, but one. A recent example is that the formerly accepted two species of giant North American mammoths (the Columbian mammoth and the woolly mammoth) were genetically the same but the two had phenotypes determined by environment.
"Epigenetics (or heritable epigenetics, or neo-Lamarckism) is a series of different processes that can cause evolutionary changes as well as dictate how organisms develop from a single fertilized egg (in the case of sexually reproducing organisms, at least) to what we look like as adults. Some say it’s just a minor tweak of already understood processes and that it’s of little importance in the broader scheme of evolutionary change or the past or even future history of life. But to others epigenetics, while still poorly understood, is potentially of far greater importance than mainstream evolutionary theory, and mainstream evolutionists have heretofore accepted that. To a few, its ongoing discovery is causing an unfolding scientific revolution. But the discoveries have not happened evenly among the many fields within what we call “biology.” The great breakthroughs have mainly been studies looking at cells, and the molecules within cells, including DNA and RNA and other aspects of genetics. But to date there has been little if any progress in tying epigenetic change to the many events evidenced by fossils and the fossil record."
Here’s where epigenetics differs from traditional Darwinian evolution:
"The second kind of epigenetic change causes unforeseen modification to an organism without altering the genetic coding for specific genes, but it also passes on these changes. It can cause change ranging from minor to profound, and can be heritable. “Lamarckian” change is where something encountered in its environment, and not necessarily expected in the life of an organism, causes chemical changes to the DNA through the addition of tiny molecules, or through a shape change of the scaffolding that holds the twisted DNA molecules in specific shapes. Other kinds of epigenetic change can also be caused by the actions of small RNA molecules responding to some kind of external environmental change. Peter Ward, “Why the Earth Has Fewer Species Than We Think”
Comment: This fits Tony's idea about species.
Genome complexity; epigenetics: Lamarck is back
by Balance_Maintained , U.S.A., Wednesday, August 29, 2018, 22:22 (2279 days ago) @ David Turell
Peter Ward in a new book:
http://nautil.us/issue/63/horizons/why-the-earth-has-fewer-species-than-we-think
"More and more, biologists are discovering that organisms thought to be different species are, in fact, but one. A recent example is that the formerly accepted two species of giant North American mammoths (the Columbian mammoth and the woolly mammoth) were genetically the same but the two had phenotypes determined by environment.
"Epigenetics (or heritable epigenetics, or neo-Lamarckism) is a series of different processes that can cause evolutionary changes as well as dictate how organisms develop from a single fertilized egg (in the case of sexually reproducing organisms, at least) to what we look like as adults. Some say it’s just a minor tweak of already understood processes and that it’s of little importance in the broader scheme of evolutionary change or the past or even future history of life. But to others epigenetics, while still poorly understood, is potentially of far greater importance than mainstream evolutionary theory, and mainstream evolutionists have heretofore accepted that. To a few, its ongoing discovery is causing an unfolding scientific revolution. But the discoveries have not happened evenly among the many fields within what we call “biology.” The great breakthroughs have mainly been studies looking at cells, and the molecules within cells, including DNA and RNA and other aspects of genetics. But to date there has been little if any progress in tying epigenetic change to the many events evidenced by fossils and the fossil record."
Here’s where epigenetics differs from traditional Darwinian evolution:
"The second kind of epigenetic change causes unforeseen modification to an organism without altering the genetic coding for specific genes, but it also passes on these changes. It can cause change ranging from minor to profound, and can be heritable. “Lamarckian” change is where something encountered in its environment, and not necessarily expected in the life of an organism, causes chemical changes to the DNA through the addition of tiny molecules, or through a shape change of the scaffolding that holds the twisted DNA molecules in specific shapes. Other kinds of epigenetic change can also be caused by the actions of small RNA molecules responding to some kind of external environmental change. Peter Ward, “Why the Earth Has Fewer Species Than We Think”
Comment: This fits Tony's idea about species.
It would explain point eggs...
--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.
Genome complexity; epigenetics: Lamarck is back
by David Turell , Thursday, August 30, 2018, 00:58 (2279 days ago) @ Balance_Maintained
Peter Ward in a new book:
http://nautil.us/issue/63/horizons/why-the-earth-has-fewer-species-than-we-think
"More and more, biologists are discovering that organisms thought to be different species are, in fact, but one. A recent example is that the formerly accepted two species of giant North American mammoths (the Columbian mammoth and the woolly mammoth) were genetically the same but the two had phenotypes determined by environment.
"Epigenetics (or heritable epigenetics, or neo-Lamarckism) is a series of different processes that can cause evolutionary changes as well as dictate how organisms develop from a single fertilized egg (in the case of sexually reproducing organisms, at least) to what we look like as adults. Some say it’s just a minor tweak of already understood processes and that it’s of little importance in the broader scheme of evolutionary change or the past or even future history of life. But to others epigenetics, while still poorly understood, is potentially of far greater importance than mainstream evolutionary theory, and mainstream evolutionists have heretofore accepted that. To a few, its ongoing discovery is causing an unfolding scientific revolution. But the discoveries have not happened evenly among the many fields within what we call “biology.” The great breakthroughs have mainly been studies looking at cells, and the molecules within cells, including DNA and RNA and other aspects of genetics. But to date there has been little if any progress in tying epigenetic change to the many events evidenced by fossils and the fossil record."
Here’s where epigenetics differs from traditional Darwinian evolution:
"The second kind of epigenetic change causes unforeseen modification to an organism without altering the genetic coding for specific genes, but it also passes on these changes. It can cause change ranging from minor to profound, and can be heritable. “Lamarckian” change is where something encountered in its environment, and not necessarily expected in the life of an organism, causes chemical changes to the DNA through the addition of tiny molecules, or through a shape change of the scaffolding that holds the twisted DNA molecules in specific shapes. Other kinds of epigenetic change can also be caused by the actions of small RNA molecules responding to some kind of external environmental change. Peter Ward, “Why the Earth Has Fewer Species Than We Think”
DAvid: Comment: This fits Tony's idea about species.
Tony: It would explain point eggs...
If only an epigenetic change in DNA can do it.
Genome complexity; epigenetics: Lamarck is back
by dhw, Thursday, August 30, 2018, 08:12 (2279 days ago) @ David Turell
QUOTE: The second kind of epigenetic change causes unforeseen modification to an organism without altering the genetic coding for specific genes, but it also passes on these changes. It can cause change ranging from minor to profound, and can be heritable. “Lamarckian” change is where something encountered in its environment, and not necessarily expected in the life of an organism, causes chemical changes to the DNA through the addition of tiny molecules, or through a shape change of the scaffolding that holds the twisted DNA molecules in specific shapes. Other kinds of epigenetic change can also be caused by the actions of small RNA molecules responding to some kind of external environmental change. Peter Ward, “Why the Earth Has Fewer Species Than We Think”
DAVID: This fits Tony's idea about species.
It fits the idea that environmental change is the trigger for organismal change, whether adaptation or innovation. I see no hint of advance planning here, or of new organisms suddenly appearing out of nowhere.
Genome complexity; epigenetics: Lamarck is back
by David Turell , Thursday, August 30, 2018, 18:02 (2278 days ago) @ dhw
QUOTE: The second kind of epigenetic change causes unforeseen modification to an organism without altering the genetic coding for specific genes, but it also passes on these changes. It can cause change ranging from minor to profound, and can be heritable. “Lamarckian” change is where something encountered in its environment, and not necessarily expected in the life of an organism, causes chemical changes to the DNA through the addition of tiny molecules, or through a shape change of the scaffolding that holds the twisted DNA molecules in specific shapes. Other kinds of epigenetic change can also be caused by the actions of small RNA molecules responding to some kind of external environmental change. Peter Ward, “Why the Earth Has Fewer Species Than We Think”
DAVID: This fits Tony's idea about species.
dhw: It fits the idea that environmental change is the trigger for organismal change, whether adaptation or innovation. I see no hint of advance planning here, or of new organisms suddenly appearing out of nowhere.
Advanced planning has evidence in a huge gap like the Cambrian Explosion. No explanation as yet for the Cambrian animals who appear out of nowhere
Genome complexity; epigenetics: Lamarck is back
by dhw, Friday, August 31, 2018, 13:42 (2278 days ago) @ David Turell
QUOTE: The second kind of epigenetic change causes unforeseen modification to an organism without altering the genetic coding for specific genes, but it also passes on these changes. It can cause change ranging from minor to profound, and can be heritable. “Lamarckian” change is where something encountered in its environment, and not necessarily expected in the life of an organism, causes chemical changes to the DNA through the addition of tiny molecules, or through a shape change of the scaffolding that holds the twisted DNA molecules in specific shapes. Other kinds of epigenetic change can also be caused by the actions of small RNA molecules responding to some kind of external environmental change. Peter Ward, “Why the Earth Has Fewer Species Than We Think”
DAVID: This fits Tony's idea about species.
dhw: It fits the idea that environmental change is the trigger for organismal change, whether adaptation or innovation. I see no hint of advance planning here, or of new organisms suddenly appearing out of nowhere.
DAVID: Advanced planning has evidence in a huge gap like the Cambrian Explosion. No explanation as yet for the Cambrian animals who appear out of nowhere.
You claimed that Lamarckian change, as quoted above, fitted Tony’s ideas about species. These include advance planning and new organisms appearing out of nowhere. I have simply pointed out that Lamarckian change, as quoted above, makes no mention of advance planning or of new organisms coming out of nowhere. So how does it fit Tony's ideas about species?
Genome complexity; epigenetics: Lamarck is back
by David Turell , Friday, August 31, 2018, 19:18 (2277 days ago) @ dhw
QUOTE: The second kind of epigenetic change causes unforeseen modification to an organism without altering the genetic coding for specific genes, but it also passes on these changes. It can cause change ranging from minor to profound, and can be heritable. “Lamarckian” change is where something encountered in its environment, and not necessarily expected in the life of an organism, causes chemical changes to the DNA through the addition of tiny molecules, or through a shape change of the scaffolding that holds the twisted DNA molecules in specific shapes. Other kinds of epigenetic change can also be caused by the actions of small RNA molecules responding to some kind of external environmental change. Peter Ward, “Why the Earth Has Fewer Species Than We Think”
DAVID: This fits Tony's idea about species.
dhw: It fits the idea that environmental change is the trigger for organismal change, whether adaptation or innovation. I see no hint of advance planning here, or of new organisms suddenly appearing out of nowhere.
DAVID: Advanced planning has evidence in a huge gap like the Cambrian Explosion. No explanation as yet for the Cambrian animals who appear out of nowhere.
dhw: You claimed that Lamarckian change, as quoted above, fitted Tony’s ideas about species. These include advance planning and new organisms appearing out of nowhere. I have simply pointed out that Lamarckian change, as quoted above, makes no mention of advance planning or of new organisms coming out of nowhere. So how does it fit Tony's ideas about species?
Ward's point is some species are really Lamarckian adaptations of existing species and therefore not a new species. Tony's 'staged advances' from existing forms is simply a similar thought pattern I think. The evidence for advanced planning lies in the Cambrian gap in phenotypes.
Genome complexity; epigenetics: Lamarck is back
by Balance_Maintained , U.S.A., Friday, August 31, 2018, 21:14 (2277 days ago) @ David Turell
QUOTE: The second kind of epigenetic change causes unforeseen modification to an organism without altering the genetic coding for specific genes, but it also passes on these changes. It can cause change ranging from minor to profound, and can be heritable. “Lamarckian” change is where something encountered in its environment, and not necessarily expected in the life of an organism, causes chemical changes to the DNA through the addition of tiny molecules, or through a shape change of the scaffolding that holds the twisted DNA molecules in specific shapes. Other kinds of epigenetic change can also be caused by the actions of small RNA molecules responding to some kind of external environmental change. Peter Ward, “Why the Earth Has Fewer Species Than We Think”
DAVID: This fits Tony's idea about species.
dhw: It fits the idea that environmental change is the trigger for organismal change, whether adaptation or innovation. I see no hint of advance planning here, or of new organisms suddenly appearing out of nowhere.
DAVID: Advanced planning has evidence in a huge gap like the Cambrian Explosion. No explanation as yet for the Cambrian animals who appear out of nowhere.
dhw: You claimed that Lamarckian change, as quoted above, fitted Tony’s ideas about species. These include advance planning and new organisms appearing out of nowhere. I have simply pointed out that Lamarckian change, as quoted above, makes no mention of advance planning or of new organisms coming out of nowhere. So how does it fit Tony's ideas about species?
David: Ward's point is some species are really Lamarckian adaptations of existing species and therefore not a new species. Tony's 'staged advances' from existing forms is simply a similar thought pattern I think. The evidence for advanced planning lies in the Cambrian gap in phenotypes.
Actually, it was more to the point that we are finding fewer 'kinds' and are still able to account for the programmatic variation in a mechanical way. Further, the interplay between genetic stability and epigenetic changes causing the bushy 'leaves' that hid the fact that there are only a few branches is far too complex to not have been designed.
DNA is incredibly complex and informationally dense. Epigenetics will likely prove to be incredibly complex and informationally dense as we understand it more. To have such incredible finesse and control, complete with safeguards and redundancies and repair systems is absolutely not possible by chance.
In the end, we will find periodic creation of flora and fauna in limited branches at the cusp of great atmospheric or geologic changes in which the arriving types play a significant roll in the further development of the earth, such as balancing CO2 and O2 and other gasses in the atmosphere, or perhaps bacteria creating oil resevoirs as a form of planetary lubricant to deal with the internal stresses caused by the start of plate tectonics.
I would lay even money that every single creature on this earth has some role, some fundamental function in the ongoing development of this planet. And that is something that CAN be tested.
--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.
Genome complexity; epigenetics: Lamarck is back
by David Turell , Friday, August 31, 2018, 23:54 (2277 days ago) @ Balance_Maintained
dhw: You claimed that Lamarckian change, as quoted above, fitted Tony’s ideas about species. These include advance planning and new organisms appearing out of nowhere. I have simply pointed out that Lamarckian change, as quoted above, makes no mention of advance planning or of new organisms coming out of nowhere. So how does it fit Tony's ideas about species?
David: Ward's point is some species are really Lamarckian adaptations of existing species and therefore not a new species. Tony's 'staged advances' from existing forms is simply a similar thought pattern I think. The evidence for advanced planning lies in the Cambrian gap in phenotypes.
Tony: Actually, it was more to the point that we are finding fewer 'kinds' and are still able to account for the programmatic variation in a mechanical way. Further, the interplay between genetic stability and epigenetic changes causing the bushy 'leaves' that hid the fact that there are only a few branches is far too complex to not have been designed.DNA is incredibly complex and informationally dense. Epigenetics will likely prove to be incredibly complex and informationally dense as we understand it more. To have such incredible finesse and control, complete with safeguards and redundancies and repair systems is absolutely not possible by chance.
In the end, we will find periodic creation of flora and fauna in limited branches at the cusp of great atmospheric or geologic changes in which the arriving types play a significant roll in the further development of the earth, such as balancing CO2 and O2 and other gasses in the atmosphere, or perhaps bacteria creating oil resevoirs as a form of planetary lubricant to deal with the internal stresses caused by the start of plate tectonics.
I would lay even money that every single creature on this earth has some role, some fundamental function in the ongoing development of this planet. And that is something that CAN be tested.
I agree with you. The balance between every individual in studies of eco-niches shows that top predators are a requirement, i.e., the wolves of Yellowstone. Everyone at every level has a role to play.
Genome complexity; epigenetics: Lamarck is back
by dhw, Saturday, September 01, 2018, 10:00 (2277 days ago) @ David Turell
dhw: You claimed that Lamarckian change, as quoted above, fitted Tony’s ideas about species. These include advance planning and new organisms appearing out of nowhere. I have simply pointed out that Lamarckian change, as quoted above, makes no mention of advance planning or of new organisms coming out of nowhere. So how does it fit Tony's ideas about species?
DAVID: Ward's point is some species are really Lamarckian adaptations of existing species and therefore not a new species. Tony's 'staged advances' from existing forms is simply a similar thought pattern I think.
That concerns the definition of species, which I think we have all agreed on now as referring to organisms which cannot interbreed. I thought you were referring to Tony’s ideas about species being planned and appearing out of nowhere, so I’m glad we’ve clarified the misunderstanding.
TONY: DNA is incredibly complex and informationally dense. Epigenetics will likely prove to be incredibly complex and informationally dense as we understand it more. To have such incredible finesse and control, complete with safeguards and redundancies and repair systems is absolutely not possible by chance.
Until we get a supporter of the chance theory to join us, there will be no discussion on this. The only open question is how design comes about.
TONY: In the end, we will find periodic creation of flora and fauna in limited branches at the cusp of great atmospheric or geologic changes in which the arriving types play a significant roll in the further development of the earth, such as balancing CO2 and O2 and other gasses in the atmosphere, or perhaps bacteria creating oil resevoirs as a form of planetary lubricant to deal with the internal stresses caused by the start of plate tectonics.
I would lay even money that every single creature on this earth has some role, some fundamental function in the ongoing development of this planet. And that is something that CAN be tested.
And how do you propose to test the fundamental function performed by the millions of life forms (root types and their variants) that have disappeared?
Genome complexity; epigenetics: Lamarck is back
by David Turell , Saturday, September 01, 2018, 15:25 (2277 days ago) @ dhw
dhw: You claimed that Lamarckian change, as quoted above, fitted Tony’s ideas about species. These include advance planning and new organisms appearing out of nowhere. I have simply pointed out that Lamarckian change, as quoted above, makes no mention of advance planning or of new organisms coming out of nowhere. So how does it fit Tony's ideas about species?
DAVID: Ward's point is some species are really Lamarckian adaptations of existing species and therefore not a new species. Tony's 'staged advances' from existing forms is simply a similar thought pattern I think.
dhw:v That concerns the definition of species, which I think we have all agreed on now as referring to organisms which cannot interbreed. I thought you were referring to Tony’s ideas about species being planned and appearing out of nowhere, so I’m glad we’ve clarified the misunderstanding.
TONY: DNA is incredibly complex and informationally dense. Epigenetics will likely prove to be incredibly complex and informationally dense as we understand it more. To have such incredible finesse and control, complete with safeguards and redundancies and repair systems is absolutely not possible by chance.
dhw: Until we get a supporter of the chance theory to join us, there will be no discussion on this. The only open question is how design comes about.
TONY: In the end, we will find periodic creation of flora and fauna in limited branches at the cusp of great atmospheric or geologic changes in which the arriving types play a significant roll in the further development of the earth, such as balancing CO2 and O2 and other gasses in the atmosphere, or perhaps bacteria creating oil resevoirs as a form of planetary lubricant to deal with the internal stresses caused by the start of plate tectonics.
I would lay even money that every single creature on this earth has some role, some fundamental function in the ongoing development of this planet. And that is something that CAN be tested.[/i]
dhw: And how do you propose to test the fundamental function performed by the millions of life forms (root types and their variants) that have disappeared?
Evolution implies replacement and in the case of evolution from simple to more complex
Genome complexity; epigenetics: Lamarck is back
by Balance_Maintained , U.S.A., Saturday, September 01, 2018, 23:03 (2276 days ago) @ David Turell
dhw: You claimed that Lamarckian change, as quoted above, fitted Tony’s ideas about species. These include advance planning and new organisms appearing out of nowhere. I have simply pointed out that Lamarckian change, as quoted above, makes no mention of advance planning or of new organisms coming out of nowhere. So how does it fit Tony's ideas about species?
DAVID: Ward's point is some species are really Lamarckian adaptations of existing species and therefore not a new species. Tony's 'staged advances' from existing forms is simply a similar thought pattern I think.
dhw:v That concerns the definition of species, which I think we have all agreed on now as referring to organisms which cannot interbreed. I thought you were referring to Tony’s ideas about species being planned and appearing out of nowhere, so I’m glad we’ve clarified the misunderstanding.
TONY: DNA is incredibly complex and informationally dense. Epigenetics will likely prove to be incredibly complex and informationally dense as we understand it more. To have such incredible finesse and control, complete with safeguards and redundancies and repair systems is absolutely not possible by chance.
dhw: Until we get a supporter of the chance theory to join us, there will be no discussion on this. The only open question is how design comes about.
TONY: In the end, we will find periodic creation of flora and fauna in limited branches at the cusp of great atmospheric or geologic changes in which the arriving types play a significant roll in the further development of the earth, such as balancing CO2 and O2 and other gasses in the atmosphere, or perhaps bacteria creating oil resevoirs as a form of planetary lubricant to deal with the internal stresses caused by the start of plate tectonics.
I would lay even money that every single creature on this earth has some role, some fundamental function in the ongoing development of this planet. And that is something that CAN be tested.[/i]
dhw: And how do you propose to test the fundamental function performed by the millions of life forms (root types and their variants) that have disappeared?
david Evolution implies replacement and in the case of evolution from simple to more complex
Start by testing the ones that are currently living. How does their lives, input and output, impact the environment.
--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.
Genome complexity; epigenetics: Lamarck is back
by David Turell , Sunday, September 02, 2018, 15:12 (2276 days ago) @ Balance_Maintained
.
TONY: In the end, we will find periodic creation of flora and fauna in limited branches at the cusp of great atmospheric or geologic changes in which the arriving types play a significant roll in the further development of the earth, such as balancing CO2 and O2 and other gasses in the atmosphere, or perhaps bacteria creating oil resevoirs as a form of planetary lubricant to deal with the internal stresses caused by the start of plate tectonics.
I would lay even money that every single creature on this earth has some role, some fundamental function in the ongoing development of this planet. And that is something that CAN be tested.[/i]
dhw: And how do you propose to test the fundamental function performed by the millions of life forms (root types and their variants) that have disappeared?
david: Evolution implies replacement and in the case of evolution from simple to more complex
David: Start by testing the ones that are currently living. How does their lives, input and output, impact the environment.
I've published here the wolves Yellowstone study of changes down to how it affected river sides vegetation .
Genome complexity; epigenetics: Lamarck is back
by dhw, Sunday, September 02, 2018, 09:17 (2276 days ago) @ David Turell
TONY: I would lay even money that every single creature on this earth has some role, some fundamental function in the ongoing development of this planet. And that is something that CAN be tested.
dhw: And how do you propose to test the fundamental function performed by the millions of life forms (root types and their variants) that have disappeared?
DAVID: Evolution implies replacement and in the case of evolution from simple to more complex.
Agreed. How will that enable us to test the fundamental function performed by the millions of life forms that have disappeared?
TONY: Start by testing the ones that are currently living. How does their lives, input and output, impact the environment.
I’ll look forward to your findings, Tony! And I’ll look forward even more to hearing how you plan to test the fundamental function of all the pre-historic organisms that disappeared because their fundamental function was no longer fundamental, and of all the organisms that have disappeared during the modern age.
Genome complexity; epigenetics: Lamarck is back
by David Turell , Sunday, September 02, 2018, 15:24 (2276 days ago) @ dhw
TONY: I would lay even money that every single creature on this earth has some role, some fundamental function in the ongoing development of this planet. And that is something that CAN be tested.
dhw: And how do you propose to test the fundamental function performed by the millions of life forms (root types and their variants) that have disappeared?
DAVID: Evolution implies replacement and in the case of evolution from simple to more complex.
Agreed. How will that enable us to test the fundamental function performed by the millions of life forms that have disappeared?
TONY: Start by testing the ones that are currently living. How does their lives, input and output, impact the environment.
dhw: I’ll look forward to your findings, Tony! And I’ll look forward even more to hearing how you plan to test the fundamental function of all the pre-historic organisms that disappeared because their fundamental function was no longer fundamental, and of all the organisms that have disappeared during the modern age.
Already seen in the wolves Yellowstone studies.
Genome complexity; epigenetics: Lamarck is back
by David Turell , Thursday, October 21, 2021, 21:06 (1130 days ago) @ David Turell
edited by David Turell, Thursday, October 21, 2021, 21:11
Poaching caused fenmale elephant tusk loss:
https://www.newscientist.com/article/2294549-female-african-elephants-evolved-to-lose-t...
"Female elephants in Mozambique rapidly evolved to become tuskless as a result of intense ivory poaching during the country’s civil war, even though one of the mutations involved kills male offspring.
"During the war, from 1977 to 1992, both sides hunted elephants for ivory, and the elephant population of Gorongosa National Park plummeted. Now an analysis of historical video footage and contemporary sightings by Shane Campbell-Staton at Princeton University and his colleagues has shown that the proportion of tuskless females rose from 19 to 51 per cent during the conflict, and a statistical analysis indicated this was extremely unlikely to have occurred in the absence of a selective pressure. The proportion of tuskless elephants has been declining since the war ended.
"This loss of tusks due to ivory hunting or poaching has happened in many other places too. For instance, in Sri Lanka less than 5 per cent of male Asian elephants still have tusks.
"Oddly, though, all male African elephants have retained their tusks despite the pressure of hunting. This appears to be the result of a genetic quirk.
"The team hasn’t yet found the precise genetic changes that cause tusklessness in females, but it appears two mutations are involved. One is probably in a gene on the X chromosome called AMELX, which plays a part in tooth formation.
"It appears this mutation also affects other, crucial genes nearby. Females have two copies of the X chromosome, so if one copy isn’t mutated, the genes it carries will still function normally and the elephant will still be healthy. But males have only one X chromosome, so this mutation is lethal to any males that inherit it.
"Much the same genetic condition can occur in people, says Campbell-Staton. Women with it lack upper lateral incisors – the equivalent of tusks – and male fetuses that inherit the mutation are usually lost in the third trimester."
Comment: Cutting off rat tails by August Weismann supposedly killed Lamarck's theory, so why is the same sort of event working now?
Genome complexity; communication along DNA
by David Turell , Wednesday, October 27, 2021, 22:16 (1124 days ago) @ David Turell
There are messages that travel along the spiral c hanging function:
https://wis-wander.weizmann.ac.il/chemistry/calling-through-dna-wire
"Proteins can communicate through DNA, conducting a long-distance dialogue that serves as a kind of genetic “switch,” according to Weizmann Institute of Science researchers. They found that the binding of proteins to one site of a DNA molecule can physically affect another binding site at a distant location, and that this “peer effect” activates certain genes. This effect had previously been observed in artificial systems, but the Weizmann study is the first to show it takes place in the DNA of living organisms.
"A team headed by Dr. Hagen Hofmann of the Chemical and Structural Biology Department made this discovery while studying a peculiar phenomenon in the soil bacteria Bacillus subtilis. A small minority of these bacteria demonstrate a unique skill: an ability to enrich their genomes by taking up bacterial gene segments scattered in the soil around them. This ability depends on a protein called ComK, a transcription factor, which binds to the DNA to activate the genes that make the scavenging possible. However, it was unknown how exactly this activation works.
***
"They found that when two ComK molecules bind to one of the sites, it sets off a signal that facilitates the binding of two additional ComK molecules at the second site. The signal can travel between the sites because physical changes triggered by the original proteins’ binding create tension that is transmitted along the DNA, something like twisting a rope from one end. Once all four molecules are bound to the DNA, a threshold is passed, switching on the bacterium’s gene scavenging ability.
“'We were surprised to discover that DNA, in addition to containing the genetic code, acts like a communication cable, transmitting information over a relatively long distance from one protein binding site to another,” Rosenblum says.
"By manipulating the bacterial DNA and monitoring the effects of these manipulations, the scientists clarified the details of the long-distance communication within the DNA. They found that for communication – or cooperation – between two sites to occur, these sites must be located at a particular distance from one another, and they must face the same direction on the DNA helix. Any deviation from these two conditions – for example, increasing the distance – weakened the communication. The sequence of genetic letters running between the two sites was found to have little effect on this communication, whereas a break in the DNA interrupted it completely, providing further evidence that this communication occurs through a physical connection.
“'Long-distance communication within a DNA molecule is a new type of regulatory mechanism – one that opens up previously unavailable methods for designing the genetic circuits of the future,” Hofmann says."
Comment: More magic in DNA, an amazing molecule with all sorts of hidden designed functions. Not by chance mutations
Genome complexity; fat control
by David Turell , Thursday, February 14, 2013, 15:10 (4301 days ago) @ David Turell
Long non-coding RNA (lncRNA) controls the production of fat cells:-http://medicalxpress.com/news/2013-02-noncoding-rnas-fat-cells.html#ajTabs
Genome complexity; gene expression
by David Turell , Monday, February 18, 2013, 15:58 (4297 days ago) @ David Turell
Long non-coding RNa controls gene expression. Important in fetal development; forms loops with DNA:-http://www.sciencedaily.com/releases/2013/02/130217134240.htm-"To discover how such enhancer-like RNAs function, the Shiekhatter laboratory deleted candidate molecules with known roles in activating gene expression, and assessed if they were related to RNA-dependent activation. They found that depleting components of the protein complex known as Mediator specifically and potently diminished the ability of ncRNA-a to start the process of transcribing a gene into RNA. Further, they found that these activating ncRNAs can attach to Mediator at multiple locations within the Mediator protein complex, and Mediator itself can interact with the enhancer element site on DNA that encodes these activating ncRNAs. Their results also determined how mutations in a protein that makes up the Mediator complex, called MED12, drastically diminishes Mediator's ability to associate with activating ncRNAs."-Yes, complexity
Genome complexity: Helicase speed
by David Turell , Thursday, February 21, 2013, 05:18 (4295 days ago) @ David Turell
The enzyme that unwinds DNA for replication or manufacture can spin up to 10,000 times a minute.-http://www.evolutionnews.org/2013/02/unwinding_the_d_1069371.html-"DNA helicase travels ahead of the replication fork, continuously opening and unwinding the DNA double helix to provide the template needed by the DNA Polymerase. With a rotational speed of up to 10,000 rotations per minute, the helicase rivals the rotational speed of jet engine turbines.'-Talk about a nanomachine!!
Genome complexity: RNA controls
by David Turell , Thursday, February 21, 2013, 15:32 (4294 days ago) @ David Turell
Destroying or organizing RNA in a cell is up to the exosome, a conplex set of organic molecules. Exactly how it works is not fully understood, but it exists in all forms of cellular life, conseved at all levels of evolution:-"Any errors that occur during the synthesis of RNA molecules or unwanted accumulation of RNAs can be damaging to the cell. The elimination of defective RNAs or of RNAs that are no longer needed are therefore key steps in the metabolism of a cell. The Exosome, a multi-protein complex, is a key machine that shreds RNA into pieces. In addition, the Exosome also processes certain RNA molecules into their mature form. However, the molecular mechanism of how the Exosome performs these functions has been elusive."- Read more at: http://phys.org/news/2013-02-macromolecular-shredder-rna-unravel-machinery.html#jCp
Genome complexity: a new RNA
by David Turell , Wednesday, February 27, 2013, 18:30 (4288 days ago) @ David Turell
Circular Rnas, very large, can control micro RNAs and reverse their function. Another very complex layer of gene expression controls.-http://www.nature.com/news/circular-rnas-throw-genetics-for-a-loop-1.12513?WT.ec_id=NATURE-20130228
Genome complexity: a new RNA
by David Turell , Monday, March 04, 2013, 18:12 (4283 days ago) @ David Turell
More info. A whole new level of gene regulation:-http://www.genomeweb.com//node/1199156?hq_e=el&hq_m=1518660&hq_l=1&hq_v=734b9bdc58-Circular RNA's are in various organs
Genome complexity: a new RNA, circular
by David Turell , Tuesday, August 01, 2017, 18:35 (2672 days ago) @ David Turell
Known about for many years but the function, if any is still unknown:
http://www.the-scientist.com/?articles.view/articleNo/49873/title/Uncovering-Functions-...
"Kadener’s work was published earlier this year,1 back-to-back in Molecular Cell with another group’s study—on human and mouse cells—that had simultaneously come to the same conclusion: translation of circRNAs can and does occur in living cells.2 For now, neither group has any hint of the function of these proteins, or of how common circRNA translation really is, but “you can imagine that it has some biological importance,” Kadener notes. RNA researcher William Jeck, currently a fellow at Harvard Medical School, agrees. Many scientists had “written off translation,” he says. “This is extremely exciting evidence that other circles may produce peptides that may be biologically relevant. . . . It’s really changed the paradigm.”
***
"Now, research on circRNAs is exploding, and the molecules’ biogenesis is gradually becoming clearer. At least two proteins, Muscleblind and Quaking, have been linked to circle formation, which generally occurs when the cell’s splicing machinery connects a downstream splice donor to an upstream splice acceptor, such as joining an exon’s 5´ end to its own 3´ end or an upstream exon’s 3´ end, in a process known as backsplicing. Recently, several additional mechanisms have been proposed (see “Making the Rounds” here), and some circRNAs contain introns, either instead of or in addition to exons. Regardless of their genetic makeup, the lack of ends makes circles less vulnerable to exonuclease enzymes, allowing them to persist in cells for days, unlike their linear counterparts, whose life spans are measured in hours or minutes.
"Despite a growing appreciation for the abundance—and now translation—of circRNAs in eukaryotes, there’s still very little understanding of what exactly circRNAs do. “We don’t even know how much of it is functional,” says Jeremy Wilusz, an RNA researcher at the University of Pennsylvania Perelman School of Medicine. “What’s the point of these circles? Why are they made?”
***
"CircRNAs also appear to associate with proteins, suggesting another suite of potential regulatory functions. For example, researchers recently showed that a circRNA produced by the Foxo3 gene (called circ-Foxo3) interacts with proteins involved in cell proliferation, including a key cyclin-dependent kinase and one of its inhibitors, suggesting a role in the cell cycle. And while most exon-containing circles accumulate in the cytoplasm, those that retain introns are often found in the nucleus, where they encounter proteins involved in transcription. In 2015, scientists in China showed that a group of exon-intron circRNAs promoted transcription of their parent genes via interaction with RNA polymerase II.10 Other studies have shown circles interacting with different RNA-binding proteins as well, including proteins now linked to circRNA biogenesis, such as Muscleblind and Quaking, and Argonaute proteins, well-known for their participation in RNAi-based gene regulation.
***
"Of course, how circRNAs come to be understood in the lab and possibly one day used in the clinic remains to be seen, as the study of these looped molecules represents an area that’s still young. But if the past five years are any indication, the study of circRNAs is rapidly ramping up. “What’s amazing to me is how fast this field has grown,” says Wilusz, whose lab supplies plasmids expressing circRNAs to other research groups and has recorded a dramatic uptick in requests in the last couple of years. “It’s really taking off.”
"Rajewsky, whose group is now focusing on circRNAs’ interactions in the brain, agrees that the best is very much ahead. “We’re really just at the beginning of an exciting journey,” he says. “It doesn’t happen often in molecular biology that you find such a fundamentally new phenomenon.'”
Comment: So far some hints of gene regulation, but the overall reason for circRNA is still not clear.
Genome complexity:cell controls of gene expression
by David Turell , Thursday, August 03, 2017, 18:04 (2670 days ago) @ David Turell
A new study shows how a newly found RNAi works. It is a giant molecule. Be sure to see the diagrams:
https://phys.org/news/2017-08-view-rnai-effect-repressing-gene.html
"Like other creatures, we humans depend on RNAi to fine-tune the expression of our genes. We could not survive without it.
"Today in Molecular Cell, a team led by structural biologist Leemor Joshua-Tor, an HHMI Investigator and professor at Cold Spring Harbor Laboratory (CSHL), publishes atomic-resolution pictures and a comprehensive analysis of the workings of a part of the RNAi machinery. Although much is already known about this machinery, important mysteries about its function have remained unsolved.
"The new discoveries pertain to the way several parts of the machinery come together and work in concert to tamp down gene expression. They can do this in various ways, but the new pictures are about one way in particular: events occurring after the attachment of the machinery to an RNA message (mRNA) copied from a gene. This association of the RNAi machinery and a gene's message is prelude to destruction of the message before it arrives at a cellular protein factory called the ribosome. When the machinery works properly in this mode, the protein never gets made.
"The primary component of the RNAi machinery is called RISC - the RNA-induced silencing complex. It contains two essential parts, a small RNA molecule called a microRNA (miRNA) which guides RISC to its mRNA target; and a much larger component into which the guide RNA fits, a protein called Argonaute, which, Joshua-Tor showed in 2004, actually performs the "slicing up" of the mRNA.
"Now Joshua-Tor's team has succeeded in showing how in humans, a protein called GW182 physically associates with RISC. It was known that there are three possible binding sites on GW182 for Argonaute. An atomic level view of one, called a hook motif, reveals a gate-like interaction. The pictures show that human Argonaute has a single binding site for GW182, and that binding of the guide sequence increases the affinity of the Argonaute and GW182.
"Showing that human GW182 can "multivalently" recruit up to three copies of Argonaute at once, experimenters in the lab led by first author Elad Elkayam suggest a possible source of synergy. "There may be greater efficiency in destroying the mRNA target, we speculate, because of 'crosstalk' between the RISC complexes and GW182," Joshua-Tor says."
Comment: This giant molecule is vital for life to control gene expression. It certainly looks designed, and I think it was.
Genome complexity: origins of DNA folding
by David Turell , Friday, August 11, 2017, 00:23 (2663 days ago) @ David Turell
Apparently all the way back to Archaea:
https://phys.org/news/2017-08-dna-archaea.html
"The archaeal DNA folding, described today in the journal Science, hints at the evolutionary origins of genome folding, a process that involves bending DNA and one that is remarkably conserved across all eukaryotes (organisms that have a defined nucleus surrounded by a membrane).
"Like Eukarya and Bacteria, Arachaea represent one of the three domains of life. But Archaea are thought to include the closest living relatives to an ancient ancestor that first hit on the idea of folding DNA.
"Scientists have long known that cells in all eukaryotes, from fish to trees to people, pack DNA in exactly the same way. DNA strands are wound around a 'hockey puck' composed of eight histone proteins, forming what's called a nucleosome. Nucleosomes are strung together on a strand of DNA, forming a "beads on a string" structure. The universal conservation of this genetic necklace raises the question of its origin.
"If all eukaryotes have the same DNA bending style, "then it must have evolved in a common ancestor," said study co-author John Reeve, a microbiologist at Ohio State University. "But what that ancestor was, is a question no one asked."
***
"The researchers revealed that despite using a single type of histone (and not four as do eukaryotes), the archaea were folding DNA in a very familiar way, creating the same sort of bends as those found in eukaryotic nucleosomes.
"But there were differences, too. Instead of individual beads on a string, the archaeal DNA formed a long superhelix, a single, large curve of already twisty DNA strands.
"In Archaea, you have one single building block," Luger said. "There is nothing to stop it. It's almost like it's a continuous nucleosome, really."
"This superhelix formation, it turns out, is important. When CU Boulder postdoctoral researcher Francesca Mattiroli, together with Thomas Santangelo's lab at Colorado State University, created mutations that interfered with this structure, the cells had trouble growing under stressful conditions. What's more, the cells seemed to not be using a set of their genes properly.
"'It's clear with these mutations that they can't form these stretches," Mattiroli said.
The results suggest that the archaeal DNA folding is an early prototype of the eukaryotic nucleosome.
"'I don't think there's any doubt that it's ancestral," Reeve said."
Comment: this is the best sort of evidence that evolution is a process of common descent. Archaea are the oldest of the three domains of life, and closest to original life forms.
Genome complexity: circular DNA in brains
by David Turell , Friday, August 11, 2017, 04:50 (2663 days ago) @ David Turell
It is not clear what they do:
https://phys.org/news/2017-08-circular-rna-linked-brain-function.html
"While hundreds of circular RNAs (circRNAs) are abundant in mammalian brains, one big question has remained unanswered: What are they actually good for?
***
"RNA is much more than the mundane messenger between DNA and the protein it encodes. Indeed, there are several different kinds of non-coding RNA molecules. They can be long non-coding RNAs (lncRNAs) or short regulatory RNAs (miRs); they can interfere with protein production (siRNAs) or help make it possible (tRNAs). In the past 20 years, scientists have discovered some two dozen RNA varieties that form intricate networks within the molecular microcosm. The most enigmatic among them are circRNAs, an unusual class of RNAs whose heads are connected to their tails to form a covalently closed ring. These structures had for decades been dismissed as a rare, exotic RNA species. In fact, the opposite is true. Current RNA-sequencing analyses have revealed that they are a large class of RNA, which is highly expressed in brain tissues.
***
"Intriguingly, most circular RNAs are unusually stable, floating in the cytoplasm for hours and even days on end. The systems biologists proposed that—at least sometimes - circRNAs serve gene regulation. Cdr1as, a large single-stranded RNA loop that is 1,500 nucleotides around, might act as a "sponge" for microRNAs. For example, it offers more than 70 binding sites for a microRNA called miR-7. MicroRNAs are short RNA molecules that typically bind to complementary sequences in messenger RNAs, thereby controlling the amounts of specific proteins produced by cells.
"Additionally, Rajewsky and his collaborators mined databases and discovered thousands of different circRNAs in nematode worms, mice and humans. Most of them were highly conserved throughout evolution. "We had found a parallel universe of unexplored RNAs," says Rajewsky. "Since publication the field has exploded; hundreds of new studies have been carried out."
"For the current paper in Science, the systems biologists teamed up with Carmen Birchmeier's lab at the MDC to reconsider Cdr1as. "This particular circle can be found in excitatory neurons but not in glial cells," says Monika Piwecka, one of the first authors of the paper and coordinator of most of the experiments. "In brain tissues of mice and humans, there are two microRNAs called miR-7 and miR-671 that bind to it." In a next step, Rajewsky and his collaborators selectively deleted the circRNA Cdr1as in mice using the genome editing technology CRISPR/Cas9. In these animals, the expression of most microRNAs in four studied brain regions remained unperturbed. However, miR-7 was downregulated and miR-671 upregulated. These changes were post-transcriptional, consistent with the idea that Cdr1as usually interacts with these microRNAs in the cytoplasm.
***
"The changes in microRNA concentration had dramatic effects on the mRNA and proteins produced by nerve cells, especially for a group called "immediate early genes." They are part of the first wave of responses when stimuli are presented to neurons. Also affected were messenger RNAs that encode proteins involved in the maintenance of the animals' sleep-wake cycles.
***
"'Functionally, our data suggest that Cdr1as and its direct interactions with microRNAs are important for sensorimotor gating and synaptic transmission," says Nikolaus Rajewsky. "More generally, since the brain is an organ with exceptionally high and diverse expression of circular RNAs, we believe that our data suggest the existence of a previously unknown layer of biological functions carried out by these circles.'"
Comment: the genome control gets more and more complex with more layers of control. It could be expected, as complex as the brain is, there are many layers of control over its plasticity.
Genome complexity: circular DNA in brains
by David Turell , Saturday, August 12, 2017, 01:03 (2662 days ago) @ David Turell
More work reported:
http://www.the-scientist.com/?articles.view/articleNo/50061/title/First-In-Vivo-Functio...
"Using mouse and human postmortem brains, the team showed that miR-7, and to a much lesser extent, another microRNA, miR-671, both bind to Cdr1as.
"Then, the researchers employed CRISPR-Cas9 to delete the locus in mice and create Cdr1as-deficient mutants. Although the knockout animals were outwardly normal—they were viable, fertile, and showed no obvious changes in brain anatomy—the team detected altered levels of free microRNA in areas of the brain where Cdr1as would normally have been expressed: miR-671 was slightly upregulated, while miR-7 levels were markedly lowered—a result that could reflect the circle’s role in preventing degradation of this microRNA by binding to it in wild-type animals, Rajewsky notes.
"Because microRNAs play a role in regulating messenger RNA, the researchers next looked for changes in gene expression in Cdr1as-deficient animals. They found that knockout mice showed altered expression of a set of genes associated with brain activity called immediate early genes—several of which have already been identified as targets of miR-7. “It’s known that neuronal activity is often marked by upregulation of immediate early genes,” Rajewsky says. In the brains of knockout mice, “it was very clear that immediate early genes, as a group, go up.”
"Consistent with this change in gene expression, the researchers found on closer inspection that mutant mice did indeed show abnormalities in neuronal activity. Among other things, single-cell analyses of neurons revealed that, compared to controls, knockout mice had more than double the frequency of miniature excitatory postsynaptic currents—a sign of disrupted neurotransmission.
"Finally, the team ran a suite of experiments to look for behavioral consequences of Cdr1as-deficiency. Although knockout mice exhibited normal anxiety levels and no obvious memory defects, the researchers found that the mutants performed poorly in prepulse inhibition experiments, which measure an animal’s ability to suppress a startle response to an aversive stimulus, such as a sudden loud noise, if a preceding, weaker version of the stimulus has already been played as a warning."
Comment: Just adding another layer of genome complexity in the brain. How much complexity must be shown in the layers of the genome before the need for a designer is recognized?
Genome complexity: controlling cell specificity
by David Turell , Tuesday, August 22, 2017, 22:30 (2651 days ago) @ David Turell
All cells have the same starting DNA with an allele from each parent, but not all alleles are expressed in different tissues. "Enhancer" areas in the DNA exert controls over the process of developing different functional tissues:
https://www.sciencedaily.com/releases/2017/08/170818092138.htm
"Every gene in (almost) every cell of the body is present in two variants -- so called alleles: one is deriving from the mother, the other one from the father. In most cases both alleles are active and transcribed by the cells into an RNA message. However, for a few genes, only one allele is expressed, while the other one is silenced. The decision whether the maternal or the paternal version is shut down occurs early in embryonic development -- one reason, why for long it was thought that the pattern of active alleles is nearly homogeneous in the various tissues of the organism.
"The new study (DOI:10.7554/eLife.25125), where CeMM PhD Student Daniel Andergassen is first author, uncovers a different picture. By performing the first comprehensive analysis of all active alleles in 23 different tissues and developmental stages of mice, the team of scientists revealed that each tissue showed a specific distribution of active alleles.
***
"The scientists found that both genetic and epigenetic differences between the maternal and paternal allele contributed to the observed tissue-specific activity patterns. "Our results indicate that a large part of those patterns are induced by so-called 'enhancers'," co-senior author Quanah Hudson, now at IMBA (Institute for molecular Biotechnology of the Austrian Academy of Sciences) explains. "Enhancers are DNA regions that are often located at quite some distance from the observed allele, but nevertheless have a direct influence on their activity."
"'This study reveals for the first time a comprehensive picture of all active alleles in different tissues -- we have uncovered the first complete allelome" Florian Pauler, now at ISTA (Institute of Science and Technology Austria) and co-senior author, adds.
***
"Some of the genes that contributed to the tissue-specific activity patterns were located on the X chromosome and escaped so-called "X-chromosome inactivation," where one of the two X chromosomes in females gets shut down. Previously it was reported that around 3% of X-chromosomal genes in mice and 15% in humans escape inactivation. However, this study revealed that mice are more similar to humans than previously thought, with an average of around 10% of active genes escaping X-inactivation per tissue. By examining a broad range of organs the researchers showed that the number of escapers varies dramatically between tissues.
***
"Finally, the allelome offers a near complete picture of "genomic imprinting," the process that leads to epigenetic silencing of either the maternal or paternal allele that is initiated by an epigenetic mark placed in either the egg or sperm. Previously, it was reported that approximately 100 genes can be subject to imprinted silencing -- but in many cases, the tissue specificity was not known. This study led to the discovery of 18 new imprinted genes, validated some known genes and resolved the disputed status of some others to provide a gold standard list of 93 imprinted genes in mouse. The scientists found that those new genes were located near to other imprinted genes, indicating that they were co -- regulated. Interestingly, this study demonstrated that Igfr2, the first imprinted gene discovered by Denise Barlow in 1991, is surrounding by a large cluster of imprinted genes that extend over 10% of the chromosome, making it the largest co-regulated domain in the genome outside of the X chromosome. Fittingly, after her lab found the first imprinted gene, and discovered the first imprinted non-coding RNA shown to control imprinted silencing."
Comment: DNA doesn't just make protein. It has to use these complex arrangements to specify cells and tissues in production. This is specified complexity, which cannot have happened by chance.
Genome complexity:a protein controls chromosomes
by David Turell , Friday, August 25, 2017, 00:56 (2649 days ago) @ David Turell
A specific protein has been found to control chromosomes and form the nucleus:
https://www.sciencedaily.com/releases/2017/08/170824124708.htm
"A protein that crosslinks the DNA to allow proper nuclear envelope reformation.
Every one of our cells stores its genome within the nucleus -- the quintessential subcellular structure that distinguishes eukaryotic cells from bacteria. When animal cells divide, they disassemble their nucleus, releasing individual chromosomes for proper segregation to daughter cells. At the end of cell division, the daughter cells reassemble a single nucleus around a complete set of chromosomes. The formation of a single nucleus is critical for the maintenance of genomic integrity. Individual chromosomes packaged into separate, small nuclei are prone to massive DNA damage, leading to mutations as well as chromosome rearrangement and loss.....how cells package their genome into just one nucleus has been a mystery.
"The Gerlich lab at the IMBA set out to solve this problem by screening for genes that are required to assemble a single nucleus in human cells. They uncovered "barrier-to-autointegration factor" (BAF), a multifunctional protein that binds DNA as well as many proteins. Without BAF, cells formed fragmented nuclei at the end of cell division. BAF was already known to link DNA to specific proteins at the nuclear membrane. Unexpectedly, Gerlich's lab discovered that nuclear assembly did not require BAF's association with nuclear membrane proteins. Instead, they found that BAF's ability to bind and bridge distant DNA sites was essential to shape a single nucleus.
"How does BAF's association with DNA regulate formation of the nucleus? The authors found that BAF forms a compact and mechanically stiff network with DNA. This created a coherent surface mesh around the set of chromosomes, which is impenetrable for nuclear membranes. This barrier prevents membranes from separately enwrapping individual chromosomes, and therefore guides the formation of a single nucleus.
"The work, published in the current issue of Cell, answers a fundamental question in biology and reveals an entirely unanticipated function for BAF. "Our findings suggest an entirely new role for DNA cross-bridging beyond genomic functions such as regulating gene expression and recombination, by forming boundaries and mechanical scaffolds of subcellular compartments. We are excited to further uncover the molecular mechanisms that shape mitotic chromosomes and control their interactions with other cellular components" says Gerlich."
Comment: Once again we see evidence of careful design. Cells constantly divide and the chromosomes must be carefully reproduced and packaged into a single nucleus. Evolved by chance, no way!
Genome complexity:cell controls of gene expression
by David Turell , Wednesday, August 30, 2017, 22:56 (2643 days ago) @ David Turell
Another control mechanism is discovered:
https://phys.org/news/2017-08-key-factor-gene-silencing.html
"Wang and colleagues describe a key role for a protein called RSF1 in silencing genes. Besides the molecular biology details, the researchers also showed that disruption of RSF1 expression in the embryos of African clawed frogs caused severe developmental defects in the tadpoles—through a dysregulation of mesodermal cell fate specification.
"RSF1 acts on chromatin, the organized structure of the chromosome where the 6-foot-long DNA of each human cell is highly condensed by wrapping around spools of histone proteins. Chromatin is not static, however—it is highly dynamic and changes in its structure to control different physiological processes.
"One contributor to chromatin fluidity is modifications of the histone proteins made by adding or removing chemical groups to the histone tails. The histones can be modified by acetylation, phosphorylation, methylation, ubiquitination or ADP-ribosylation.
"In his current work, Wang, an associate professor of biochemistry and molecular genetics in the UAB School of Medicine, focused on the addition of ubiquitin to the histone subunit H2A. This prevalent modification is linked to gene silencing, and removal of ubiquitin from H2A leads to gene activation. Wang and colleagues discovered that RSF1 mediates the gene-silencing function of ubiquitinated-H2A.
"They found that RSF1—which stands for remodeling and spacing factor 1, a subunit of the RSF complex—is a ubiquitinated-H2A binding protein that reads ubiquitinated-H2A through a previously uncharacterized and obligatory ubiquitinated-H2A binding domain.
"In human and mouse cells, the genes regulated by RSF1 were found to overlap significantly with those controlled by part of a complex that ubiquitinates H2A. Knockout of RSF1 in cells derepressed the genes regulated by RSF1, and this was accompanied by changes in ubiquitinated-H2A chromatin organization and release of linker histone H1.
"In the paper, Wang and colleagues proposed a model for the action of RSF1 in gene silencing.
"'RSF1 binds to ubiquitinated-H2A nucleosomes to establish and maintain the stable ubiquitinated-H2A nucleosome pattern at promoter regions," they wrote. "The stable nucleosome array leads to a chromatin architecture that is refractory to further remodeling required for ubiquitinated-H2A target gene activation. When RSF1 is knocked out, ubiquitinated-H2A nucleosome patterns are disturbed and nucleosomes become less stable, despite the presence of ubiquitinated-H2A. These ubiquitinated-H2A nucleosomes are subjected to chromatin remodeling for gene activation."
"Wang says knowledge of the ubiquitinated-H2A binding site may help in the discovery of other ubiquitinated histone-binding proteins. "
Comment: Ubiquitination does several things:
"The addition of ubiquitin to a substrate protein is called ubiquitination or less frequently ubiquitylation. Ubiquitination affects proteins in many ways: it can mark them for degradation via the proteasome, alter their cellular location, affect their activity, and promote or prevent protein interactions."
https://en.wikipedia.org/wiki/Ubiquitin
The complexity of these molecular controls is truly amazing and highly suggestive of design.
Genome complexity: 3-D DNA packing
by David Turell , Thursday, September 07, 2017, 05:35 (2636 days ago) @ David Turell
It is tightly packed in very short segments. Functional studies sow he following:
https://evolutionnews.org/2017/09/researchers-highlight-logistics-nightmare-facing-chro...
"What O’Shea’s team saw, in both resting and dividing cells, was chromatin whose “beads on a string” did not form any higher-order structure like the theorized 30 or 120 or 320 nanometers. Instead, it formed a semi-flexible chain, which they painstakingly measured as varying continuously along its length between just 5 and 24 nanometers, bending and flexing to achieve different levels of compaction. This suggests that it is chromatin’s packing density, and not some higher-order structure, that determines which areas of the genome are active and which are suppressed.
"We show that chromatin does not need to form discrete higher-order structures to fit in the nucleus,” adds O’Shea. “It’s the packing density that could change and limit the accessibility of chromatin, providing a local and global structural basis through which different combinations of DNA sequences, nucleosome variations and modifications could be integrated in the nucleus to exquisitely fine-tune the functional activity and accessibility of our genomes.”
"An entry in the Oxford Science Blog asks, “How does a cell know which combination of the 20,000 genes it should activate to produce its specific toolkit?” Look in the formerly named junk DNA for clues:
"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.
"Switches are not junk. To show that they have important functional roles, the team looked at one enhancer called CTCF.
"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.
“'Cells divide at least a billion times in the average person, usually without any problem.” Nevertheless, rare abnormalities do occur, as in the case with Down syndrome, when the wrong number of chromosomes (aneuploidy) results. ( my bold)
"Using high resolution microscopes to video the inner workings of live human cells, Dr Draviam and her colleagues at the University of Cambridge (UK) and the European Molecular Biology Laboratory in Heidelberg (Germany), discovered that two proteins — Aurora-B kinase and BubR1-bound PP2A phosphatase — act in opposition to each other, adding or removing phosphate groups respectively, to correctly control the attachment of microtubules to the chromosomes.
"Co-author Duccio Conti, who is Dr Draviam’s PhD student, said: “We found that a balance between Aurora-B kinase and BubR1-bound phosphatase is important to maintain correct chromosome numbers in human cells.'”
Comment: Packing DNA in a cell nucleus requires great complex compactification in order to give the right 3-D relationships for genes to be next to switches enhancers for proper expression of the genes. this is how 'Junk DNA' plays a major role, and obviously isn't junk. Obviously required design by God. Note my bold. The level of mistakes must be very small, but like a good designer, God recognized the need for backup corrective mechanisms to cover that possibility.
Genome complexity: 3-D DNA packing
by dhw, Thursday, September 07, 2017, 10:57 (2636 days ago) @ David Turell
QUOTE: “'Cells divide at least a billion times in the average person, usually without any problem.” Nevertheless, rare abnormalities do occur, as in the case with Down syndrome, when the wrong number of chromosomes (aneuploidy) results. ( DAVID’s bold)
DAVID: Note my bold. The level of mistakes must be very small, but like a good designer, God recognized the need for backup corrective mechanisms to cover that possibility.
There is no cure for Down’s syndrome.
Genome complexity: 3-D DNA packing
by David Turell , Thursday, September 07, 2017, 13:50 (2636 days ago) @ dhw
QUOTE: “'Cells divide at least a billion times in the average person, usually without any problem.” Nevertheless, rare abnormalities do occur, as in the case with Down syndrome, when the wrong number of chromosomes (aneuploidy) results. ( DAVID’s bold)
DAVID: Note my bold. The level of mistakes must be very small, but like a good designer, God recognized the need for backup corrective mechanisms to cover that possibility.
dhw: There is no cure for Down’s syndrome.
And there are many others, not as well known. What we have been given has never been completely perfect.
Genome complexity: bacterial gene fusion
by David Turell , Friday, September 08, 2017, 14:06 (2635 days ago) @ David Turell
A new study finds it helps with survivability and produces new protein:
https://phys.org/news/2017-09-bacteria-genes-fuse-production-proteins.html
"All organisms must continuously adapt to their environment in order to survive. Such adaptation is brought about by changes in their genetic material. Together with colleagues from New Zealand, Paul Rainey from the Max Planck Institute for Evolutionary Biology in Plön has been studying the emergence of new, better adapted cell types in the laboratory. The researchers have discovered that one mechanism by which bacteria can develop new characteristics is through the fusion of two existing genes. In some of the cells, this resulted in genes coming under the control of a new promoter, resulting in the synthesis of larger quantities of the protein encoded by the gene. In another case, two neighbouring genes fused together. The protein encoded by the resulting gene – composed of parts of the two original genes – has a different localization within the cell. This effect is also known from other organisms, including humans. A gene fusion of this type results in bacterial cells which are better adapted to their environment.
"Changes to the genetic code in existing genes – mutations – can equip an organism with new characteristics. Duplication of genes and the insertion of extra sections of DNA can also increase an organism's adaptability. Over the course of evolution, it is even possible for completely new genes to be created. This involves changes in previously non-functional stretches of DNA, which result in them becoming functional templates for protein synthesis. Another known mechanism of gene creation is the fusion of two genes, resulting in the production of a novel protein.
***
"According to Rainey and his colleagues, mat formation is caused by a variety of mutational changes in genes that regulate di-guanylate cyclase activity. These mutations switch off negative regulators causing the di-guanylate cyclases to assume an active state. When the researchers eliminated pathways subject to negative regulation they discovered a set of previously unknown mutations that caused the wrinkly mat-forming phenotype. In some of these, the di-guanylate cyclase gene had come under the control of a different promoter, resulting in increased di-guanylate cyclase production.
"In some wrinkly cells, however, the activity of this gene was unchanged. Analysis of the mutations in these cells showed that these mutants contained a chimeric gene formed from the di-guanylate cyclase gene and a neighbouring gene. The protein encoded by the latter is normally active in the cell membrane. "There must, therefore, have been a fusion event between two genes encoding proteins which are usually found at different locations within the cell," explains Rainey. The new protein possesses a membrane domain and is embedded in the cell membrane. This activates the protein, resulting in increased cellulose production.
"In other organisms too, proteins produced by gene fusions frequently end up having a different localization within the cell. In humans, for example, the Kua-UEV gene is the result of the fusion of the Kua and UEV genes. The new UEV protein now localizes to internal cell membranes and performs a new function. In humans, 64 percent of gene families for mitochondrial proteins contain a gene for a protein which is active elsewhere in the cell. "Although in our experiments gene fusion events made up only about 0.1 percent of mutations resulting in the wrinkly phenotype, outside the laboratory they may be more common," says Rainey."
Comment: This study supports Shapiro's work on bacteria manipulating their DNA. It does not explain the underlying mechanism which I think is existing informational instructions in the genome.
Genome complexity: waking sleeping ribosomes
by David Turell , Tuesday, September 12, 2017, 18:31 (2630 days ago) @ David Turell
Under stress bacterial ribosomes will become inactive to conserve energy. This is how they are awakened:
https://phys.org/news/2017-09-hibernating-ribosomes.html
"In research published in Proceedings of the National Academy of Sciences (PNAS), Mee-Ngan F. Yap, Ph.D., assistant professor of biochemistry and molecular biology at Saint Louis University, has uncovered the way a bacterial ribosome moves from an inactive to an active form, and how that "wake up call" is key to its survival.
"Often described as a cell's protein factory, ribosomes translate messenger RNA and link amino acids together to form new proteins. Ribosomes catalyze proteins that are essential for all life.
"In bacteria, ribosomes can take an inactive form called hibernating 100S ribosome. Because protein synthesis accounts for more than half of a cell's energy costs, the inactive ribosome form helps bacteria survive under stressful conditions. During limited nutrient access, antibiotic stress, host colonization, adaptation to the dark and biofilm formation, bacteria aim to conserve energy by shutting down the protein factory.
"Scientists have observed that the hibernating form of the ribosome is not a permanent state and that if conditions are favorable, it can "wake up" and return to its active form, called 70S, and begin to initiate new cycles of protein synthesis.
"'The 100S form is not held together forever," Yap said. "However, until now, the disassociation of 100S ribosome has been a complete black box. We haven't known how ribosomes move from one form to the other."
"Yap was looking for the protein factor that caused the 100S form to return to the intermediate 30S and 50S forms and subsequently into the active 70S form. Studying Staphylococcus aureus, commonly known as staph, Yap found that a GTP hydrolase enzyme called HflX is the wake-up call that will re-activate the ribosome.
"'HflX is one way to break up the 100S ribosome structure so that it can return to the active 70S form," Yap said.
"HflX GTPases are a family of enzymes that are evolutionarily conserved proteins, meaning they also exist in plants, humans and other bacteria. Yap is intrigued by this finding, because while there has been virtually no study of the protein in human cells, it appears in genetic sequencing mapped to cancer patients and those with neurological symptoms, including tic disorder-like syndromes. Scientists do not yet know what this connection means."
Comment: Logically, this entire protection system had to be developed in one step, the sleep and wake-up process available from the onset. It requires foresight and design from a planning mind.
Genome complexity: DNA repair two ways
by David Turell , Thursday, September 21, 2017, 17:27 (2621 days ago) @ David Turell
There is a slow and a fast repair:
http://www.salk.edu/news-release/right-way-repair-dna/
Is it better to do a task quickly and make mistakes, or to do it slowly but perfectly? When it comes to deciding how to fix breaks in DNA, cells face the same choice between two major repair pathways. The decision matters, because the wrong choice could cause even more DNA damage and lead to cancer.
Salk Institute scientists found that a tiny protein called CYREN helps cells choose the right pathway at the right time, clarifying a longstanding mystery about DNA repair.
***
Double-strand breaks, the most serious injuries that happen to DNA, can be repaired by one of two pathways: a fast but error-prone process known as NHEJ (non-homologous end joining) and a slower, error-free pathway known as HR (homologous recombination). The faster pathway efficiently rejoins broken strands, but in the case of multiple breaks it can join the wrong two ends together, making things much worse for a cell. The slower pathway is error-free because it relies on having an undamaged DNA sequence to guide the repair, but this means it can only operate after a cell has copied its genetic information in order to divide. Given that, the fast pathway operates exclusively before DNA is copied, though its machinery is so efficient and prolific that scientists have wondered why it doesn’t outcompete the slower, more-exact pathway after copying, too. Scientists have long suspected that something must be holding the faster option back in those cases.
That something, the new work reveals, is a microprotein called CYREN, which inhibits the faster pathway when a DNA copy is available for the slower pathway to use. CYREN was discovered by another Salk scientist, Alan Saghatelian, as part of a 2015 effort to identify small proteins called “short ORF-encoded peptides” or SEPs, which are increasingly being found to have critical biological roles.
***
The Salk team ... found that with CYREN present, no repairs occurred after the cell copies its DNA, suggesting that it does flip off the master switch, Ku. Without CYREN around, Ku’s fast pathway was active both before DNA was copied and after.
***
These experiments revealed that CYREN directly attaches to Ku to inhibit the fast pathway both depending on timing (before or after DNA copying) and the type of DNA break (smooth versus jagged, for example). Its activity can even tune the ratio of fast to slow repairs.
“Our study shows that CYREN is an important regulator of DNA-repair-pathway choice,” says Karlseder, who holds the Donald and Darlene Shiley Chair at Salk.
Comment: accurate DNA repair is essential for life to continue to exist in proper forms. Dividing cells do make decisions as this research shows, safely going slow when DNA is well organized. This is obviously an automatic system which depends on the status of DNA organization. Too complex to be developed by chance.
Genome complexity: 3-D DNA football controls
by David Turell , Wednesday, September 27, 2017, 14:56 (2616 days ago) @ David Turell
Very sophisticated molecular techniques have found controlling 'footballs' of transcription factors that fit in tightly packed DNA to speed reaction times:
https://phys.org/news/2017-09-scientists-genes-nano-footballs.html
"Crucially, they discovered that transcription factors operate not as single molecules as was previously thought, but as a spherical football-like cluster of around seven to ten molecules of roughly 30 nanometres in diameter.
***
"'We had no idea that we would discover that transcription factors operated in this clustered way. The textbooks all suggested that single molecules were used to switch genes on and off, not these crazy nano footballs that we observed."
"The team believe the clustering process is due to an ingenious strategy of the cell to allow transcription factors to reach their target genes as quickly as possible.
"Professor Leake said: "We found out that the size of these nano footballs is a remarkably close match to the gaps between DNA when it is scrunched up inside a cell. As the DNA inside a nucleus is really squeezed in, you get little gaps between separate strands of DNA which are like the mesh in a fishing net. The size of this mesh is really close to the size of the nano footballs we see.
"'This means that nano footballs can roll along segments of DNA but then hop to another nearby segment. This allows the nano football to find the specific gene it controls much more quickly than if no nano hopping was possible. In other words, cells can respond as quickly as possible to signals from the outside, which is an enormous advantage in the fight for survival.'"
Comment: Life's processes run at very high speed. This 3-D arrangement is logical planning to help get that speed. This must be designed from the beginning of life, or we must assume life ran very slowly at the start.
Genome complexity:3-D DNA neighborhood controls
by David Turell , Friday, September 29, 2017, 18:59 (2613 days ago) @ David Turell
By keeping neighborhoods together as DNA is coiled gene networks can continue to cooperate in a faster fashion:
https://phys.org/news/2017-09-molecular-motor-chromosomes.html
"A molecular "motor" that organizes the genome into distinct neighborhoods by forming loops of DNA has been characterized by researchers at MIT and the Pasteur Institute in France.
"In a study published in 2016, a team led by Leonid Mirny, a professor of physics in MIT's Institute for Medical Engineering and Sciences, proposed that molecular motors transform chromosomes from a loosely tangled state into a dynamic series of expanding loops.
"The process, known as loop extrusion, is thought to bring regulatory elements together with the genes they control. The team also suggested that DNA is decorated with barriers—akin to stop signs—that limit the process of extrusion.
"In this way, loop extrusion divides chromosomes into separate regulatory neighborhoods, known as topologically associating domains (TADs).
***
"Now, in a paper published in the journal Nature, a team led by Mirny and Francois Spitz at the Pasteur Institute, have demonstrated that cohesin does indeed play the role of a motor in the loop extrusion process.
"'Each of these machines lands on the DNA and starts extruding loops, but there are boundaries on DNA that these motors cannot get through," Mirny says. "So as a result of this motor activity, the genome is organized into many dynamic loops that do not cross the boundaries, so the genome becomes divided into a series of neighborhoods."
"The researchers also discovered that a different mechanism, that does not use cohesin, is at work organizing active and inactive regions of DNA into separate compartments in the cell's nucleus.
***
"The team believes the cohesin motors allow each gene to reach out to its regulatory elements, which control whether genes should be switched on or off.
"What's more, it appears that the cohesin motors are stopped by another protein, CTCF, which demarcates the boundaries of each neighborhood. In a recent study in the journal Cell, the Mirny lab, in collaboration with researchers at the University of California at San Francisco and the University of Massachusetts Medical School has demonstrated that if this demarcating protein is removed, the borders between neighborhoods disappear, allowing genes in one neighborhood to talk to regulatory elements they should not be talking to in another neighborhood, and leading to misregulation of genes in the cell.
"'Cohesin is central for gene regulation, and we emphasize that this is a motor function, so it is not just that they (genes and their regulatory elements) find each other somewhere randomly in space, but they were brought together by this motor activity," Mirny says.
***
"'In this work the Mirny and Spitz labs combine mouse models with genomic approaches to study chromosome folding to reveal that the machine that loads the cohesin complex is critical for TAD formation," Dekker says. "From this and another previous study, a molecular mechanism is coming into view where TADs form by cohesin and Nipbl-dependent chromatin loop extrusion, which is blocked by sites bound by CTCF."
"The researchers are now attempting to characterize how the absence of the molecular motor would affect gene regulation. They are also carrying out computer simulations in a bid to determine how the cohesin-based loop extrusion takes place at the same time as the genome is undergoing the independent process of segregating into active and inactive compartments."
Comment: Note the tight controls of the 3-D DNA relationships. Such complexity cannot have been developed step by step. The 3-D relationships allow living cells to reproduce at high speed and to do so accurately by genes and controls being kept close to each other. Only a planning mind can create such a mechanism. Evidence that God exists.
Genome complexity:4-D DNA neighborhood controls
by David Turell , Friday, October 06, 2017, 22:04 (2606 days ago) @ David Turell
Studies now are looking at DNA changes with time:
https://phys.org/news/2017-10-human-genome-d.html
"For decades, researchers have suspected that when a human cell responds to a stimulus, DNA elements that lie far apart in the genome quickly find one another, forming loops along the chromosome. By rearranging these DNA elements in space, the cell is able to change which genes are active.
***
"To track the folding process over time, the research team began by disrupting cohesin, a ring-shaped protein complex that was located at the boundaries of nearly all known loops. In 2015, the team proposed that cohesin creates DNA loops in the cell nucleus by a process of extrusion.
"'Extrusion works like the strap-length adjustor on a backpack," explained Dr. Erez Lieberman Aiden, director of the Center for Genome Architecture at Baylor College of Medicine and senior author on the new study. "When you feed the strap through either side, it forms a loop. DNA seems to be doing the same thing – except that cohesin rings appear to play the role of the adjustor."
"Aiden said a crucial prediction of the 2015 model is that all the loops should disappear in the absence of cohesin. In the new research, Aiden, Rao and colleagues tested that assumption.
"'We found that when we disrupted cohesin, thousands of loops disappeared," said Rao, a medical student at Stanford University, Hertz Fellow and member of the Aiden lab. "Then, when we put cohesin back, all those loops came back – often in a matter of minutes. This is precisely what you would predict from the extrusion model, and it suggests that the speed at which cohesin moves along DNA is among the fastest for any known human protein."
"But not everything happened as the researchers expected. In some cases, loops did the exact opposite of what the researchers anticipated.
"'As we watched thousands of loops across the genome get weaker, we noticed a funny pattern," said Aiden, also a McNair Scholar, Hertz Fellow and a senior investigator at Rice University's Center for Theoretical Biological Physics. "There were a few odd loops that were actually becoming stronger. Then, as we put cohesin back, most loops recovered fully – but these odd loops again did the opposite – they disappeared!"
"By scrutinizing how the maps changed over time, the team realized that extrusion was not the only mechanism bringing DNA elements together. A second mechanism, called compartmentalization, did not involve cohesin.
"'The second mechanism we observed is quite different from extrusion," explained Rao. "Extrusion tends to bring DNA elements together two at a time, and only if they lie on the same chromosome. This other mechanism can connect big groups of elements to one another, even if they lie on different chromosomes. And it seems to be just as fast as extrusion."
"Broad Institute Director Eric Lander, a study co-author, said, "We're beginning to understand the rules by which DNA elements come together in the nucleus. Now that we can track the elements as they move over time, the underlying mechanisms are starting to become clearer.'"
Comment: The fact that DNA can rearrange itself so quickly to respond as necessary indicates there are chemical controls that are yet to be understood. It looks as if DNA can think, but that is beyond possibility. The complexity of the underlying organization it presents demands that the system is designed. Not by chance.
Genome complexity: DNA epigenetic controls
by David Turell , Monday, October 30, 2017, 17:44 (2582 days ago) @ David Turell
Switching DNA genes on and off is conducted by epigenetic mechanisms:
https://www.sciencedaily.com/releases/2017/10/171030095704.htm
"DNA contains the blueprint of an entire organism. Based on the information in this blueprint, every cell knows what it must become and what function it must perform. Throughout the entire lifespan of an organism, the genetic information has to be read correctly to ensure that genes are active at the right time and in the right cells. If these processes are defective, cells acquire the wrong identity -- which can ultimately lead to cancer.
"However, the program that determines which genes are switched on or off as a cell develops does not depend solely on DNA, but is also determined by epigenetic marks. Methylation marks on DNA act as a molecular switch that regulate gene activity in order to coordinate the cell's specialization within the organism.
***
"Tuncay Baubec, professor at the Department of Molecular Mechanisms of Disease at the University of Zurich, and his team have shown that one particular protein plays an important part in this process: The DNA methyltransferase 3A (DNMT3A) enzyme is responsible for positioning the methylation to the right place on the DNA. "DNMT3A places itself preferably in close vicinity to genes that play an important role for development and makes sure that the DNA methylation around these genes is maintained," explains Massimiliano Manzo, lead author of the study. "The DNA methylation around these genes works like a container that ensures that H3K27me3, another epigenetic modification, which normally regulates these genes, is positioned correctly." This means that these essential genes are regulated by two epigenetic layers."
Comment: Once again we see the discovery of giant enzyme molecules in charge of DNA expression. Current Darwin theories do not describe how such large specialized molecules are found in the process of evolution. A designer is required.
Genome complexity: DNA enzyme controls
by David Turell , Monday, October 30, 2017, 18:01 (2582 days ago) @ David Turell
Another enzyme molecule is analyzed which controls DNA expression. see the article to see how complex these enzymes can be:
https://phys.org/news/2017-10-scientists-unveil-protein-critical-gene.html
"The study, led by Dr Lori Passmore opens in new window from the MRC Laboratory of Molecular Biology, is the first to reveal the structure of an important part of the protein, called cleavage and polyadenylation factor (CPF).
"CPF is a complex enzyme made up of many subunits. Cryo-electron microscopy has revolutionised scientists' ability to discover the structure of large, flexible and complex proteins like this in their natural form.
"Dr Lori Passmore, senior author on the paper and group leader at the MRC LMB, said: "Understanding the structure and function of intact CPF, and how it is assembled, has been a central question in the field of gene expression for decades – it's such a fundamental protein but we still don't understand how it works. This was a huge technical challenge because very few structures have been built entirely from scratch using cryo-EM data. We were very excited to finally build the first atomic model of the structure of part of CPF."
"Gene expression - turning the instructions encoded in DNA into proteins - requires a number of important steps. Enzymes copy the gene and produce a single-stranded version of the DNA, called messenger RNA (mRNA).
"The mRNA can travel out of the nucleus of the cell, where the DNA is housed, to the cytoplasm where cellular machinery uses the mRNA's instructions to assemble a protein.
The CPF enzyme is a necessary part of this process – it adds a long string of adenosine molecules, called a 'poly-A tail', to the end of each new mRNA.
"This tail is important because the length of the tail specifies the amount of time that the mRNA is present in the cell, and how often it is translated into proteins. The poly-A tail is also necessary for the mRNA to be transported out of the nucleus.
"Viral infections, such as influenza, target CPF within the cell and disrupt gene expression. The researchers identified a site on CPF where a protein from the virus can bind in a way that may block CPF from interacting with mRNA, and thereby halt gene expression in the cell to the virus' advantage.
"The scientists say this structure will also help them to better understand how CPF works and how defects in poly-A tail addition contribute to diseases - including β-thalassemia, thrombophilia, and cancer."
Comment: Be sure to look at the structure. A blind Darwinian process cannot invent this sort of protein. Designer required.
Genome complexity: Archaea and nuclei
by David Turell , Wednesday, November 08, 2017, 17:32 (2573 days ago) @ David Turell
Eukaryotes have nuclei requiring packing proteins to handle long DNA. Related proteins are found in Archaea:
https://phys.org/news/2017-11-human-cells-hardy-microbes-common.html
"Santangelo, associate professor in the Department of Biochemistry and Molecular Biology, was on a team that found striking parallels between how archaeal cells and more complex cells, including humans' and animals', package and store their genetic material. The breakthrough study, published in Science earlier this year, provided evidence that archaea and eukaryotic cells share a common mechanism to compact, organize and structure their genomes.
***
"Science paper collaborator John Reeve had discovered in the 1990s that histone proteins were not limited to eukaryotes, but were also found in nucleus-free archaea cells. Reeves and Luger began a collaboration to crystallize histone-based archaeal chromatin and compare that structure with eukaryotic chromatin.
"After years of stops and starts and trouble growing reliable archaeal histone crystals – Luger called it a "gnarly crystallographic problem" – the scientists succeeded in resolving the structure of archaeal chromatin, revealing its structural similarity to eukaryotes.
***
"A little high school biology review: Eukaryotes are cells with a nucleus and membrane-bound organelles, and they include fungal, plant and animal – including human – cells. They're set apart from their less complex counterparts, prokaryotes, by the absence of a nucleus. While archaea and bacteria are both prokaryotes, they are only distantly related. Archaea are the likely progenitors of eukaryotes and share many of the same proteins that control gene expression.
"One of life's most fundamental processes – the mechanics by which DNA bends, folds and crams itself into a cell nucleus – is common across all eukaryotes, from microscopic protists to plants to humans.
"Packed inside the nucleus of every eukaryotic cell is several feet of genetic material that is compacted in a very specific way. Small sections of DNA are wrapped, like thread around a spool, roughly two times around eight small proteins called histones. This entire DNA-histone complex is called a nucleosome, and a string of compacted nucleosomes is called chromatin."
Comment: More evidence for pre-planning the future of evolution, just like a change in monkey lumbar changes.
Read more at: https://phys.org/news/2017-11-human-cells-hardy-microbes-common.html#jCp
Genome complexity: DNA is all sizes
by David Turell , Friday, November 10, 2017, 23:03 (2571 days ago) @ David Turell
Looking at all organisms, DNA comes in all sizes totally unexplained:
https://www.quantamagazine.org/shrinking-bat-dna-and-elastic-genomes-20170801/
'Take an onion. Slice it very thin. Thinner than paper thin: single-cell thin. Then dip a slice in a succession of chemical baths cooked up to stain DNA. The dyed strands should appear in radiant magenta — the fingerprints of life’s instructions as vivid as rose petals on a marital bed. Now you can count how much DNA there is in each cell. It’s simply a matter of volume and density. A computer can flash the answer in seconds: 17 picograms. That’s about 16 billion base pairs — the molecular links of a DNA chain.
'Maybe that number doesn’t mean much to you. Or maybe you’re scratching your head, recalling that your own hereditary blueprint weighs in at only 3 billion base pairs. “Huh?” joked Ilia Leitch, an evolutionary biologist at the Royal Botanic Gardens, Kew, in England. Her reaction mimicked the befuddlement of countless anthropocentric minds who have puzzled over this discrepancy since scientists began comparing species’ genomes more than 70 years ago. “Why would an onion have five times more DNA than we have? Are they five times more clever?”
'Of course, it wasn’t just the onion that upended assumptions about a link between an organism’s complexity and the heft of its genetic code. In the first broad survey of animal genome sizes, published in 1951, Arthur Mirsky and Hans Ris —pioneers in molecular biology and electron microscopy, respectively — reported with disbelief that the snakelike salamander Amphiuma contains 70 times as much DNA as a chicken, “a far more highly developed animal.” The decades that followed brought more surprises: flying birds with smaller genomes than grasshoppers; primitive lungfish with bigger genomes than mammals; flowering plants with 50 times less DNA than humans, and flowering plants with 50 times more; single-celled protozoans with some of the largest known genomes of all.
***
'Mammals are not especially diverse when it comes to genome size. In many animal groups, such as insects and amphibians, genomes vary more than a hundredfold. By contrast, the largest genome in mammals (in the red viscacha rat) is only five times as big as the smallest (in the bent-wing bat). Many researchers took this to mean that mammalian genomes just don’t have much going on. As Susumu Ohno, the noted geneticist and expert in molecular evolution, put it in 1969: “In this respect, evolution of mammals is not very interesting.”
***
'Or perhaps genomes are unpredictable in the same way life is unpredictable — with exceptions to every rule. “Biological systems are like Rube Goldberg machines,” said Jeff Bennetzen, a plant geneticist at the University of Georgia. “If something works, it will be done, but it can be done in the most absurd, complicated, multistep way. This creates novelty. It also creates the potential for that novelty to change in a million different ways.'”
Comment: I've skipped all the theorizing about why sizes are what they are. There is no coherent theory. Transposons play a key role:
"By then, scientists had learned that B chromosomes are only a tiny fraction of the molecular parasites making genomes fat. The most prolific freeloaders are mobile strings of DNA called transposons, identified in 1944 by Barbara McClintock, the groundbreaking cytogeneticist who was honored with a Nobel Prize for that discovery. Transposons are popularly known as “jumping genes,” although they are rarely in fact true genes. They can get passed down from one generation to the next or transmitted between species, like viruses, and they come in several flavors. Some encode enzymes that snip a transposon out of its place in a genome and paste it elsewhere. Others copy themselves by manufacturing RNA templates or stealing enzymes from other transposons." (plucked out of the article)
Genome complexity: amazing translation efficiency
by David Turell , Friday, November 17, 2017, 15:09 (2564 days ago) @ David Turell
Information in the genome must be translated into proteins and functions. It turns out to be amazingly efficient as compared to computer energy use:
https://phys.org/news/2017-11-astonishing-efficiency-life.html
"All life on earth performs computations – and all computations require energy. From single-celled amoeba to multicellular organisms like humans, one of the most basic biological computations common across life is translation: processing information from a genome and writing that into proteins.
"Translation, it turns out, is highly efficient.
***
"To discover just how efficient translation is, the researchers started with Landauer's Bound. This is a principle of thermodynamics establishing the minimum amount of energy that any physical process needs to perform a computation.
"'What we found is that biological translation is roughly 20 times less efficient than the absolute lower physical bound," says lead author Christopher Kempes, an SFI Omidyar Fellow. "And that's about 100,000 times more efficient than a computer." DNA replication, another basic computation common across life, is about 165 times worse than Landauer's Bound. "That's not as efficient as biological translation, but still stunningly good compared to computers."
"Scaling up to calculate the thermodynamic efficiency of higher-level biological computations like thought, and to understand how important efficiency is to natural selection, offer challenging questions for further research."
Comment: Life maintains its homeostasis through the genome. Limiting the energy required helps life survive its requirement for a constant energy addition. When life originated it is unlikely the process stumbled into this efficiency by chance. It was designed.
Genome complexity: How Archaea handle DNA
by David Turell , Thursday, March 11, 2021, 18:18 (1354 days ago) @ David Turell
They coil it like a slinky:
https://www.sciencenews.org/article/archaea-microbes-fold-twist-contort-dna-extreme-ways
"Single-celled archaea microbes pack their DNA into flexible coils that expand and stretch much like a Slinky does. This kind of molecular gymnastics had never been seen before in other organisms and may represent a way for archaea to get easy access to their genetic material, researchers report March 2 in eLife.
***
“'You would think that this would really contort the DNA in an awful shape, but it actually flows very naturally.”
***
"In 2017, Luger and her colleagues discovered that archaea — microbes that resemble bacteria under the microscope but are quite distinct — can spool their DNA around small proteins called histones (SN: 8/10/17). This process is strikingly similar to how plants, animals and fungi bend and fold their own genomes into compact, disk-shaped units known as nucleosomes.
"But nobody knew what these structures looked like in archaea, or how the microbes gained access to their spooled DNA. Using computer simulations and electron microscopy experiments on the genetic material of Methanothermus fervidus, a heat-loving archaeal species, the researchers found the Slinky-like shapes opened and closed in a clamshell motion.
“'My gut reaction was: ‘Wow! So pretty!’” says Luger. “My second reaction was: ‘Of course! This makes so much sense!’”
"Complex organisms such as humans, palm trees or mushrooms depend on a sophisticated machinery to loosen their highly compacted nucleosomes and gain access to specific genes. Archaea microbes might instead simply be contorting their DNA to turn genes on and off –– allowing proteins to “read” the genes when the Slinkies open, and cutting off access when they close."
Comment: Archaea are our oldest ancestors. This means complex DNA code reading came with or shortly after the appearance of life.
Genome complexity:3-D DNA
by David Turell , Monday, April 23, 2018, 18:16 (2407 days ago) @ David Turell
Comes in five different forms when DNA is active in cells:
https://cosmosmagazine.com/biology/helix-no-more-researchers-find-a-new-dna-shape
"A team of Australian researchers at Sydney’s Garvan Institute has identified a knotty version of DNA, known as an I-motif, that appears within DNA when it is actively being read.
***
"According to John Mattick, the out-going director of the Garvan, who was not involved in the research, “This shows another level of dynamic regulation of the DNA code. It’s not just a twisted railway track; it’s got signposts and sidings along the way.”
***
"But over the past couple of decades, mischievous scientists have succeeded in showing that DNA structures other than the elegant helix appear under the microscope. All in all, there are five besides the “standard” shape, known as B-DNA: A-DNA, Z-DNA, triplex DNA, G quadruplex, and I-motif DNA.
***
"To explore whether I-motif DNA existed in living cells, the Garvan team developed an antibody that would bind to it and no other form.
"Injecting the antibody into a variety of cells, the researchers found that the it zeroed in on several targets across the cells – mostly in parts that do not code for proteins – including the regulatory regions that switch genes on and off (known as promotors) and the chromosome tips (called telomeres).
"The I-motif was not detectable all the time. Rather, the antibody, visible because of its green fluorescent tag, came and went as the cells progressed through their cycles of division. However, they were most visible in the late Gap 1 phase, when cells are actively reading their DNA in order to synthesise mRNA and proteins prior to dividing.
“'What excited us most is that we could see the green spots – the I-motifs – appearing and disappearing over time,” says Mahdi Zeraati, the first author of the paper. “It seems likely that they are there to help switch genes on or off.”
"Rather shockingly, the I-motif doesn’t just disobey the structural rules, it also disobeys the normally strict base-pairing rules for DNA, which hold that adenine always binds to thymine, and cytosine always hooks up with guanine. In this instance, the structure is formed by two cytosines pairing up.
"Given that 98% of the genome does not code for proteins, on to decode this information. “Its probably not one dimensional but three or four dimensional”, says Mattick.
As senior author Marcel Dinger puts it, “These findings will set the stage for a whole new push to understand what this new DNA shape is really for.'”
Comment: It is obvious that DNA is much more than a simple linear code, but most of the huge molecule is an active participant in running all phases of life, well beyond simple protein production. Obviously too complex for any chance invention
Genome complexity: DNA repair mechanisms
by David Turell , Sunday, September 02, 2018, 18:20 (2275 days ago) @ David Turell
Without accurate repair mechanisms DNA can become cancer or defects which cause disease conditions:
https://www.sciencedaily.com/releases/2018/09/180901110632.htm
"Researchers from Tokyo Metropolitan University and the FIRC Institute of Molecular Oncology (IFOM) in Italy have uncovered a previously unknown function of the DDX11 helicase enzyme. Mutations in the gene which codes for DDX11 are known to be implicated in Warsaw Breakage Syndrome. They showed that DDX11 plays an important role in DNA repair, and functions as a backup to the Fanconi Anemia (FA) pathway, whose malfunction is associated with another life-debilitating condition.
"DNA plays a central role in the biological function of the cell, but it is constantly being damaged, both spontaneously and through environmental factors. Failure to successfully repair these lesions can lead to malignant tumors or cancer.
***
"Warsaw Breakage Syndrome (WABS) is a genetic disorder; afflicted individuals suffer from mild to severe intellectual disability and growth impairment amongst other potential abnormalities. It was known that mutations in the DDX11 gene in Chromosome 12 in the human genome and the enzyme it codes for, the DDX11 helicase, were responsible for the onset of WABS, yet the mechanism by which DDX11 acted remained unclear.
***
"What they found was that DDX11 played a vital role in DNA repair, acting together with the 9-1-1 checkpoint complex protein, which, as the name suggests, checks the integrity of DNA strands after replication. In doing so, DDX11 is critical in the repair of a wide-range of bulky lesions and also serves as a backup to the so-called FA pathway, specialized in the repair of interstrand crosslinks (ICLs), a harmful type of lesion that can lead to cell death and developmental problems. This finding explains the apparent similarity between WABS and FA cells exposed to ICLs, which caused WABS to be classified as a FA-like disorder. The researchers also discovered that DDX11 is involved in immunoglobulin-variable gene diversification, a key mechanism in the healthy function and adaptability of a healthy immune system. As immunoglobulin-variable gene diversification is induced by abasic sites, the most common endogenous lesion in mammalian cells, one implication is that DDX11 and 9-1-1 promote DNA damage tolerance of abasic sites, a finding that potentially explains the essential role of DDX11 and its similarity with 9-1-1 during development.
"Besides shedding light on the mechanism underlying WABS, the study advances our understanding of the biological mechanisms behind genomic stability and how disorders arise at the cellular level. These results have profound medical significance for several conditions, including cancer and developmental disorders associated with DNA repair deficiency."
Comment: We recognize the complexity of DNA itself. In their own way the enzymes that repair DNA are equally complex given their enormous size as protein molecules. It is obvious that when DNA appeared, these repair enzymes had to be in place or life would not have continued as it has. Only planned design fits this scenario.
Genome complexity: 3 types of bees from one DNA
by David Turell , Wednesday, September 12, 2018, 15:11 (2266 days ago) @ David Turell
A study of the modifications which seem to control the three types of bees, queens, drones, and workers:
https://www.the-scientist.com/news-opinion/as-bees-specialize--so-does-their-dna-packag...
"The bee genome has a superpower. Not only can the exact same DNA sequence yield three types of insect—worker, drone, and queen—that look and behave very differently, but, in the case of workers, it dictates different sets of behaviors.
"A key to the genome’s versatility seems to be epigenetic changes—chemical tags that, when added or removed from DNA, change the activity of a gene. Previous studies had shown distinct patterns of tags known as methyl groups on the genomes of bees performing different roles within their hives.
"In a study published in Genome Research last month, Paul Hurd, an epigenetics researcher at Queen Mary University of London, and colleagues looked at a different type of epigenetic change: histone modifications. DNA wraps around histones, and chemical modifications to these proteins are thought to affect how available genes are to be transcribed.
"In their new study, the researchers report that queen and worker bees each have characteristic patterns of histone modifications on their genomes, and that these differences emerge very early in development, suggesting they may be key to determining the insects’ fates.
"The very different individuals that arise from hive members’ identical genomes have made the honeybee “one of the most well-known and striking examples of phenotypic plasticity,” says Gene Robinson, a genomicist at the University of Illinois who was not involved in the study. Bees are a model, he says, for “understanding how environmental signals are transduced and then trigger these alternate developmental pathways.”
"Larvae are sent down different developmental pathways from the time of hatching by nurse bees (a type of worker), which tailor the insects’ diets according to their future castes. Worker bees that tend to queen larvae and mature queens make their special food, so-called royal jelly, themselves, and it contains a compound known to directly influence histone modifications, the authors note in their paper.
***
"To investigate their role, the research team collected worker and queen bee eggs and larvae from Apis mellifera hives and sampled the larvae 96 hours after they hatched. The team then analyzed the bee genomes for the positions of three different types of histone modifications.
"At 96 hours, the researchers found, the genomes of future workers and queens already had “striking differences” in their patterns of histone modifications, says Robert Lowe, a computational biologist at Queen Mary University of London and one of the paper’s authors. And the locations of the histones that were modified differently in workers and queens corresponded with the sites of genes that have different expression levels between the two populations.
"The authors suggest that the histone modifications drive differences in gene transcription among bees of different castes, which in turn guide them down different developmental paths."
Comment: This is a complex society, well coordinated in their tasks an efficient hive. It certainly looks designed that way and not evolved with steps over time.
Genome complexity: genes and what they control
by David Turell , Thursday, September 20, 2018, 23:39 (2257 days ago) @ David Turell
We still know much about the genome and how genes relate to functions is really not clear:
https://www.sciencedaily.com/releases/2018/09/180917090856.htm
Ever since the decoding of the human genome in 2003, genetic research has been focused heavily on understanding genes so that they could be read like tea leaves to predict an individual's future and, perhaps, help them stave off disease.
A new USC Dornsife study suggests a reason why that prediction has been so challenging, even for the most-studied diseases and disorders: The relationship between an individual's genes, environment, and traits can significantly change when a single, new mutation is introduced.
"Individuals have genetic and environmental differences that cause these mutations to show different effects, and those make it difficult to predict how mutations will behave, " said Ian Ehrenreich, a lead author and biologist at the USC Dornsife College of Letters, Arts and Sciences. "For example, mutations that break the cell's ability to perform DNA mismatch repair are linked to colorectal cancer, but some individuals that harbor these mutations never develop the disease."
***
A growing number of large-scale, genome-wide association studies have revealed which genes are linked to certain diseases, behaviors or other traits. These studies overlook how interactions between genetic differences, the environment, and new mutations -- what scientists have termed "background effects" -- differ from individual to individual.
***
The authors found that background effects result from many, often environment-specific, interactions between mutations and genetic differences. In fact, most of these interactions involved multiple genetic differences interacting with not only a mutation, but also with each other and the environment.
These findings imply that background effects result from complicated interactions between mutations, pre-existing genetic differences, and the environment.
"In the extreme, we found that that these complicated interactions could influence whether a perfectly healthy cell lived or died after a mutation was introduced," Ehrenreich said.
"The role of genetic and environmental context in shaping the effects of genetic mutations on traits may be significantly underappreciated," he said.
"There is an obvious goal here -- to help people prevent disease or lower their risk," Ehrenreich said. "The challenge is that we don't fully understand how genetics work. These critical experiments in yeast and other model organisms help clarify what we might be missing. An important next step would be to examine whether these conclusions hold true for humans." (my bold)
Comment: We have touched only a thin sliver of how the genome works with only two percent of it coding for protein and 80% actively influencing what goes on. The coiled construction and folding allows for 3-D relationships that defy any simple understanding. We are many years for any full understanding.
Genome complexity: genes and what they control
by Balance_Maintained , U.S.A., Friday, September 21, 2018, 04:35 (2257 days ago) @ David Turell
We still know much about the genome and how genes relate to functions is really not clear:
https://www.sciencedaily.com/releases/2018/09/180917090856.htm
Ever since the decoding of the human genome in 2003, genetic research has been focused heavily on understanding genes so that they could be read like tea leaves to predict an individual's future and, perhaps, help them stave off disease.
A new USC Dornsife study suggests a reason why that prediction has been so challenging, even for the most-studied diseases and disorders: The relationship between an individual's genes, environment, and traits can significantly change when a single, new mutation is introduced.
"Individuals have genetic and environmental differences that cause these mutations to show different effects, and those make it difficult to predict how mutations will behave, " said Ian Ehrenreich, a lead author and biologist at the USC Dornsife College of Letters, Arts and Sciences. "For example, mutations that break the cell's ability to perform DNA mismatch repair are linked to colorectal cancer, but some individuals that harbor these mutations never develop the disease."
***
A growing number of large-scale, genome-wide association studies have revealed which genes are linked to certain diseases, behaviors or other traits. These studies overlook how interactions between genetic differences, the environment, and new mutations -- what scientists have termed "background effects" -- differ from individual to individual.
***
The authors found that background effects result from many, often environment-specific, interactions between mutations and genetic differences. In fact, most of these interactions involved multiple genetic differences interacting with not only a mutation, but also with each other and the environment.
These findings imply that background effects result from complicated interactions between mutations, pre-existing genetic differences, and the environment.
This is precisely what I was talking about with the bees.
--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.
Genome complexity: HOX genes appeared early in evolution
by David Turell , Thursday, September 27, 2018, 19:48 (2250 days ago) @ Balance_Maintained
HOX genes are major control genes over body plans and there is evidence now they were set up early in evolution:
https://phys.org/news/2018-09-probes-ancient-body-code.html
"These findings, published in the September 28, 2018, issue of Science, give researchers a better understanding of these genes' ancestral function, and a grasp on an important step in evolutionary biology.
"'The sea anemone offers us a window into the possible ancient past of Hox gene function," says Stowers Investigator Matthew Gibson, Ph.D., who led the study.
"The roles of Hox genes in bilaterian animals have been well established. These are animals that have a head-to-tail axis, have largely symmetrical left and right sides, and include everything from humans to dogs to fish to spiders. Hox genes control the identity of different segments of these animals as they develop, setting in motion the genetic programs that form various body structures such as limbs and organs. Segment identity depends on which Hox genes are expressed—or the Hox code—in that region of the developing organism.
"Although Hox genes have been identified in the group of animals known as Cnidaria, which include radially symmetrical animals like sea anemones, jellyfish, and corals, their particular roles in cnidarian body plan regulation were previously unknown.
"'We've never had functional evidence for where the Hox code originated and how it may have controlled development before the emergence of the bilaterians," Gibson said. "By studying the function of Hox genes in a sea anemone we can begin to understand the possible role of these genes in our ancient common ancestor, some 600 million years in the past."
***
"'It's entirely possible that the ancestral role of the Hox genes was to both drive segment formation and confer segment identity," Gibson said. "In extant bilaterians, these functions may have separated such that Hox genes just control segment identity."'
"'These findings uncover the existence of a Hox code in a developing cnidarian, providing evolutionary biologists with new insights into the process of Hox code evolution," said Shuonan He, a predoctoral researcher at the Graduate School of the Stowers Institute for Medical Research and first author of the paper. "These genes already existed before the split of bilaterians and cnidarians from their common ancestor," he said. "Now we can look at more cnidarian branches to test if these genes are employed in similar fashion."
"Gibson said that these findings also provide further evidence that evolution doesn't necessarily make the gene code more complex. "There is a popular notion that the process of evolution increases sophistication and complexity inexorably upward, but we now know in many cases that's not what happens at all," he said. "Our ancient animal ancestors had complex biology regulated by the same types of genes that are present in humans today. They were just employed in a different way.'"
Comment: In the past I have proposed that God set up the genome to be easily modified as evolution was to progress. This article shows exactly that pattern to have basic master genes for body plans, which make later modification easier to the coding/dabbling.
Genome complexity: HOX genes appeared early in evolution
by Balance_Maintained , U.S.A., Thursday, September 27, 2018, 20:10 (2250 days ago) @ David Turell
HOX genes are major control genes over body plans and there is evidence now they were set up early in evolution:
https://phys.org/news/2018-09-probes-ancient-body-code.html
"These findings, published in the September 28, 2018, issue of Science, give researchers a better understanding of these genes' ancestral function, and a grasp on an important step in evolutionary biology."'The sea anemone offers us a window into the possible ancient past of Hox gene function," says Stowers Investigator Matthew Gibson, Ph.D., who led the study.
"The roles of Hox genes in bilaterian animals have been well established. These are animals that have a head-to-tail axis, have largely symmetrical left and right sides, and include everything from humans to dogs to fish to spiders. Hox genes control the identity of different segments of these animals as they develop, setting in motion the genetic programs that form various body structures such as limbs and organs. Segment identity depends on which Hox genes are expressed—or the Hox code—in that region of the developing organism.
"Although Hox genes have been identified in the group of animals known as Cnidaria, which include radially symmetrical animals like sea anemones, jellyfish, and corals, their particular roles in cnidarian body plan regulation were previously unknown.
"'We've never had functional evidence for where the Hox code originated and how it may have controlled development before the emergence of the bilaterians," Gibson said. "By studying the function of Hox genes in a sea anemone we can begin to understand the possible role of these genes in our ancient common ancestor, some 600 million years in the past."
***
"'It's entirely possible that the ancestral role of the Hox genes was to both drive segment formation and confer segment identity," Gibson said. "In extant bilaterians, these functions may have separated such that Hox genes just control segment identity."'
"'These findings uncover the existence of a Hox code in a developing cnidarian, providing evolutionary biologists with new insights into the process of Hox code evolution," said Shuonan He, a predoctoral researcher at the Graduate School of the Stowers Institute for Medical Research and first author of the paper. "These genes already existed before the split of bilaterians and cnidarians from their common ancestor," he said. "Now we can look at more cnidarian branches to test if these genes are employed in similar fashion."
"Gibson said that these findings also provide further evidence that evolution doesn't necessarily make the gene code more complex. "There is a popular notion that the process of evolution increases sophistication and complexity inexorably upward, but we now know in many cases that's not what happens at all," he said. "Our ancient animal ancestors had complex biology regulated by the same types of genes that are present in humans today. They were just employed in a different way.'"
David Comment: In the past I have proposed that God set up the genome to be easily modified as evolution was to progress. This article shows exactly that pattern to have basic master genes for body plans, which make later modification easier to the coding/dabbling.
I also see common coding functions across 'unrelated' species (bilaterians/Cnidarians).
--
What is the purpose of living? How about, 'to reduce needless suffering. It seems to me to be a worthy purpose.
Genome complexity: protecting DNA integrity
by David Turell , Wednesday, October 03, 2018, 15:43 (2245 days ago) @ Balance_Maintained
A whole complex of proteins has been found to keep DNA intact:
https://the-scientist.com/the-literature/chromosome-clusters-help-keep-the-genome-toget...
"Between cell divisions, pericentromeric DNA—noncoding, repetitive satellite DNA abundant around centromeres—bunches together across several chromosomes to cluster them into structures called chromocenters.
"The function of pericentromeric DNA and of chromocenters had remained largely unknown until cell biologist Yukiko Yamashita and her team at the University of Michigan set out to see what would happen to fruit fly cells without them. Simply mutating or excising pericentromeric DNA, which occurs as long sequences of tandem repeats, would have been impractical. So Yamashita’s group instead targeted a protein, D1, that’s known to interact with satellite DNA. When D1 was mutated, fruit fly germ cells did not survive for long. The researchers stained these mutant, dying germ cells with an antibody for Vasa, a cytoplasmic protein, and saw dark spots that turned out to be micronuclei, aberrant structures that can form when rogue chromosomes escape from their chromocenters and cause bits of the nuclear membrane to bud off around them.
"Yamashita’s team proposes that the protein D1 binds to pericentromeric DNA on multiple chromosomes, in effect locking them together in chromocenters. Without this protein or the requisite DNA binding sites, the chromosomes simply float away from each other, leaving behind incomplete nuclei. To see if these results held up in mammals, the team carried out similar experiments in mouse cells, and found that knocking down a D1 analog called HMGA1 caused micronuclei to form.
"Next, Yamashita and her colleagues expressed the D1 protein from fruit flies in mouse cells and saw that fewer chromocenters formed with higher levels of D1 in a dose-dependent way—indicating that in cells with elevated levels of the fruit fly protein, the chromosomes were forming larger bunches. Even though D1 and HMGA1 bind to different DNA sequences in their native species, the former had evidently interacted with mouse pericentromeric DNA.
"In another experiment in flies, the team attached D1 to DNA sites that don’t naturally interact with the protein and saw that those regions were pulled into the chromocenters.
"Thus, pericentromeric DNA’s function may be to ensure that all the chromosomes that make up a genome stay together.
"Aaron Straight, who studies chromosome biology at Stanford University and was not involved in the study, says the disruption of the nuclear membrane and budding of micronuclei is an unexpected result of knocking down the proteins that bind pericentromeric DNA. “That, I don’t think, could have been predicted,” he says. He adds that whether the absence of chromocenters leads to micronuclei formations remains to be seen.
"Yamashita notes that the makeup of such satellite DNA diverges significantly even between closely related species. The team speculates that incompatibility between satellite DNA and chromocenter-forming proteins may make it difficult for would-be hybrids to form chromocenters, potentially affecting their viability and helping to drive speciation.
Comment: A cleverly designed system that had to be place by design to protect DNA when it was created. See the diagrams
Genome complexity: genes control different stress responses
by David Turell , Wednesday, October 03, 2018, 18:43 (2244 days ago) @ David Turell
Studies in E. coli shows that cells can have different responses to different stresses:
https://phys.org/news/2018-10-cells-specialised-protein-factories-stress.html
"Prevailing dogma in biological research holds that the cell's protein factories, the ribosomes, function the same way in all cells and in all conditions. In an international study with participation from Weill Cornell Medicine and Uppsala University, published today in the journal Cell Reports, the researchers show that this is a truth that seems to not hold true.
"Most functions in a cell are controlled by proteins. They are formed inside the cells in special protein factories called ribosomes. Different cells, i.e. in different tissues, need different sets of proteins and there are several ways that a cell can control how they are produced. However, it has long been an established "truth" that the composition and function of the ribosomes are the same in all cells and in all conditions. (my bold)
"This truth is now being disputed and in the present study the researchers show that E. coli bacteria can form specialised ribosomes that influence which proteins are produced.
"We exposed the bacteria to stress conditions by reducing the nutrient levels and found that a certain type of ribosome was produced in larger amounts. We could also link the increase in this type of ribosome to an activation of the cells' general stress response," says Theresa Vincent, group leader at the Department of Immunology, Genetics and Pathology, who participated in the study together with Professor Scott Blanchard at Weill Cornell Medicine in New York.
"A ribosome consists of a large number of molecules that are all encoded by genes in the cell. In the study the researchers could show that variations in the DNA sequence in one of these genes gives rise to the specialised ribosomes.
"'Our results support the finding that specialised ribosomes exist, that they are a result of natural gene variations and that they can control gene activity and the production of proteins. Since it has previously been believed that ribosomes have a passive role during the production of proteins, their importance in for instance diseases has not been investigated.
"But specialised ribosomes also exist in animal cells and it is warranted to study if and how the gene variations behind those ribosomes affect the function of the cells.'"
Comment: This study in a stand-alone bacterium logically was bound to show this result, as the animal must accept all the different stresses and stimuli that might appear. It had to be designed that way. In a multicellular animal organ cells will also have different protein responses although since they are responsible for a specific organ function and their responses may be coordinated. Note the automaticity: the genes are programmed to know how to respond to specific challenges with specific proteins.
Genome complexity: genes control different stress responses
by dhw, Thursday, October 04, 2018, 10:56 (2244 days ago) @ David Turell
DAVID: Studies in E. coli shows that cells can have different responses to different stresses:
https://phys.org/news/2018-10-cells-specialised-protein-factories-stress.html
QUOTES: "Most functions in a cell are controlled by proteins. They are formed inside the cells in special protein factories called ribosomes. Different cells, i.e. in different tissues, need different sets of proteins and there are several ways that a cell can control how they are produced. However, it has long been an established "truth" that the composition and function of the ribosomes are the same in all cells and in all conditions. (David’s bold)
"This truth is now being disputed and in the present study the researchers show that E. coli bacteria can form specialised ribosomes that influence which proteins are produced. (dhw’s bold)
DAVID: This study in a stand-alone bacterium logically was bound to show this result, as the animal must accept all the different stresses and stimuli that might appear. It had to be designed that way. In a multicellular animal organ cells will also have different protein responses although since they are responsible for a specific organ function and their responses may be coordinated. Note the automaticity: the genes are programmed to know how to respond to specific challenges with specific proteins.
No animal “must accept every stress and stimulus that might appear”. Over time, the vast majority have failed to accept them and have gone extinct. Were they designed that way, i.e. preprogrammed 3.8 billion years ago to fail? Or were the coordinating cell communities simply unable to cope? But apparently your God preprogrammed lucky old E-coli 3.8 billion years ago to cover every single challenge they will meet for the rest of life’s history. Here’s a theistic alternative: he gave them the means to work out for themselves how to respond to specific challenges. This is not my fantasy. Some scientists who specialize in the study of bacteria strongly support the concept of bacterial intelligence, as opposed to “noting the automaticity”.
Genome complexity: DNA's physical properties
by David Turell , Tuesday, March 09, 2021, 20:04 (1356 days ago) @ David Turell
Under amazingly designed controls:
https://physicsworld.com/a/make-or-break-building-soft-materials-with-dna/
"DNA molecules are constantly getting broken up and glued back together again with a new topology (figure 2). But there’s one big difference: the DNA needs to preserve its genetic sequence otherwise cells might die or diseases could be triggered.
***
"Nature requires proteins to perform topological operations on DNA while maintaining the original information (the DNA sequence) intact.
"This has a fundamental impact on how topological operations are performed on DNA. Unlike worm-like micelles – where the operations can occur at random anywhere along the micelle and at any time – the topological changes on DNA have to happen at the right place and the right time (they have to be “regulated” as biologists love to say).
***
"To break DNA, for example, you need “restriction enzymes”, which cut the chain only where a certain DNA sequence is recognized. Topoisomerase proteins, meanwhile, have to be precisely positioned at certain locations on chromosomes where entanglements and mechanical stress often accumulate. Similarly, when two pieces of DNA reconnect and recombine – for example when parental genetic material is shuffled in gametes (the precursor of egg and sperm cells) – the process is tightly regulated in space and time to avoid aberrant chromosomes in cells. It’s almost as if DNA (thanks to proteins) is a smart worm-like micelle."
Comment: To do this type of research the author must use enzymes that are used by life's processes. He cannot just step in on his own and invent new chemistry. He is dealing with designed molecules that have electrochemical properties, which by design produce very specific results. However by learning how to manipulate DNA with the proper enzymes, he can produce artificial DNA with new properties. Using CRISPR to slice and dice DNA is one current example.
Genome complexity: Adjusting x chromosomes in cells
by David Turell , Tuesday, March 09, 2021, 22:13 (1356 days ago) @ David Turell
Male and female x's must be equalized in cells:
https://phys.org/news/2021-03-genes-sex-chromosomes.html
"Because human females have two X chromosomes and males have one X and one Y, somatic cells have special mechanisms that keep expression levels of genes on the X chromosome the same between both sexes. This process is called dosage compensation and has been extensively studied in the fruit fly Drosophila. Now, researchers at the University of Tsukuba (UT) continued work with Drosophila to show that dosage compensation does not occur in the germ cells of male flies.
"In an article published in Scientific Reports, the UT researchers investigated this phenomenon in fly primordial germ cells (PGCs), which are present in embryos and are the precursor cells to what ultimately become sperm and eggs in adults. Previous reports on dosage compensation in this cell type were controversial.
"Genetic research in somatic cells has shown that expression of X-linked genes in male fruit flies is upregulated to reach equivalent levels to that of their female counterparts. A group of proteins, called the male-specific lethal (MSL) complex, is responsible for carrying out this role. These findings made the UT group interested in if this mechanism also occurs in the male germ cells. Distinct molecular events occur in the PGCs during embryonic development between male and female fruit flies.
"'The MSL complex leaves a signature mark, called acetylation, on a specific amino acid of the histone H4 protein of the X chromosome," says Professor Satoru Kobayashi, senior author of the study. "The acetyl group being added tells the cell to express the X-linked genes at a higher level, which results in dosage compensation."
"To address their questions, the researchers used a process called transcriptome analysis to compare gene expression levels between male and female fruit fly PGCs. They also examined the histone H4 protein to determine if acetylation had occurred.
"'We found that X-linked gene expression in male PGCs was about half that of female PGCs," describes Professor Kobayashi. "We also could not detect the acetylation signature of the MSL complex."
"The authors also determined that the main components of the MSL complex are only present in very low amounts in the fly PGCs. Interestingly, they then created transgenic flies that were engineered to express higher levels of the MSL complex proteins. Male PGCs in these flies showed greater activation of X-linked genes, as well as the acetylation signature."
Comment: A complex mechanism to handle x chromosomes properly requires precise design.
Genome complexity: new editing systems found
by David Turell , Thursday, September 30, 2021, 22:19 (1151 days ago) @ David Turell
Transposons controlling RNA's found in early new research:
https://www.science.org/doi/full/10.1126/science.abj6856?af=R
"Abstract
IscB proteins are putative nucleases encoded in a distinct family of IS200/IS605 transposons and are likely ancestors of the RNA-guided endonuclease Cas9, but the functions of IscB and its interactions with any RNA remain uncharacterized. Using evolutionary analysis, RNA sequencing, and biochemical experiments, we reconstructed the evolution of CRISPR-Cas9 systems from IS200/IS605 transposons. We found that IscB uses a single noncoding RNA for RNA-guided cleavage of double-stranded DNA and can be harnessed for genome editing in human cells. We also demonstrate the RNA-guided nuclease activity of TnpB, another IS200/IS605 transposon-encoded protein and the likely ancestor of Cas12 endonucleases. This work reveals a widespread class of transposon-encoded RNA-guided nucleases, which we name OMEGA (obligate mobile element–guided activity), with strong potential for developing as biotechnologies.
***
"Discussion
Naturally programmable biological systems offer an efficient solution for diverse organisms to achieve scalable complexity via modularity of their components. RNA-guided defense and regulatory systems, which are widespread in prokaryotes and eukaryotes, are a prominent case in point, and have served as the basis of numerous biotechnology applications thanks to the ease with which they can be engineered and reprogrammed.
Here, through the exploration of Cas9 evolution, we discovered the programmable RNA-guided mechanism of three highly abundant but previously uncharacterized transposon-encoded nucleases: IscB, IsrB, and TnpB, which we collectively refer to as OMEGA (obligate mobile element–guided activity) because the mobile element localization and movement likely determines the identity of their guides. Although the biological functions of OMEGA systems remain unknown, several hypotheses are compatible with the available evidence, including roles in facilitating TnpA-catalyzed, RNA-guided transposition, or acting as a toxin, with the transposon acting as the antitoxin, securing maintenance of IS200/IS605 insertions."
Comment: This highly complex mechanism is not fully understood as yet. But it is obviously irreducibly complex and was designed at the initiation of DNA coding. Chance cannot produce this.
Genome complexity: protecting DNA integrity
by David Turell , Wednesday, October 03, 2018, 19:21 (2244 days ago) @ David Turell
Another system is described. Finding a multiplicity of protections is not surprising, since DNA replication must be exact:
https://www.sciencedaily.com/releases/2018/10/181003090314.htm
"Researchers from Tokyo Metropolitan University and the FIRC Institute of Molecular Oncology (IFOM) in Italy have succeeded in depleting AND-1, a key protein for DNA replication, by using a recently developed conditional protein degradation system. Consequently, they were able to gain unprecedented access to the mechanism behind how AND-1 works during DNA replication and cell proliferation in vertebrate cells, demonstrating that AND-1 has two different functions during DNA replication mediated by different domains of AND-1.
***
"The AND-1/Ctf4 protein is a key player in DNA replication, and is found in a vast range of living organisms, from fungi to vertebrates. Ctf4/AND-1 is essential in some organisms, but whether it is an essential gene for cell proliferation in vertebrates has not been shown experimentally. Moreover, how loss of AND-1 affects cell proliferation is not known.
***
"When done correctly, DNA replication should result in the formation of new double-stranded DNA helices. Authors used transmission electron microscopy (TEM) to visualize DNA replication intermediates and observed newly synthesized DNA having abnormally long single stranded DNA at the fork branching point in the absence of AND-1. They hypothesized that this was due to a DNA cleaving enzyme, a nuclease, disrupting the process of strands being disassembled. On further addition of a compound that suppresses the action of a particular nuclease, MRE11, they were able to successfully revert the abnormal replication fork phenotype and recover cell division, explicitly demonstrating the key role played by AND-1 in preventing nascent DNA cleavage by the nuclease during replication. Further analysis revealed that a specific part of the protein called WD40 repeats was responsible for preventing the accumulation of damage to the strand."
Comment: An expected finding. By design.
Genome complexity: automatic mechanism to kill early cancer
by David Turell , Thursday, November 01, 2018, 23:42 (2215 days ago) @ David Turell
The RNA mechanism has been found:
https://www.sciencedaily.com/releases/2018/10/181029084050.htm
"A kill code is embedded in every cell in the body whose function may be to cause the self-destruction of cells that become cancerous, reports a new Northwestern Medicine study. As soon as the cell's inner bodyguards sense it is mutating into cancer, they punch in the kill code to extinguish the mutating cell.
"The code is embedded in large protein-coding ribonucleic acids (RNAs) and in small RNAs, called microRNAs, which scientists estimate evolved more than 800 million years ago in part to protect the body from cancer. The toxic small RNA molecules also are triggered by chemotherapy, Northwestern scientists report.
***
"In published research in 2017, Peter showed cancer cells die when he introduced certain small RNA molecules. He also discovered cancer cells treated with the RNA molecules never become resistant because the molecules simultaneously eliminate multiple genes cancer cells need for survival.
***
"But he didn't know what mechanism caused the cells to self-destruct. What he knew was a sequence of just six nucleotides (6mers) present in small RNAs made them toxic to cancer cells. Nucleotides are organic molecules that are the building blocks of DNA and RNA. They are G, C, A or T (in DNA), or U (in RNA).
"In the first of the new studies, Peter then tested all 4,096 different combinations of nucleotide bases in the 6mers until he found the most toxic combination, which happens to be G-rich, and discovered microRNAs expressed in the body to fight cancer use this 6mer to kill cancer cells.
"In the second new study, Peter showed the cells chop a gene (Fas ligand) involved in cancer cell growth into small pieces that then act like microRNAs and are highly toxic to cancer. Peter's group found about three percent of all protein-coding large RNAs in the genome can be processed in this way.
"'Based on what we have learned in these two studies, we can now design artificial microRNAs that are much more powerful in killing cancer cells than even the ones developed by nature," Peter said."
Comment: It is obvious this mechanism doesn't work all the time, but is another example of automaticity the cells exhibit. Obviously it is an intelligent response.
Genome complexity: 3-D DNA contortions ad complexity
by David Turell , Saturday, November 03, 2018, 18:01 (2213 days ago) @ David Turell
DNA just doesn't sit there. It is constant motion twisting and untwisting delivering genetic instructions:
https://www.quantamagazine.org/dna-supercoils-change-the-way-that-cells-work-20160105/
"DNA is probably best known for its iconic shape — the double helix that James Watson and Francis Crick first described more than 60 years ago. But the molecule rarely takes that form in living cells. Instead, 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.”
***
"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.
***
"Like the string, it prefers to be in its most relaxed state — the iconic double helix. But 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.
"These interactions represent the inner workings of the cell, the basis of all life. 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.
***
"Researchers have known since the 1970s that twisting DNA opposite the direction of the helix — called negative supercoiling — can split open the two strands. This split serves a dual purpose. It both relieves pent-up molecular stress and exposes the code hidden within the helix, granting access to the molecular machines that replicate DNA and make RNA.
"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.
"Levens says these structural changes also help DNA communicate along its length. Just as pressing an inner tube makes a weak spot bulge, changes in the shape of one part of the DNA molecule might trigger stress elsewhere along its length, which in turn might help regulate genes.
"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 process — DNA and proteins each influences how the other acts and reacts.'”
Comment: This 3-D dance in cells is constant as life maintains its balance or homeostasis. It has to be automatically making necessary choices or life's processes could be scrambled by imperfect reactions. Bit by bit we are unearthing the hidden layers of genome complexity, but there is one item we don't understand at all: we may know what gene controls what process or event, but we have no idea how it exerts its control. Finding the code for protein production was only a tiny step in understanding how complex the genome actually is.
Genome complexity: 3-D DNA contortions ad complexity
by dhw, Sunday, November 04, 2018, 12:33 (2213 days ago) @ David Turell
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: This 3-D dance in cells is constant as life maintains its balance or homeostasis. It has to be automatically making necessary choices or life's processes could be scrambled by imperfect reactions. Bit by bit we are unearthing the hidden layers of genome complexity, but there is one item we don't understand at all: we may know what gene controls what process or event, but we have no idea how it exerts its control. Finding the code for protein production was only a tiny step in understanding how complex the genome actually is.
Thank you for another important article. “We have no idea how it exerts its control” is fair comment, but it doesn’t have to be AUTOMATICALLY making necessary choices. The cell/cell communities could simply be making necessary choices. Macrocosm and microcosm: macrocosmic humans and to a lesser degree our fellow animals autonomously use what we call the mind to make intelligent choices (“drive the bus”), although we have no idea what actually constitutes the mind or “how it exerts its control”. Some scientists would say the same about microcosmic cells and cell communities. That doesn't mean they have a human/animal mind - just their own particular form of intelligence. If you would only stop inserting "automatically" in your comments, I wouldn't have to indulge in all this repetition!
Genome complexity: 3-D DNA contortions ad complexity
by David Turell , Sunday, November 04, 2018, 18:35 (2212 days ago) @ dhw
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: This 3-D dance in cells is constant as life maintains its balance or homeostasis. It has to be automatically making necessary choices or life's processes could be scrambled by imperfect reactions. Bit by bit we are unearthing the hidden layers of genome complexity, but there is one item we don't understand at all: we may know what gene controls what process or event, but we have no idea how it exerts its control. Finding the code for protein production was only a tiny step in understanding how complex the genome actually is.
dhw: Thank you for another important article. “We have no idea how it exerts its control” is fair comment, but it doesn’t have to be AUTOMATICALLY making necessary choices. The cell/cell communities could simply be making necessary choices. Macrocosm and microcosm: macrocosmic humans and to a lesser degree our fellow animals autonomously use what we call the mind to make intelligent choices (“drive the bus”), although we have no idea what actually constitutes the mind or “how it exerts its control”. Some scientists would say the same about microcosmic cells and cell communities. That doesn't mean they have a human/animal mind - just their own particular form of intelligence. If you would only stop inserting "automatically" in your comments, I wouldn't have to indulge in all this repetition!
Why stop when it is what I believe from the chemical evidence? Life requires constant maintenance which means exact repetition, which means automatic. Your kidney controls sodium levels in the blood exactly in a tiny range of value. The decisions are automatic, not simply necessary, which really means automatic. Stop playing with words that don't change what is obvious.
Genome complexity: protecting DNA integrity in reproduction
by David Turell , Sunday, November 04, 2018, 15:00 (2212 days ago) @ David Turell
In this study DNA protections are reviewed as sperm and egg produce a new individual:
https://phys.org/news/2018-11-invading-genes-thwarted.html
"Since Carnegie Institution's Barbara McClintock received her Nobel Prize on her discovery of jumping genes in 1983, we have learned that almost half of our DNA is made up of jumping genes—called transposons. Given their ability of jumping around the genome in developing sperm and egg cells, their invasion triggers DNA damage and mutations. This often leads to animal sterility or even death, threatening species survival. The high abundance of jumping genes implies that organisms have survived millions, if not billions, of transposon invasions. However, little is known about where this adaptability comes from. Now, a team of Carnegie researchers has discovered that, upon jumping gene invasion, reproductive stem cells boost production of non-coding RNA elements (piRNA) that suppress their activity and activates a DNA repair process allowing for normal egg development.
***
"They found that reproductive stem cells use a novel adaptive response to "rapidly tame" the invading elements by activating the so-called DNA damage checkpoint. This is a process that activates a pause in the cell cycle, before cell division, to repair damaged DNA. A checkpoint component, called Chk2, was found to be key. This pause in the repair process amplified the production of piRNA—those non-coding RNA elements that silence the jumping genes. They found that this pause period is necessary for adaptation and for permanently silencing the invading jumping genes, which allowed for normal egg production that could begin within four days.
"'Jumping gene invasion triggers catastrophic genomic instability in all organisms," remarked Zhao Zhang. "They greatly reduce the viability or fertility of the invaded animals and can lead to a population crisis. We believe that the ability of reproductive stem cells to rapidly adapt and restore fertility in this manner allows species to resist such a population crash. This mechanism is a lynchpin to species survival.'" (my bold)
Comment: My bolded sentence makes that obvious point that design is necessary from the beginning of sexual reproduction. Since transposons cause such trouble, control mechanisms had to be present from the beginning.
Genome complexity: controlling DNA in the cell
by David Turell , Sunday, November 04, 2018, 19:52 (2212 days ago) @ David Turell
There are molecules which lasso DNA:
https://www.sciencedaily.com/releases/2018/11/181102105950.htm
"The Rice lab of José Onuchic has determined the structure of the condensin protein complex. The work settles the controversy over whether the complex is a single ring that lassos two double strands of DNA or a molecular "handcuff" composed of two connected rings that each wrangle a double strand.
***
"Their work is the first step toward understanding the activity of proteins over the structure of chromosomes throughout mitosis and all phases of the cell life cycle.
***
"Condensin does what the word suggests: It helps condense the chromosomes into the cell's nucleus. Recent research has demonstrated that condensin and its protein partner cohesin extrude DNA. But until now, nobody has settled on how condensin proteins come together into their functional forms.
"Krepel started her analysis from bacterial condensin complexes made up of five subunits, including two structural maintenance of chromosomes (SMC) proteins that come together as a hinge and long kleisin proteins that make up the rest of the ring. Complexes in human eukaryotic nuclei -- a target for future analysis -- are similar to their more archaic counterparts.
" Krepel pieced the puzzle together by combining and comparing existing data about the atomic structures and genetic sequences of the individual proteins. The structures came from available X-ray crystallography of protein fragments, and sequence information through direct coupling analysis (DCA), a statistics-based program introduced by Onuchic and his colleagues in 2011 that compares amino acid residues in proteins that coevolve.
"'We used DCA to infer coevolving pairs of amino acids, and we had little bits of protein fragments from experiments," Krepel said. "That was a good starting point, and then we had to put them together like a puzzle. We wanted to get a full structure and settle the conflict over whether it's a single or double ring."
***
"Onuchic's group at Rice's Center for Theoretical Biological Physics (CTBP) has published a series of papers that extend its theories on protein folding to the much larger genome. He expects ongoing work will eventually reveal condensin's mechanisms. "These things have to condense the chromosomes," he said. "People know that. But nobody knows how they do it."
"Onuchic said studies by others suggest the flexible hinge may help open and close the ring, serving as a gate that allows DNA strands in and out, a process also hinted at by the Rice study. But without knowing the position of every molecule in the complex, there is no way to completely understand its function and dynamics.
"'We know the condensin complex is involved, because if you remove it, mitosis doesn't happen," he said. "But nobody understands the mechanism. Now that we have this structure, we have the first shot at understanding the molecular details.'"
Comment: Translation of this paper: we can see what the molecules do, but we do not know how the molecules are controlled. Molecules cannot act on their own, but are driven by reactions that are intelligently purposeful. The complexity requires design.
Genome complexity: controlling DNA in the cell
by dhw, Monday, November 05, 2018, 10:03 (2212 days ago) @ David Turell
QUOTE: "'Jumping gene invasion triggers catastrophic genomic instability in all organisms," remarked Zhao Zhang. "They greatly reduce the viability or fertility of the invaded animals and can lead to a population crisis. We believe that the ability of reproductive stem cells to rapidly adapt and restore fertility in this manner allows species to resist such a population crash. This mechanism is a lynchpin to species survival.'" (David's bold)
DAVID: My bolded sentence makes that obvious point that design is necessary from the beginning of sexual reproduction. Since transposons cause such trouble, control mechanisms had to be present from the beginning.
In that case I can’t help wondering why transposons were designed in such a way that they would cause so much trouble. It’s as if the different types of cell have to work out their own means of achieving the equilibrium or homeostasis necessary for life to continue. I would love to know more about the capabilities of stem cells. Their ability to adapt and to change their identity might lie at the core of evolutionary development.
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: This 3-D dance in cells is constant as life maintains its balance or homeostasis. It has to be automatically making necessary choices or life's processes could be scrambled by imperfect reactions. Bit by bit we are unearthing the hidden layers of genome complexity, but there is one item we don't understand at all: we may know what gene controls what process or event, but we have no idea how it exerts its control. […]
dhw: Thank you for another important article. “We have no idea how it exerts its control” is fair comment, but it doesn’t have to be AUTOMATICALLY making necessary choices. The cell/cell communities could simply be making necessary choices. Macrocosm and microcosm: macrocosmic humans and to a lesser degree our fellow animals autonomously use what we call the mind to make intelligent choices (“drive the bus”), although we have no idea what actually constitutes the mind or “how it exerts its control”. Some scientists would say the same about microcosmic cells and cell communities. That doesn't mean they have a human/animal mind - just their own particular form of intelligence. If you would only stop inserting "automatically" in your comments, I wouldn't have to indulge in all this repetition!
DAVID: Why stop when it is what I believe from the chemical evidence? Life requires constant maintenance which means exact repetition, which means automatic. Your kidney controls sodium levels in the blood exactly in a tiny range of value. The decisions are automatic, not simply necessary, which really means automatic. Stop playing with words that don't change what is obvious.
More repetition: yes, most of cellular activity is automatic. It ceases to be automatic when the cell/cell community is confronted with new problems. That is how scientists test for intelligence!
Quote: "'We know the condensin complex is involved, because if you remove it, mitosis doesn't happen," he said. "But nobody understands the mechanism. Now that we have this structure, we have the first shot at understanding the molecular details.'"
DAVID’s comment: Translation of this paper: we can see what the molecules do, but we do not know how the molecules are controlled. Molecules cannot act on their own, but are driven by reactions that are intelligently purposeful. The complexity requires design.
Thank you for summarizing the message so concisely. Yes, the complexity requires design. But the question remains: what is the mechanism that controls the actions of the molecules? If actions/reactions are intelligently purposeful, you are faced with a stark choice. Either every single one was preprogrammed 3.8 billion years ago, or your God personally intervenes when there is a new problem, or (theistic version of my hypothesis) he endowed cells with a mechanism that would enable them to deal AUTONOMOUSLY with problems as they arose.
Genome complexity: controlling DNA in the cell
by David Turell , Monday, November 05, 2018, 20:20 (2211 days ago) @ dhw
dhw: Thank you for another important article. “We have no idea how it exerts its control” is fair comment, but it doesn’t have to be AUTOMATICALLY making necessary choices. The cell/cell communities could simply be making necessary choices. Macrocosm and microcosm: macrocosmic humans and to a lesser degree our fellow animals autonomously use what we call the mind to make intelligent choices (“drive the bus”), although we have no idea what actually constitutes the mind or “how it exerts its control”. Some scientists would say the same about microcosmic cells and cell communities. That doesn't mean they have a human/animal mind - just their own particular form of intelligence. If you would only stop inserting "automatically" in your comments, I wouldn't have to indulge in all this repetition!
DAVID: Why stop when it is what I believe from the chemical evidence? Life requires constant maintenance which means exact repetition, which means automatic. Your kidney controls sodium levels in the blood exactly in a tiny range of value. The decisions are automatic, not simply necessary, which really means automatic. Stop playing with words that don't change what is obvious.
dhw: More repetition: yes, most of cellular activity is automatic. It ceases to be automatic when the cell/cell community is confronted with new problems. That is how scientists test for intelligence!
Which can interpreted, just as well, by recognizing intelligent automatic instructions for all responses.
Quote: "'We know the condensin complex is involved, because if you remove it, mitosis doesn't happen," he said. "But nobody understands the mechanism. Now that we have this structure, we have the first shot at understanding the molecular details.'"DAVID’s comment: Translation of this paper: we can see what the molecules do, but we do not know how the molecules are controlled. Molecules cannot act on their own, but are driven by reactions that are intelligently purposeful. The complexity requires design.
dhw: Thank you for summarizing the message so concisely. Yes, the complexity requires design. But the question remains: what is the mechanism that controls the actions of the molecules? If actions/reactions are intelligently purposeful, you are faced with a stark choice. Either every single one was preprogrammed 3.8 billion years ago, or your God personally intervenes when there is a new problem, or (theistic version of my hypothesis) he endowed cells with a mechanism that would enable them to deal AUTONOMOUSLY with problems as they arose.
Interpretation of the comment: 'New problems' imply new circumstances for living organisms which require modification by new designs which can only be created by a designing mind. God could certainly have provided organisms with an inventive mechanism with guidelines for future species in evolution.
Genome complexity: controlling DNA in the cell
by dhw, Tuesday, November 06, 2018, 08:33 (2211 days ago) @ David Turell
dhw: More repetition: yes, most of cellular activity is automatic. It ceases to be automatic when the cell/cell community is confronted with new problems. That is how scientists test for intelligence!
DAVID: Which can interpreted, just as well, by recognizing intelligent automatic instructions for all responses.
So (a) please stop focusing solely on the automatic activities, as if they proved that there is no intelligence in the problem-solving activities, and (b) please recognize that what you have just written acknowledges that the solving of problems can “just as well” be interpreted as evidence that cells/cell communities are autonomously intelligent.
DAVID’s comment: Translation of this paper: we can see what the molecules do, but we do not know how the molecules are controlled. Molecules cannot act on their own, but are driven by reactions that are intelligently purposeful. The complexity requires design.
dhw: Thank you for summarizing the message so concisely. Yes, the complexity requires design. But the question remains: what is the mechanism that controls the actions of the molecules? If actions/reactions are intelligently purposeful, you are faced with a stark choice. Either every single one was preprogrammed 3.8 billion years ago, or your God personally intervenes when there is a new problem, or (theistic version of my hypothesis) he endowed cells with a mechanism that would enable them to deal AUTONOMOUSLY with problems as they arose.
DAVID: Interpretation of the comment: 'New problems' imply new circumstances for living organisms which require modification by new designs which can only be created by a designing mind. God could certainly have provided organisms with an inventive mechanism with guidelines for future species in evolution.
Your “interpretation” is correct, except that my hypothesis does not include “can only be created by a designing mind” if by that you mean your God. And my hypothesis leaves out your nebulous “with guidelines”, which takes away the all-important autonomy which I suggest has led to the vast variety of life forms. In other words, your God could certainly have provided organisms with an autonomous inventive mechanism for future species in evolution.
Genome complexity: controlling DNA in the cell
by David Turell , Tuesday, November 06, 2018, 14:50 (2210 days ago) @ dhw
dhw: More repetition: yes, most of cellular activity is automatic. It ceases to be automatic when the cell/cell community is confronted with new problems. That is how scientists test for intelligence!
DAVID: Which can interpreted, just as well, by recognizing intelligent automatic instructions for all responses.
dhw: So (a) please stop focusing solely on the automatic activities, as if they proved that there is no intelligence in the problem-solving activities, and (b) please recognize that what you have just written acknowledges that the solving of problems can “just as well” be interpreted as evidence that cells/cell communities are autonomously intelligent.
All biochemical research shows that molecules act robotically in the series of reactions exposed.
DAVID’s comment: Translation of this paper: we can see what the molecules do, but we do not know how the molecules are controlled. Molecules cannot act on their own, but are driven by reactions that are intelligently purposeful. The complexity requires design.dhw: Thank you for summarizing the message so concisely. Yes, the complexity requires design. But the question remains: what is the mechanism that controls the actions of the molecules? If actions/reactions are intelligently purposeful, you are faced with a stark choice. Either every single one was preprogrammed 3.8 billion years ago, or your God personally intervenes when there is a new problem, or (theistic version of my hypothesis) he endowed cells with a mechanism that would enable them to deal AUTONOMOUSLY with problems as they arose.
DAVID: Interpretation of the comment: 'New problems' imply new circumstances for living organisms which require modification by new designs which can only be created by a designing mind. God could certainly have provided organisms with an inventive mechanism with guidelines for future species in evolution.
dhw: Your “interpretation” is correct, except that my hypothesis does not include “can only be created by a designing mind” if by that you mean your God. And my hypothesis leaves out your nebulous “with guidelines”, which takes away the all-important autonomy which I suggest has led to the vast variety of life forms. In other words, your God could certainly have provided organisms with an autonomous inventive mechanism for future species in evolution.
He is my God. We disagree about how He works. Diversity is needed for balance of nature, and therefore is part of the world God created. Why wouldn't God create the diversity on His own? You are asking for helter skelter creation. It was obviously controlled.
Genome complexity: controlling DNA in the cell
by dhw, Wednesday, November 07, 2018, 12:17 (2210 days ago) @ David Turell
dhw: More repetition: yes, most of cellular activity is automatic. It ceases to be automatic when the cell/cell community is confronted with new problems. That is how scientists test for intelligence!
DAVID: Which can interpreted, just as well, by recognizing intelligent automatic instructions for all responses.
dhw: So (a) please stop focusing solely on the automatic activities, as if they proved that there is no intelligence in the problem-solving activities, and (b) please recognize that what you have just written acknowledges that the solving of problems can “just as well” be interpreted as evidence that cells/cell communities are autonomously intelligent.
DAVID: All biochemical research shows that molecules act robotically in the series of reactions exposed.
Why have you changed cells/cell communities to molecules? I’m amazed that you think “my” advocates of cellular intelligence, who have spent a lifetime researching the behaviour of cells, have done no research on the behaviour of cells.
DAVID (under “big brain birth canal”: Only neurons can be organized into a mind that can design. Are your 'cells' somehow magically neurons?
dhw: An astonishing statement from someone who claims to be a dualist, and an astonishing assumption which runs counter to your admission that cellular problem-solving can “just as well” be interpreted as automatic – which puts automaticity on a par with the hypothesis that non-neurons can be autonomously intelligent, as advocated by some scientists who have spent a lifetime studying them.
DAVID: The automaticity discussion involves intracellular reactions, not inventing a new pelvis, which is the subject under discussion. Your lifetime group studied cells not major evolutionary changes. Your hypothesis is a huge extrapolation from the single cell reactions to whole body alterations.
Agreed a thousand times over, and that is why it is a hypothesis. But the automaticity discussion is not confined to my extrapolation. It relates to the basis from which I extrapolate my hypothesis – namely, that of cellular intelligence, which you continue to try and dismiss although at the same time you admit to a “just as well” parity of possibilities.
dhw: Your “interpretation” is correct, except that my hypothesis does not include “can only be created by a designing mind” if by that you mean your God. And my hypothesis leaves out your nebulous “with guidelines”, which takes away the all-important autonomy which I suggest has led to the vast variety of life forms. In other words, your God could certainly have provided organisms with an autonomous inventive mechanism for future species in evolution.
DAVID: He is my God. We disagree about how He works. Diversity is needed for balance of nature, and therefore is part of the world God created. Why wouldn't God create the diversity on His own? You are asking for helter skelter creation. It was obviously controlled.
If your God exists, there is no question that diversity is part of the world he created, and the constantly shifting balance of nature must be linked to constantly changing conditions which in turn lead to diversity. But you are right, he is your God, and you can imagine him doing whatever you want him to do: so yes, he could deliberately have created every single life form, lifestyle and natural wonder extant and extinct in the whole history of life, controlling every action by every organism, and probably controlling every change in conditions as well (since the changing balance of nature depends on changing conditions). How all this fits in with his purpose of creating the brain and body of H. sapiens is a mystery, but God’s logic is different from ours so we shouldn’t try to fit the different parts of the hypothesis together. And we shouldn’t consider a different hypothesis whose parts actually do fit together, because…because…? Well, he is your God and you can imagine him doing...etc.
Genome complexity: controlling DNA in the cell
by David Turell , Wednesday, November 07, 2018, 18:43 (2209 days ago) @ dhw
dhw: So (a) please stop focusing solely on the automatic activities, as if they proved that there is no intelligence in the problem-solving activities, and (b) please recognize that what you have just written acknowledges that the solving of problems can “just as well” be interpreted as evidence that cells/cell communities are autonomously intelligent.
DAVID: All biochemical research shows that molecules act robotically in the series of reactions exposed.
dhw: Why have you changed cells/cell communities to molecules? I’m amazed that you think “my” advocates of cellular intelligence, who have spent a lifetime researching the behaviour of cells, have done no research on the behaviour of cells.
What do you think your guys study except molecular reactions in cells? That is what biological research is at the intracellular level!.
DAVID: The automaticity discussion involves intracellular reactions, not inventing a new pelvis, which is the subject under discussion. Your lifetime group studied cells not major evolutionary changes. Your hypothesis is a huge extrapolation from the single cell reactions to whole body alterations.dhw: Agreed a thousand times over, and that is why it is a hypothesis. But the automaticity discussion is not confined to my extrapolation. It relates to the basis from which I extrapolate my hypothesis – namely, that of cellular intelligence, which you continue to try and dismiss although at the same time you admit to a “just as well” parity of possibilities.
Intelligent molecular reactions in cells cannot create evolution All they are doing is performing life's homeostasis. Do any of your folks think cellular intelligence leads to evolution?
dhw: Your “interpretation” is correct, except that my hypothesis does not include “can only be created by a designing mind” if by that you mean your God. And my hypothesis leaves out your nebulous “with guidelines”, which takes away the all-important autonomy which I suggest has led to the vast variety of life forms. In other words, your God could certainly have provided organisms with an autonomous inventive mechanism for future species in evolution.DAVID: He is my God. We disagree about how He works. Diversity is needed for balance of nature, and therefore is part of the world God created. Why wouldn't God create the diversity on His own? You are asking for helter skelter creation. It was obviously controlled.
See my fungus entry today. Perfect example of preplanning by God.
dhw: If your God exists, there is no question that diversity is part of the world he created, and the constantly shifting balance of nature must be linked to constantly changing conditions which in turn lead to diversity. But you are right, he is your God, and you can imagine him doing whatever you want him to do: so yes, he could deliberately have created every single life form, lifestyle and natural wonder extant and extinct in the whole history of life, controlling every action by every organism, and probably controlling every change in conditions as well (since the changing balance of nature depends on changing conditions). How all this fits in with his purpose of creating the brain and body of H. sapiens is a mystery, but God’s logic is different from ours so we shouldn’t try to fit the different parts of the hypothesis together. And we shouldn’t consider a different hypothesis whose parts actually do fit together, because…because…? Well, he is your God and you can imagine him doing...etc.
I fully understand where your rump is placed on the picket fence. You admit design is needed to explain the tremendous changes in evolution, but can't explain where the design originated
so you invent what to me are preposterous hypotheses based on a monstrous extrapolation of cellular intelligence, when all they are doing is intelligently running life's homeostasis because of how they are designed. Which is why this website exists to help clear up agnostic confusion.
Genome complexity: controlling DNA in the cell
by dhw, Thursday, November 08, 2018, 11:41 (2209 days ago) @ David Turell
DAVID: All biochemical research shows that molecules act robotically in the series of reactions exposed.
dhw: Why have you changed cells/cell communities to molecules? I’m amazed that you think “my” advocates of cellular intelligence, who have spent a lifetime researching the behaviour of cells, have done no research on the behaviour of cells.
DAVID: What do you think your guys study except molecular reactions in cells? That is what biological research is at the intracellular level!
The question does not revolve around molecular reactions but around what DRIVES the molecular reactions! My guys have observed how cells solve problems, and have concluded that the molecular reactions which lead to the solution of the problems are driven by cellular intelligence.
DAVID: Intelligent molecular reactions in cells cannot create evolution All they are doing is performing life's homeostasis. Do any of your folks think cellular intelligence leads to evolution?
If you bear in mind that Shapiro is a strong champion of cellular intelligence, I think his concept of natural genetic engineering suggests precisely that:
www.thethirdwayofevolution.com/people/view/james-a-shapiro
QUOTES: "The capacity of living organisms to alter their own heredity is undeniable. Our current ideas about evolution have to incorporate this basic fact of life."
(Evolution: A View from the 21st Century, p.2)
quote: “Shapiro integrates advances in symbiogenesis, epigenetics, and saltationism into a unified approach that views evolutionary change as an active cell process, regulated epigenetically and capable of making rapid large changes by horizontal DNA transfer, inter-specific hybridization, whole genome doubling, symbiogenesis, or massive genome restructuring.”
dhw: If your God exists, there is no question that diversity is part of the world he created, and the constantly shifting balance of nature must be linked to constantly changing conditions which in turn lead to diversity. But you are right, he is your God, and you can imagine him doing whatever you want him to do: so yes, he could deliberately have created every single life form, lifestyle and natural wonder extant and extinct in the whole history of life, controlling every action by every organism, and probably controlling every change in conditions as well (since the changing balance of nature depends on changing conditions). How all this fits in with his purpose of creating the brain and body of H. sapiens is a mystery, but God’s logic is different from ours so we shouldn’t try to fit the different parts of the hypothesis together. And we shouldn’t consider a different hypothesis whose parts actually do fit together, because…because…? Well, he is your God and you can imagine him doing...etc.
DAVID: I fully understand where your rump is placed on the picket fence. You admit design is needed to explain the tremendous changes in evolution, but can't explain where the design originated so you invent what to me are preposterous hypotheses based on a monstrous extrapolation of cellular intelligence, when all they are doing is intelligently running life's homeostasis because of how they are designed. Which is why this website exists to help clear up agnostic confusion.
Sorry, but your polemic does not lend any credibility to your own hypothesis, whose illogicality you admit by claiming that your God’s logic must be different from ours. On the other hand, you have agreed that my hypothesis fits in with the history of life as we know it, and since NOBODY knows the origin of speciation, but we do know that cell communities are capable of minor adaptations and of solving problems, the hypothesis that they might also have engineered the innovations we cannot explain can hardly be called “monstrous” or “preposterous”. And for those who believe in or do not disbelieve in God, the hypothesis has the added attraction that it does not in any way exclude his existence as the inventor of the mechanism. It only excludes one particular, illogical interpretation of his motives and methods.
Genome complexity: controlling DNA in the cell
by David Turell , Thursday, November 08, 2018, 18:20 (2208 days ago) @ dhw
DAVID: What do you think your guys study except molecular reactions in cells? That is what biological research is at the intracellular level!
dhw: The question does not revolve around molecular reactions but around what DRIVES the molecular reactions! My guys have observed how cells solve problems, and have concluded that the molecular reactions which lead to the solution of the problems are driven by cellular intelligence.
But all they can see in studying molecular reactions is those reactions, and assuming a background intelligence, not automaticity in the reactions, thus they must introduce an enormous assumption of a background of active intelligence, when it all can be intelligent design of responses.
DAVID: Intelligent molecular reactions in cells cannot create evolution All they are doing is performing life's homeostasis. Do any of your folks think cellular intelligence leads to evolution?dhw: If you bear in mind that Shapiro is a strong champion of cellular intelligence, I think his concept of natural genetic engineering suggests precisely that:
www.thethirdwayofevolution.com/people/view/james-a-shapiroQUOTES: "The capacity of living organisms to alter their own heredity is undeniable. Our current ideas about evolution have to incorporate this basic fact of life."
(Evolution: A View from the 21st Century, p.2)quote: “Shapiro integrates advances in symbiogenesis, epigenetics, and saltationism into a unified approach that views evolutionary change as an active cell process, regulated epigenetically and capable of making rapid large changes by horizontal DNA transfer, inter-specific hybridization, whole genome doubling, symbiogenesis, or massive genome restructuring.”
I've carefully read all of this a long time ago, based on his bacterial studies, and have integrated it into my thinking and arguments.
DAVID: I fully understand where your rump is placed on the picket fence. You admit design is needed to explain the tremendous changes in evolution, but can't explain where the design originated so you invent what to me are preposterous hypotheses based on a monstrous extrapolation of cellular intelligence, when all they are doing is intelligently running life's homeostasis because of how they are designed. Which is why this website exists to help clear up agnostic confusion.dhw: Sorry, but your polemic does not lend any credibility to your own hypothesis, whose illogicality you admit by claiming that your God’s logic must be different from ours.
How do you logically know God's logic is like ours. I believe in Him but I don't know I know His form of logic must be like mine. You must know Him better than I do.
Genome complexity: controlling DNA in the cell
by dhw, Friday, November 09, 2018, 12:39 (2208 days ago) @ David Turell
DAVID: What do you think your guys study except molecular reactions in cells? That is what biological research is at the intracellular level!
dhw: The question does not revolve around molecular reactions but around what DRIVES the molecular reactions! My guys have observed how cells solve problems, and have concluded that the molecular reactions which lead to the solution of the problems are driven by cellular intelligence.
DAVID: But all they can see in studying molecular reactions is those reactions, and assuming a background intelligence, not automaticity in the reactions, thus they must introduce an enormous assumption of a background of active intelligence, when it all can be intelligent design of responses.
I like your “can be”, which chimes in with your earlier “just as well” and your even earlier 50/50. It is not an enormous assumption, it is a rational conclusion they draw from their research, and is certainly no more enormous or unreasonable than your own assumption that the problem-solving, decision-making behaviour of cells/cell communities was preprogrammed 3.8 billion years ago by your God, except when he pops in to do a personal dabble.
DAVID: Do any of your folks think cellular intelligence leads to evolution?
dhw: If you bear in mind that Shapiro is a strong champion of cellular intelligence, I think his concept of natural genetic engineering suggests precisely that:
www.thethirdwayofevolution.com/people/view/james-a-shapiro
QUOTE: "The capacity of living organisms to alter their own heredity is undeniable. Our current ideas about evolution have to incorporate this basic fact of life."
(Evolution: A View from the 21st Century, p.2)
QUOTE: “Shapiro integrates advances in symbiogenesis, epigenetics, and saltationism into a unified approach that views evolutionary change as an active cell process, regulated epigenetically and capable of making rapid large changes by horizontal DNA transfer, inter-specific hybridization, whole genome doubling, symbiogenesis, or massive genome restructuring.”
DAVID: I've carefully read all of this a long time ago, based on his bacterial studies, and have integrated it into my thinking and arguments.
If you have carefully read that living organisms have the capacity to alter their own heredity, that evolutionary change is an active cell process, and that rejection of cellular intelligence is “large organisms chauvinism”, then you have not integrated it into your thinking and arguments but have categorically rejected it.
dhw: Sorry, but your polemic does not lend any credibility to your own hypothesis, whose illogicality you admit by claiming that your God’s logic must be different from ours.
DAVID: How do you logically know God's logic is like ours. I believe in Him but I don't know I know His form of logic must be like mine. You must know Him better than I do.
Neither of us “knows” if your God even exists, let alone how he thinks. However, in the past you have quite rightly argued that the only way we can guess how he thinks is by studying his works. We have both studied his works, and by your own admission, your hypothesis is illogical, while mine is logical. But you reject mine and cling to yours. Why is it more logical for you to believe in your illogical hypothesis than to even consider the possibility that my logical hypothesis might be correct?
Genome complexity: controlling DNA in the cell
by David Turell , Friday, November 09, 2018, 15:25 (2207 days ago) @ dhw
dhw: Sorry, but your polemic does not lend any credibility to your own hypothesis, whose illogicality you admit by claiming that your God’s logic must be different from ours.
DAVID: How do you logically know God's logic is like ours. I believe in Him but I don't know I know His form of logic must be like mine. You must know Him better than I do.
dhw: Neither of us “knows” if your God even exists, let alone how he thinks. However, in the past you have quite rightly argued that the only way we can guess how he thinks is by studying his works. We have both studied his works, and by your own admission, your hypothesis is illogical, while mine is logical. But you reject mine and cling to yours. Why is it more logical for you to believe in your illogical hypothesis than to even consider the possibility that my logical hypothesis might be correct?
I have constantly considered my thoughts as perfectly logical. I have never said I was illogical, unless you have misinterpreted what I write, which you sometimes do. You have constantly told me I am illogical to the point now where you believe I said it about myself. What are you smoking? I view your initial concepts as totally unreasonable, but have agreed your logic following the false starts have logic. So?
Genome complexity: DNA 3-D importance
by David Turell , Friday, November 09, 2018, 23:49 (2207 days ago) @ David Turell
Where and how genes and modifying sites are located is very important to gene expression and function:
https://www.quantamagazine.org/in-the-nucleus-genes-activity-might-depend-on-their-loca...
The 6 feet of DNA intricately bundled within a human cell’s tiny nucleus can look as chaotic as a ball of spaghetti or a tangle of thread. But how that DNA gets situated in three-dimensional space is critical — and not at all random. The degree of packing and folding enables genes to be accessible in the right place at the right time, so that the cell’s machinery can find and decode them, dial their activity up or down, and keep everything working as it should. Those rearrangements also put specific parts of the genome near or far from landmarks within the nucleus.
There’s been tantalizing evidence that the positioning of DNA at those nuclear locations may not be coincidental. Tightly wound, silent genes tend to be located toward the periphery of the nucleus, while open, active DNA makes its home toward the interior. During development, as cells differentiate, the DNA reorganizes itself: As some genes shift from a repressed state to an active one, they’ve also been found to move away from the periphery. That said, some other gene regions usually found near the periphery aren’t there all the time, and when they do move, they still show the same levels of activity.
***
“This implies that the location of the telomeres in the nucleus is important for cells to finish their proper cell cycle,” Qi said. He speculates that the Cajal bodies may have had this effect because they’ve previously been shown to produce an enzyme that helps maintain the length of telomeres. “We think we were potentially co-localizing the manufacturing plant with the consumer market,” he said.
But the researchers still need to root out just why these effects occurred. They’ll have to perform further experiments — targeting various genes and nuclear bodies in diverse cell types, and testing not only for effects on gene expression but also on genomic stability and other factors — to find out why and how the genome is organized as it is. At the very least, it seems to “build in an extra level of control,” Guttman said. “By creating active and inactive territories, the nucleus can prevent proteins that silence transcription from aberrantly turning off a gene that needs to be on, and vice versa.”
Susan Gasser, a molecular biologist at the Friedrich Miescher Institute for Biomedical Research in Switzerland, thinks experts will find that location in the nucleus is important for very particular processes, such as DNA repair — but that a lot of the time, “it instead fine-tunes gene expression.” The open or condensed state of the DNA itself may be more influential.
Comment: I've raised the importance of the DNA 3-D relationships before. Obviously positioning of genes is another layer of control taht we do not yet understand, but adds to the complexity about how DNA works its processes to utilize genes properly. I suspect that 22,000+/- human genes create much more than that total of outcomes.
Genome complexity: DNA 3-D importance in replication
by David Turell , Tuesday, January 01, 2019, 18:03 (2154 days ago) @ David Turell
It is now shown that cells can rearrange DNA for replication:
https://www.sciencedaily.com/releases/2018/12/181227150644.htm
" Taylor demonstrated how different segments of chromosomes duplicate in the late 1950s and published more than 100 papers on chromosome structure and replication. Roughly 60 years later, Gilbert determined how replication was regulated.
***
"Gilbert and Sima examined a single segment of the DNA in the highest possible 3D resolution and saw three sequences along the DNA molecule touching each other frequently. The researchers then used CRISPR, a sophisticated gene editing technology, to remove these three areas simultaneously.
"And with that, they found that these three elements together were the key to DNA replication.
"'Removing these elements shifted the segment's replication time from the very beginning to the very end of the process," Gilbert said. "This was one of those moments where just one result knocks your socks off."
"In addition to the effect on replication timing, the removal of the three elements caused the 3D structure of the DNA molecule to change dramatically.
"We have for the first time pinpointed specific DNA sequences in the genome that regulate chromatin structure and replication timing," Sima said. "These results reflect one possible model of how DNA folds inside cells and how these folding patterns could impact the hereditary materials' function."
"Greater understanding of how DNA replication is regulated opens new paths of research in genetics. When replication timing is altered -- as it was in Gilbert and Sima's experiment -- it can completely change how the genetic information of a cell is interpreted. This could become crucial information.
"'If you duplicate at a different place and time, you might assemble a completely different structure," Gilbert said. "A cell has different things available to it at different times. Changing when something replicates changes the packaging of the genetic information.'"
Comment: Just as Shapiro shows, DNA can be edited by cells. The implication is that this ability was present when bacteria appeared early in evolution. 3-D DNA is a major key to the amazing variations in controls DNA can exert just by its own 3-D relationships and how they change. Just where are the instructions to guide DNA contortions? Probably in other parts of the specific DNA. This is obviously key evidence as to how as few as 22,000 genes make a complex human.
Genome complexity: DNA 3-D importance in replication
by dhw, Wednesday, January 02, 2019, 12:09 (2154 days ago) @ David Turell
QUOTE: "'If you duplicate at a different place and time, you might assemble a completely different structure," Gilbert said. "A cell has different things available to it at different times. Changing when something replicates changes the packaging of the genetic information.'"
DAVID’s comment: Just as Shapiro shows, DNA can be edited by cells. The implication is that this ability was present when bacteria appeared early in evolution. 3-D DNA is a major key to the amazing variations in controls DNA can exert just by its own 3-D relationships and how they change. Just where are the instructions to guide DNA contortions? Probably in other parts of the specific DNA. This is obviously key evidence as to how as few as 22,000 genes make a complex human.
If different structures result from duplication at a different place and time, we have a clear indication that evolution (= changing structures) is heavily dependent on place and time (= the current environment). We then go back to your belief that all the instructions for all the undabbled changes were implanted 3.8 billion years ago, and to my alternative hypothesis that somewhere within the cell/cell community is an autonomous intelligence (as championed by the same Shapiro, and possibly invented by your God) which enables it to change itself in accordance with the needs or opportunities that arise from the current environment.
Genome complexity: DNA 3-D importance in replication
by David Turell , Wednesday, January 02, 2019, 15:09 (2153 days ago) @ dhw
QUOTE: "'If you duplicate at a different place and time, you might assemble a completely different structure," Gilbert said. "A cell has different things available to it at different times. Changing when something replicates changes the packaging of the genetic information.'"
DAVID’s comment: Just as Shapiro shows, DNA can be edited by cells. The implication is that this ability was present when bacteria appeared early in evolution. 3-D DNA is a major key to the amazing variations in controls DNA can exert just by its own 3-D relationships and how they change. Just where are the instructions to guide DNA contortions? Probably in other parts of the specific DNA. This is obviously key evidence as to how as few as 22,000 genes make a complex human.
dhw: If different structures result from duplication at a different place and time, we have a clear indication that evolution (= changing structures) is heavily dependent on place and time (= the current environment). We then go back to your belief that all the instructions for all the undabbled changes were implanted 3.8 billion years ago, and to my alternative hypothesis that somewhere within the cell/cell community is an autonomous intelligence (as championed by the same Shapiro, and possibly invented by your God) which enables it to change itself in accordance with the needs or opportunities that arise from the current environment.
We both now agree that DNA editing by unicellular organisms happens. I view it as part of God's information/instructions used by the cell, and you admit it is possible. We both agree about Shapiro who experimentally showed it.
Genome complexity: DNA 3-D importance in replication
by dhw, Thursday, January 03, 2019, 10:10 (2153 days ago) @ David Turell
QUOTE: "'If you duplicate at a different place and time, you might assemble a completely different structure," Gilbert said. "A cell has different things available to it at different times. Changing when something replicates changes the packaging of the genetic information.'"
DAVID’s comment: Just as Shapiro shows, DNA can be edited by cells. The implication is that this ability was present when bacteria appeared early in evolution. 3-D DNA is a major key to the amazing variations in controls DNA can exert just by its own 3-D relationships and how they change. Just where are the instructions to guide DNA contortions? Probably in other parts of the specific DNA. This is obviously key evidence as to how as few as 22,000 genes make a complex human.
dhw: If different structures result from duplication at a different place and time, we have a clear indication that evolution (= changing structures) is heavily dependent on place and time (= the current environment). We then go back to your belief that all the instructions for all the undabbled changes were implanted 3.8 billion years ago, and to my alternative hypothesis that somewhere within the cell/cell community is an autonomous intelligence (as championed by the same Shapiro, and possibly invented by your God) which enables it to change itself in accordance with the needs or opportunities that arise from the current environment.
DAVID: We both now agree that DNA editing by unicellular organisms happens. I view it as part of God's information/instructions used by the cell, and you admit it is possible. We both agree about Shapiro who experimentally showed it.
The question is not whether DNA editing happens, but whether your God’s “information/instructions used by the cell” means a specific, 3.8-billion-year-old programme for every single change in the history of evolution, switched on automatically by the cell when conditions require or allow it – which seems to me extremely unlikely – or a mechanism which enables the cell to change itself autonomously, i.e. to devise its own programme as conditions change. Shapiro clearly believes in the latter.
DAVID (under “Gulls change wing shape”): Helps them glide and fly in different ways:
https://techxplore.com/news/2019-01-zoologists-reveal-gulls-wing-morph.html
DAVID: It is not known if the original gulls had this ability from the beginning or developed it over time. If it wasn't present in the beginning they had trouble hunting over the oceans so one can wonder how they survived until they developed these adaptations of elbow joints which require exact design.
Perhaps they initially found plenty of food close at wing (like pre-whales having plenty of food close at leg) but then conditions changed and they had to hunt further afield, which occasioned the changes made by the cell communities that constitute the wings and their connections.
Genome complexity: DNA 3-D importance in replication
by David Turell , Thursday, January 03, 2019, 19:03 (2152 days ago) @ dhw
QUOTE: "'If you duplicate at a different place and time, you might assemble a completely different structure," Gilbert said. "A cell has different things available to it at different times. Changing when something replicates changes the packaging of the genetic information.'"
DAVID’s comment: Just as Shapiro shows, DNA can be edited by cells. The implication is that this ability was present when bacteria appeared early in evolution. 3-D DNA is a major key to the amazing variations in controls DNA can exert just by its own 3-D relationships and how they change. Just where are the instructions to guide DNA contortions? Probably in other parts of the specific DNA. This is obviously key evidence as to how as few as 22,000 genes make a complex human.
dhw: If different structures result from duplication at a different place and time, we have a clear indication that evolution (= changing structures) is heavily dependent on place and time (= the current environment). We then go back to your belief that all the instructions for all the undabbled changes were implanted 3.8 billion years ago, and to my alternative hypothesis that somewhere within the cell/cell community is an autonomous intelligence (as championed by the same Shapiro, and possibly invented by your God) which enables it to change itself in accordance with the needs or opportunities that arise from the current environment.
DAVID: We both now agree that DNA editing by unicellular organisms happens. I view it as part of God's information/instructions used by the cell, and you admit it is possible. We both agree about Shapiro who experimentally showed it.
dhw: The question is not whether DNA editing happens, but whether your God’s “information/instructions used by the cell” means a specific, 3.8-billion-year-old programme for every single change in the history of evolution, switched on automatically by the cell when conditions require or allow it – which seems to me extremely unlikely – or a mechanism which enables the cell to change itself autonomously, i.e. to devise its own programme as conditions change. Shapiro clearly believes in the latter.
The only issue here is I believe God gave the cells that mechanism.
DAVID (under “Gulls change wing shape”): Helps them glide and fly in different ways:
https://techxplore.com/news/2019-01-zoologists-reveal-gulls-wing-morph.htmlDAVID: It is not known if the original gulls had this ability from the beginning or developed it over time. If it wasn't present in the beginning they had trouble hunting over the oceans so one can wonder how they survived until they developed these adaptations of elbow joints which require exact design.
dhw: Perhaps they initially found plenty of food close at wing (like pre-whales having plenty of food close at leg) but then conditions changed and they had to hunt further afield, which occasioned the changes made by the cell communities that constitute the wings and their connections.
You are still using environmental changes to push evolution, but some one or some thing has to do the designing for the large body changes.
Genome complexity: DNA tiny part of the controls
by David Turell , Thursday, January 03, 2019, 19:35 (2152 days ago) @ David Turell
DNA codes for protein but we still do not know what runs life:
http://nautil.us/issue/68/context/its-the-end-of-the-gene-as-we-know-it
"The existence of a powerful code-script seemed to be confirmed with the discovery of the structure of DNA by Watson and Crick in 1953. They revealed how the sequences of components (called nucleotides) in DNA could serve as a template—a code—for a protein, much as a typewriter sequences letters to form words. 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.
***
"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.
"This can seem confusing to those of us indoctrinated in the idea that there must be a set of genetic instructions prior to development: If not in the DNA code, then where? By the 1980s, research findings started to turn that notion on its head.
***
"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.
***
"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, “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.”
***
"But 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.
***
"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.
***
" 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: the whole system of genetic controls is still a giant black box.
Genome complexity: control of DNA in embryology
by David Turell , Thursday, January 03, 2019, 23:07 (2152 days ago) @ David Turell
Spot Methylation is used in early mouse embryos to control DNA:
https://medicalxpress.com/news/2019-01-discovery-cell-genes-early-embryos.html
"Our bodies hold roughly 14 trillion cells, each containing a nucleus with DNA measuring two meters long by 20 atoms wide. To fit inside each nucleus, DNA coils around specialized proteins. These spools of wrapped DNA inhibit gene regulatory proteins from binding to protein-coding stretches along the genome, which help keep genes in the "off" position when they're not needed.
"Until now, it was unclear how this DNA packing affected development in early embryos. In a paper published this week in Science, researchers from the Perelman School of Medicine at the University of Pennsylvania found that in mouse embryos—only eight days after fertilization—compacted regions along the genome increase at protein-coding genes. Days later in the cell differentiation phase, these domains open to allow certain genes to be read and made into their corresponding proteins.
"'This is a fundamental change in our understanding of how genes are controlled in the early embryo, even if we can't yet see all the potential clinical impacts," said Ken Zaret, Ph.D., director of the Penn Institute of Regenerative Medicine and a professor of Cell and Developmental Biology. "This study demonstrates the importance of the 'off position' for gene activity in early animal development."
"First author Dario Nicetto, Ph.D., a postdoctoral fellow in Zaret's lab, explains that he and coauthors think that during the earliest stages of development, more compacted gene-coding regions arise so that a cell can make rapid "decisions" about which genes should be made into proteins. However, if genes are not open at the correct regions to be read and made into appropriate proteins, cells lose their proper identity and give rise to damaged tissue, and eventually death.
"The team also found that compacted regions were marked by three methyl molecules, which occur at specific sites of protein binding along the genome. Basically, more trimethylation leads to more compaction, which means less of the genome is available to mRNA to eventually make full-length proteins. On the other hand, less trimethylation means less compaction, so more of the genome is available for transcribing into working proteins.
"The team showed that if they deactivated the enzymes that add the methyl groups onto chromosomes, it causes out-of-place expression of cell-inappropriate genes leading to the eventual death of tissue. For example, they found that genes that are not normally "on" in liver cells are activated, which led to cell death and ultimately inadequate liver function."
Comment: As in the last entry we can see how controls are used, but still do not understand how the primary controller works.
Genome complexity: DNA 3-D importance in replication
by dhw, Friday, January 04, 2019, 13:22 (2152 days ago) @ David Turell
dhw: The question is not whether DNA editing happens, but whether your God’s “information/instructions used by the cell” means a specific, 3.8-billion-year-old programme for every single change in the history of evolution, switched on automatically by the cell when conditions require or allow it – which seems to me extremely unlikely – or a mechanism which enables the cell to change itself autonomously, i.e. to devise its own programme as conditions change. Shapiro clearly believes in the latter.
DAVID: The only issue here is I believe God gave the cells that mechanism.
I’ve read this through several times, and I’m still not sure that I dare to celebrate. Can it really be true that you have jettisoned the hypothesis of the first cells containing a 3.8-billion-year old programme for every change, and are now in favour of an autonomous mechanism whereby cells change in response to changing conditions? (I have always allowed for your God being the inventor of the mechanism.) This may be a red letter day in the history of the AgnosticWeb!
Quotes from “Genome complexity: DNA tiny part of the controls”: "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.
"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."
Once more I must thank you for your admirable integrity in offering us an article which supports the hypothesis you have so long resisted. It even uses my own favourite analogy of ant colonies. Shapiro champions cellular intelligence, and I don’t see how any organism that “learns” and creates instructions on the hoof (as opposed to being preprogrammed) can be seen as an automaton.
DAVID (under “Gulls change wing shape”): Helps them glide and fly in different ways:
https://techxplore.com/news/2019-01-zoologists-reveal-gulls-wing-morph.html
DAVID: It is not known if the original gulls had this ability from the beginning or developed it over time. If it wasn't present in the beginning they had trouble hunting over the oceans so one can wonder how they survived until they developed these adaptations of elbow joints which require exact design.
dhw: Perhaps they initially found plenty of food close at wing (like pre-whales having plenty of food close at leg) but then conditions changed and they had to hunt further afield, which occasioned the changes made by the cell communities that constitute the wings and their connections.
DAVID: You are still using environmental changes to push evolution, but some one or some thing has to do the designing for the large body changes.
Yes of course I am. Fins would not be much use if the pre-whale hadn’t taken to the water. You have just agreed that the ‘some thing’ is the cells themselves containing the mechanism which enables them to change autonomously as conditions change (provided God invented the mechanism).
Genome complexity: DNA 3-D importance in replication
by David Turell , Friday, January 04, 2019, 15:35 (2151 days ago) @ dhw
dhw: The question is not whether DNA editing happens, but whether your God’s “information/instructions used by the cell” means a specific, 3.8-billion-year-old programme for every single change in the history of evolution, switched on automatically by the cell when conditions require or allow it – which seems to me extremely unlikely – or a mechanism which enables the cell to change itself autonomously, i.e. to devise its own programme as conditions change. Shapiro clearly believes in the latter.
DAVID: The only issue here is I believe God gave the cells that mechanism.
dhw: I’ve read this through several times, and I’m still not sure that I dare to celebrate. Can it really be true that you have jettisoned the hypothesis of the first cells containing a 3.8-billion-year old programme for every change, and are now in favour of an autonomous mechanism whereby cells change in response to changing conditions? (I have always allowed for your God being the inventor of the mechanism.) This may be a red letter day in the history of the AgnosticWeb!
No letter. I've always accepted Shapiro's studies that shows bacteria can alter their DNA. In Lenski's studies with perpetual E. coli colonies they alter their use of glucose and citrate. Both mechanisms of metabolism are present, but they are able to shift when necessary to what is available and that requires some change in DNA. The 3.8 byo program gets evidence from this knowledge.
dhw: Quotes from “Genome complexity: DNA tiny part of the controls”: "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."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."
Once more I must thank you for your admirable integrity in offering us an article which supports the hypothesis you have so long resisted. It even uses my own favourite analogy of ant colonies. Shapiro champions cellular intelligence, and I don’t see how any organism that “learns” and creates instructions on the hoof (as opposed to being preprogrammed) can be seen as an automaton.
The ability to alter metabolism can well be a 3.8 byo programmed ability.
DAVID: You are still using environmental changes to push evolution, but some one or some thing has to do the designing for the large body changes.dhw: Yes of course I am. Fins would not be much use if the pre-whale hadn’t taken to the water. You have just agreed that the ‘some thing’ is the cells themselves containing the mechanism which enables them to change autonomously as conditions change (provided God invented the mechanism).
Cells in legs cannot decide to create fins and design them. Cells simply can alter metabolism as shown above. Animals are designed to fit their environments requirements which can change requiring new design or extinction. 'Bad luck' still applies. God steps in where He wishes.
Genome complexity: DNA 3-D importance in replication
by dhw, Saturday, January 05, 2019, 12:40 (2151 days ago) @ David Turell
dhw: The question is not whether DNA editing happens, but whether your God’s “information/instructions used by the cell” means a specific, 3.8-billion-year-old programme for every single change in the history of evolution, switched on automatically by the cell when conditions require or allow it – which seems to me extremely unlikely – or a mechanism which enables the cell to change itself autonomously, i.e. to devise its own programme as conditions change. Shapiro clearly believes in the latter.
DAVID: The only issue here is I believe God gave the cells that mechanism.
dhw: This may be a red letter day in the history of the AgnosticWeb!
DAVID: No letter. I've always accepted Shapiro's studies that shows bacteria can alter their DNA. In Lenski's studies with perpetual E. coli colonies they alter their use of glucose and citrate. Both mechanisms of metabolism are present, but they are able to shift when necessary to what is available and that requires some change in DNA. The 3.8 byo program gets evidence from this knowledge.
Evolution requires changes in the DNA. I gave you the choice between a 3.8 byo programme for all the changes and a mechanism which enabled the cells to change AUTONOMOUSLY in response to changing conditions. You went for the mechanism, and believe that your God gave it to the cells. If they can change their own DNA autonomously, how does that provide evidence for a 3.8 byo programme for all the changes?
dhw: Once more I must thank you for your admirable integrity in offering us an article which supports the hypothesis you have so long resisted. It even uses my own favourite analogy of ant colonies. Shapiro champions cellular intelligence, and I don’t see how any organism that “learns” and creates instructions on the hoof (as opposed to being preprogrammed) can be seen as an automaton.
DAVID: The ability to alter metabolism can well be a 3.8 byo programmed ability.
You are playing with words. The ability to make changes autonomously would be 3.8 byo. That is what I have proposed. Your proposal has been that cells are automatons and all the individual changes were programmed in the first cells 3.8 billion years ago.
DAVID: You are still using environmental changes to push evolution, but some one or some thing has to do the designing for the large body changes.
dhw: Yes of course I am. Fins would not be much use if the pre-whale hadn’t taken to the water. You have just agreed that the ‘some thing’ is the cells themselves containing the mechanism which enables them to change autonomously as conditions change (provided God invented the mechanism).
DAVID: Cells in legs cannot decide to create fins and design them. Cells simply can alter metabolism as shown above.
Cells can alter their own DNA and their own structures. We do not know the extent to which they can do this, which is why Shapiro’s “natural genetic engineering”, or my more explicit concept of autonomous (possibly God-given) cellular intelligence as the inventor of innovations, remains a hypothesis.
DAVID: Animals are designed to fit their environments requirements which can change requiring new design or extinction. 'Bad luck' still applies. God steps in where He wishes.
I’m glad you now acknowledge the vital importance of environmental influence. It is indeed bad luck if organisms can’t use their possibly God-given autonomous intelligence to solve new problems. If God exists, then of course he can dabble if he wishes, and the theistic version of my hypothesis has always allowed for this. Chixculub might be an example. (The atheistic version would be that environmental change is purely by chance – bad luck in some cases, and good in others – though it is also possible that your God set up a system to engender random environmental change.)
Genome complexity: DNA 3-D importance in replication
by David Turell , Saturday, January 05, 2019, 15:03 (2150 days ago) @ dhw
dhw: This may be a red letter day in the history of the AgnosticWeb!
DAVID: No letter. I've always accepted Shapiro's studies that shows bacteria can alter their DNA. In Lenski's studies with perpetual E. coli colonies they alter their use of glucose and citrate. Both mechanisms of metabolism are present, but they are able to shift when necessary to what is available and that requires some change in DNA. The 3.8 byo program gets evidence from this knowledge.dhw: Evolution requires changes in the DNA. I gave you the choice between a 3.8 byo programme for all the changes and a mechanism which enabled the cells to change AUTONOMOUSLY in response to changing conditions. You went for the mechanism, and believe that your God gave it to the cells. If they can change their own DNA autonomously, how does that provide evidence for a 3.8 byo programme for all the changes?
The 3.8 byo program allows the organisms to modify their DNA only for adaptations to immediate needs which provide minor changes within species. That is how I view Shapiro. Elsewhere I have provided evidence for the initial program completely providing everything (all info) from the beginning
DAVID: Cells in legs cannot decide to create fins and design them. Cells simply can alter metabolism as shown above.Cells can alter their own DNA and their own structures. We do not know the extent to which they can do this, which is why Shapiro’s “natural genetic engineering”, or my more explicit concept of autonomous (possibly God-given) cellular intelligence as the inventor of innovations, remains a hypothesis.
DAVID: Animals are designed to fit their environments requirements which can change requiring new design or extinction. 'Bad luck' still applies. God steps in where He wishes.
dhw: I’m glad you now acknowledge the vital importance of environmental influence. It is indeed bad luck if organisms can’t use their possibly God-given autonomous intelligence to solve new problems. If God exists, then of course he can dabble if he wishes, and the theistic version of my hypothesis has always allowed for this. Chixculub might be an example. (The atheistic version would be that environmental change is purely by chance – bad luck in some cases, and good in others – though it is also possible that your God set up a system to engender random environmental change.)
Of course environment plays a huge role as when mammals entered water permanently, but design for survival is required. Note design is primary.
Genome complexity: DNA 3-D importance in replication
by dhw, Sunday, January 06, 2019, 10:39 (2150 days ago) @ David Turell
dhw: Evolution requires changes in the DNA. I gave you the choice between a 3.8 byo programme for all the changes and a mechanism which enabled the cells to change AUTONOMOUSLY in response to changing conditions. You went for the mechanism, and believe that your God gave it to the cells. If they can change their own DNA autonomously, how does that provide evidence for a 3.8 byo programme for all the changes?
DAVID: The 3.8 byo program allows the organisms to modify their DNA only for adaptations to immediate needs which provide minor changes within species. That is how I view Shapiro. Elsewhere I have provided evidence for the initial program completely providing everything (all info) from the beginning.
This makes no sense. Presumably your first sentence refers to Shapiro’s hypothesis of “natural genetic engineering” (and my hypothesis of cellular intelligence as the designer of innovations), and not to your 3.8 byo programme, and your objection merely echoes the point I made myself, now in bold below.*** There is no evidence for a 3.8 byo programme for every change in the history of evolution, and when I gave you a choice, you opted for a God-given autonomous mechanism! How does an autonomous mechanism support the hypothesis that every change was preprogrammed?
***Dhw: Cells can alter their own DNA and their own structures. We do not know the extent to which they can do this, which is why Shapiro’s “natural genetic engineering”, or my more explicit concept of autonomous (possibly God-given) cellular intelligence as the inventor of innovations, remains a hypothesis.
DAVID: Animals are designed to fit their environments requirements which can change requiring new design or extinction. 'Bad luck' still applies. God steps in where He wishes.
dhw: I’m glad you now acknowledge the vital importance of environmental influence. It is indeed bad luck if organisms can’t use their possibly God-given autonomous intelligence to solve new problems. If God exists, then of course he can dabble if he wishes, and the theistic version of my hypothesis has always allowed for this. Chixculub might be an example. (The atheistic version would be that environmental change is purely by chance – bad luck in some cases, and good in others – though it is also possible that your God set up a system to engender random environmental change.)
DAVID: Of course environment plays a huge role as when mammals entered water permanently, but design for survival is required. Note design is primary.
I don’t know what you mean by “primary”. Are you referring to your theory that your God changed legs to fins before sending pre-whales into the water, all for the sake of complexity - not survival - although fins are no more complex than legs?
Genome complexity: DNA 3-D importance in replication
by David Turell , Sunday, January 06, 2019, 15:50 (2149 days ago) @ dhw
DAVID: The 3.8 byo program allows the organisms to modify their DNA only for adaptations to immediate needs which provide minor changes within species. That is how I view Shapiro. Elsewhere I have provided evidence for the initial program completely providing everything (all info) from the beginning.
dhw: This makes no sense. Presumably your first sentence refers to Shapiro’s hypothesis of “natural genetic engineering” (and my hypothesis of cellular intelligence as the designer of innovations), and not to your 3.8 byo programme, and your objection merely echoes the point I made myself, now in bold below.*** There is no evidence for a 3.8 byo programme for every change in the history of evolution, and when I gave you a choice, you opted for a God-given autonomous mechanism! How does an autonomous mechanism support the hypothesis that every change was preprogrammed?
The preprogramming allows for animals to make minor adaptations within the same species by adjusting the DNA in genes as necessary for changing circumstances. Note I said above "modify their DNA only for adaptations to immediate needs which provide minor changes within species." You and Shapiro are not describing a speciation method, only a minor adaptation ability.
***Dhw: Cells can alter their own DNA and their own structures. We do not know the extent to which they can do this, which is why Shapiro’s “natural genetic engineering”, or my more explicit concept of autonomous (possibly God-given) cellular intelligence as the inventor of innovations, remains a hypothesis.DAVID: Animals are designed to fit their environments requirements which can change requiring new design or extinction. 'Bad luck' still applies. God steps in where He wishes.
dhw: I’m glad you now acknowledge the vital importance of environmental influence. It is indeed bad luck if organisms can’t use their possibly God-given autonomous intelligence to solve new problems. If God exists, then of course he can dabble if he wishes, and the theistic version of my hypothesis has always allowed for this. Chixculub might be an example. (The atheistic version would be that environmental change is purely by chance – bad luck in some cases, and good in others – though it is also possible that your God set up a system to engender random environmental change.)
DAVID: Of course environment plays a huge role as when mammals entered water permanently, but design for survival is required. Note design is primary.
dhw: I don’t know what you mean by “primary”. Are you referring to your theory that your God changed legs to fins before sending pre-whales into the water, all for the sake of complexity - not survival - although fins are no more complex than legs?
Of course, primary always means first, and is this case design is first.
Genome complexity: chromatin makes DNA 3-D setup
by David Turell , Friday, January 10, 2020, 21:37 (1780 days ago) @ David Turell
The relationships that are arranged allows for many interpretations:
https://phys.org/news/2020-01-chromatin-d-forests-cells.html
"A single cell contains the genetic instructions for an entire organism. This genomic information is managed and processed by the complex machinery of chromatin—a mix of DNA and protein within chromosomes whose function and role in disease are of increasing interest to scientists.
"A Northwestern University research team—using mathematical modeling and optical imaging they developed themselves—has discovered how chromatin folds at the single-cell level. The researchers found chromatin is folded into a variety of tree-like domains spaced along a chromatin backbone. These small and large areas are like a mixed forest of trees growing from the forest floor. The overall structure is a 3-D forest at microscale.
"Chromatin is responsible for packing DNA into the cell nucleus. In humans, that's about six feet of DNA in each cell. The new work suggests that chromatin is more structured and hierarchical in single cells than previously thought. Learning how chromatin correctly operates will help scientists understand what goes wrong with it in cancer and other diseases.
"'By integrating theoretical and experimental work, we have produced a new chromatin folding picture that helps us see how the 3-D genome is organized at the single-cell level," said Igal Szleifer, the Christina Enroth-Cugell Professor of Biomedical Engineering at Northwestern's McCormick School of Engineering.
***
"'If genes are the hardware, chromatin is the software," said Backman, the Walter Dill Scott Professor of Biomedical Engineering and director of the Center for Physical Genomics and Engineering. "If the structure of chromatin changes, it can alter the processing of the information stored in the genome, but it does not alter the genes themselves. Understanding chromatin folding holds the key to understanding how cells differentiate and how cancer happens.'"
Comment: The 3-D relationships determines how the genes are fully interpreted. It is one of the various layers of complex information and instructions that makes each type of cell unique..
Genome complexity: how so few genes make us so complex
by David Turell , Wednesday, January 15, 2020, 19:40 (1775 days ago) @ David Turell
The human genome is small when the number of genes is measured, but those genes can mix and match code to produce many results from the same gene:
https://www.the-scientist.com/features/alternative-splicing-provides-a-broad-menu-of-pr...
"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, allows a cell to generate different RNAs, and ultimately different proteins, from the same gene...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.
***
"(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. 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)
***
"Each splicing event requires three components: the splice donor, a GU nucleotide sequence at one end of the intron; a splice acceptor, an AG nucleotide sequence at the opposite end; and a branch point, an A approximately 20–40 nucleotides away from the splice acceptor. These three “splice sites” are recognized by two core small nuclear RNAs (snRNAs) of the spliceosome, U1 and U2, followed by a protein, U2AF. The binding of these molecules to a transcript recruits a complex of three more snRNAs—U4, U5, and U6—which facilitates the splicing reaction.
"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.
***
" their studies revealed that every tissue in the body is characterized by a unique set of splicing events...They found that brain, heart, and skeletal muscle present with the most highly conserved and tissue-specific alternative splicing patterns, further underscoring the functional importance of tissue-specific alternative splicing.
***
" Giudice, found that numerous differentially spliced genes encode proteins involved in intracellular trafficking, and these splicing events are controlled by two RBPs: CELF and MBNL. All signs pointed to a splicing network. Follow-up work revealed that the expression levels of CELF and MBNL are inversely tied to one another during muscle development, and that they antagonistically regulate more than 1,000 pre-mRNA transcripts, some of which are translated into proteins critical for muscle contraction.
***
"Researchers are also exploring the possibility that chromatin architecture and epigenetics serve as another layer of splicing regulation by modulating the rate of RNAPII transcription."
Comment: Junk DNA is gone. The complexity of the human genome is only partially unraveled and what is revealed so far is an irreducible complex system that MUST be the result of design. It is highly controlled, especially in fetus formation or abnormal results will produce a defective fetus. This can only be the result of design. A designer is required.
Genome complexity:cells control degree of gene expression
by David Turell , Thursday, January 16, 2020, 20:35 (1774 days ago) @ David Turell
Shown in new study:
https://phys.org/news/2020-01-mechanisms-genome.html
"Like a dimmer light switch, each gene can be turned on (expressed) strongly or weakly, or turned off entirely. Individual cells have different gene expression profiles, which enables them to have the different functions that make them part of different tissues. For example, an immune cell expresses proteins that allow it to recognize harmful intruders, while a neuron expresses proteins that enable it to pass nerve signals to its neighbors.
"The ability for a cell to repress genes, keeping them silent, is therefore critical.
***
"The first paper looks at how cells silence transposons, parasitic genetic elements that, if not tightly controlled, are able to jump from one place to another in the genome and cause mutations in other genes while increasing their own numbers. It was known that nucleic acid molecules called piRNAs are able to recognize and suppress harmful transposons, but how they did so was unclear. In the new research, the authors report that piRNAs work together with a small protein called SUMO (small ubiquitin-like protein) that works as a tag that is attached to other proteins. piRNAs and SUMO cooperate to modify chromatin on these selfish transposons and repress them.
"The second paper focuses on roles of SUMO and chromatin in control of normal cellular genes. There are, broadly, two main classes of chromatin: heterochromatin and euchromatin.
"Euchromatin comprises the most actively expressed genes in the genome, while the genes in heterochromatin, it was believed, tend to be silenced. This new research breaks the existing paradigm and suggests that genes residing in heterochromatin are expressed because of their chromatin environment and not despite it.
"'We now know that SUMO acts as a silencing mark to suppress transposons that would otherwise interfere with the proper expression of heterochromatin genes. This is an unexpected function of SUMO," says postdoctoral scholar Maria Ninova, first author on the two new studies.
"The Caltech researchers also found that heterochromatin restricts gene expression to specific tissues and identified a novel mechanism that allows cells to maintain the proper balance between heterochromatin and euchromatin."
Comment: A finding that had to exist. All cells have the same DNA at the start.
Genome complexity: more about transposons role
by David Turell , Monday, February 22, 2021, 19:57 (1371 days ago) @ David Turell
Transposons can create new genes:
https://phys.org/news/2021-02-genes-repeatedly-evolution.html
"A study, "Recurrent Evolution of Vertebrate Transcription Factors by Transposase Capture," published Feb. 19 in Science, investigates how genetic elements called transposons, or "jumping genes," are added into the mix during evolution to assemble new genes through exon shuffling.
***
"The study, which focused on tetrapods (four-limbed vertebrates), is important because it shows that transposons represent an important force in the creation of new genes during evolution. The work also explains how genes critical for human development were born.
***
"'You are putting the bricks in in a different way and you construct a whole new thing," Feschotte said. "We are looking at the question of how genes are born. The originality is that we are looking at the role of transposons in creating proteins with novel function in evolution."
***
"The researchers identified more than 100 distinct genes fused with transposases born in the past 350 million years along different species lineages, including genes in birds, reptiles, frogs, bats and koalas, and a total of 44 genes born this way in the human genome.
"Cosby and colleagues selected four recently evolved genes and performed a wide range of experiments in cell culture to understand their functions. They found the proteins derived from these genes are able to bind to specific DNA sequences and turn off gene expression. Such genes are known as transcription factors and act as master regulator genes for development and basic physiology. One such gene, PAX6, is well studied, plays a key role as a master regulator in the formation of eyes in all animals and is highly conserved throughout evolution.
"'If you put a PAX6 gene from a mouse into a Drosophila [fruit fly], it works," Feschotte said. Though others have proposed before that PAX6 is derived from a transposase fusion, the researchers in this study further validated the hypothesis.
"Cosby and colleagues isolated one of these recently evolved genes in bats, called KRABINER, and then used CRISPR gene-editing technology to delete it from the bat genome and see what genes were affected, before adding it back in. The experiment revealed that when KRABINER was removed, hundreds of genes were dysregulated, and when they restored it, normal functioning returned. The protein expressed by the KRABINER gene bound to other related transposons in the bat genome, Cosby said.
"'The experiment revealed that it controls a large network of other genes wired through the past dispersion of related transposons throughout the bat genome—creating not just a gene but what is known as a gene regulatory network," Feschotte said."
Comment: We know that transposons jump around, but not what controls the jumping. Chance or programmed? There is not much non-purposeful DNA. It is really strange that humans are so complex with so few genes.
Genome complexity: more about transposons role
by David Turell , Wednesday, May 12, 2021, 20:48 (1292 days ago) @ David Turell
Another review:
https://www.quantamagazine.org/scientists-catch-jumping-genes-rewiring-genomes-20210512/
"For more than a decade, Feschotte has pointed to transposons as the ultimate innovators in eukaryotic genomes. Transposons are genetic elements that can copy themselves and insert those copies throughout the genome using a splicing enzyme they make. Feschotte may have finally found the smoking gun he has been looking for: As he and his colleagues recently reported in Science, these jumping genes have fused with other genes nearly 100 times in tetrapods over the past 300 million years, and many of the resulting genetic mashups are likely to encode transcription factors.
"David Adelson, chair of bioinformatics and computational genetics at the University of Adelaide in Australia, who was not involved with the study, said, “This study provides a good mechanistic understanding of how these new genes can form, and it squarely implicates the transposon activity itself as the cause.”
"Scientists have long known that transposons can fuse with established genes because they have seen the unique genetic signatures of transposons in a handful of them, but the precise mechanism behind these unlikely fusion events has largely been unknown. By analyzing genes with transposon signatures from nearly 600 tetrapods, the researchers found 106 distinct genes that may have fused with a transposon. The human genome carries 44 genes likely to have been born this way.
"The structure of genes in eukaryotes is complicated, because their blueprints for making proteins are broken up by introns. These noncoding sequences are transcribed, but they get snipped out of the messenger RNA transcripts before translation into protein occurs. But according to Feschotte’s new study, a transposon can occasionally hop into an intron and change what gets translated. In some of these cases, the protein made by the fusion gene is a mashup of the original product and the transposon’s splicing enzyme (transposase).
***
"Cosby described the 106 fusion genes described in the study as the “tiniest tip of the iceberg.” Adelson agreed and explained why: Events that randomly create fusion genes for functional, non-harmful proteins rely on a series of coincidences and must be exceedingly rare; for the fusion genes to spread throughout a population and withstand the test of time, nature must also positively select for them in some way. For the researchers to have found the examples described in the study so readily, transposons must surely cause fusion events much more often, he said.
***
"Transposons comprise a hefty chunk of eukaryotic DNA, yet organisms take extreme measures to carefully regulate their activity and prevent the havoc caused by problems such as genomic instability and harmful mutations. These dangers made Adelson wonder if fusion genes sometimes endanger orderly gene regulation. “Not only are you perturbing one thing, but you’re perturbing this whole cascade of things,” he said. “How is it that you can change expression of all these things and not have a three-headed bat?” Cosby, however, thinks it’s unlikely that a fusion gene leading to harmful morphogenic changes would readily propagate through a population.
"Damon Lisch, a plant geneticist at Purdue University who studies transposable elements and was not involved with the study, said he hopes this study pushes back against a widespread but misguided notion that transposons are “junk DNA.” Transposable elements generate tremendous amounts of diversity and have been implicated in the evolution of the placenta and the adaptive immune system, he explained. “These are not junk — they’re living little creatures in your genome that are under very active selection over long periods of time, and what that means is that they evolve new functions to stay in your genome,” he said.
"Though this study highlights the mechanism underlying transposase fusion genes, the vast majority of new genetic material is thought to form through genetic duplication, in which genes are accidentally copied and the extras diverge through mutation. But a large quantity of genetic material does not mean that new protein functions will be significant, said Cosby, who is continuing to investigate the function of the fusion proteins.
“'Evolution is the ultimate tinkerer and ultimate opportunist,” said David Schatz, a molecular geneticist at Yale University who was not involved with the study. “If you give evolution a tool, it may not use it right away, but sooner or later it will take advantage of it.'” (my bold)
Comment: The last paragraph treats evolution as if if is a personage. Why not simply God in action?
Genome complexity: How butterfly wings are made
by David Turell , Saturday, October 22, 2022, 17:27 (764 days ago) @ David Turell
Ancient non-coding DNA regulates genes:
https://www.sciencedaily.com/releases/2022/10/221021145842.htm
"Butterfly wing patterns have a basic plan to them, which is manipulated by non-coding regulatory DNA to create the diversity of wings seen in different species, according to new research.
"The study, "Deep cis-regulatory homology of the butterfly wing pattern ground plan," published as the cover story in the Oct. 21 issue of Science, explains how DNA that sits between genes -- called 'junk' DNA or non-coding regulatory DNA -- accommodates a basic plan conserved over tens to hundreds of millions of years while at the same time allowing wing patterns to evolve extremely quickly.
"The research supports the idea that an ancient color pattern ground plan is already encoded in the genome and that non-coding regulatory DNA works like switches to turn up some patterns and turn down others.
***
"/We see that there's a very conserved group of switches [non-coding DNA] that are working in different positions and are activated and driving the gene," Mazo-Vargas said.
***
"This study focused on the effect of non-coding DNA on the WntA gene. Specifically, the researchers ran experiments on 46 of these non-coding elements in five species of nymphalid butterflies, which is the largest family of butterflies.
***
"The researchers found that across four of the species -- Junonia coenia (buckeye), Vanessa cardui (painted lady), Heliconius himera and Agraulis vanillae (gulf fritillary) -- each of these non-coding elements had similar functions with respect to the WntA gene, proving they were ancient and conserved, likely originating in a distant common ancestor.
"They also found that D. plexippus (monarch) used different regulatory elements from the other four species to control its WntA gene, perhaps because it lost some of its genetic information over its history and had to reinvent its own regulatory system to develop its unique color patterns.
"'We have progressively come to understand that most evolution occurs because of mutations in these non-coding regions," Reed said."
Comment: repeating the same successful plan over and over makes perfect sense. Reed's comment is right on point. To make a new species genes must be re-regulated to produce a new form.
Genome complexity: controlling RNA in oocytes:
by David Turell , Wednesday, January 25, 2023, 16:57 (669 days ago) @ dhw
In mammals in a membraneless compartment:
https://www.the-scientist.com/news-opinion/mammalian-oocytes-store-mrna-in-newly-found-...
"During the final stages of oocyte growth, these germ cells become transcriptionally inactive while preparing to resume meiosis and jumpstart their maturation into eggs. At this austere time, oocytes can only use maternal messenger RNAs (mRNAs) they have previously stored to get through their maturation process and early embryonic development if fertilized. Oocytes from the worm Caenorhabditis elegans store mRNA in P granules, those of fruit flies do so in polar granules, and aquatic frogs and zebrafish rely on a structure called the Balbiani body—all of which are membraneless organelles. But for mammals, the storage site has been terra incognita so far.
***
"A study published online today (October 20) in Science sheds light on the enigma, showing that these oocytes accumulate mRNA in a membraneless compartment that is associated with mitochondria. The study’s authors report that they observed this newly discovered structure in various mammalian species, including mice and humans.
***
"To answer it, he and his colleagues first used various staining techniques to establish that both RNA-binding proteins and mRNA are colocalized with mitochondria in mouse, pig, cow, and human oocytes. These molecules cluster around mitochondria throughout the cytoplasm, forming a structure the team named the mitochondria-associated ribonucleoprotein domain (MARDO). They observed that MARDO becomes more prominent as oocytes grow larger, and that its formation is dependent on the parallel increase in mitochondrial membrane potential.
"Cheng and his colleagues further showed that the RNA-binding protein ZAR1, which had been previously associated with oocyte maturation and mRNA regulation, plays an essential role in both MARDO assembly and dissolution in mouse oocytes. In the team’s experiments, ZAR1 promoted MARDO coalescence and its association with mitochondria. Once the oocyte transforms into a fertilized egg and the embryo starts to grow, transcription is restored and maternal mRNAs are no longer needed to drive embryonic development. During this transition, the team found that ZAR1 is degraded by the proteosome, and with that, MARDO is dissolved."
Comment: the mRNAs contain the information to control preparations for fusion with the male sperm.
Genome complexity: controlling DNA over copying
by David Turell , Wednesday, January 25, 2023, 21:19 (669 days ago) @ David Turell
A new system found:
https://www.sciencedaily.com/releases/2023/01/230124101607.htm
"The cells of humans and all other higher organisms use a complex system of checkpoints and "licensing" proteins to ensure that they replicate their genomes precisely once before dividing. In preparation for cell division, the licensing proteins attach to specific regions in the DNA, designating them as replication origins. When the DNA synthesis phase of the cell cycle begins, replication begins only at those licensed sites, and only initiates, or "fires" once, according to the current model.
"That model was missing a crucial point, though. "The same factor that is allowing for this licensing to happen is only degraded after these replication origins have fired," said senior author Dr. Tobias Meyer, the Joseph Hinsey Professor in Cell and Developmental Biology at Weill Cornell Medicine. "In principle, the cell could load these licensing machines onto DNA that's already replicated, so, instead of two copies, you're getting three or four copies of that segment of the DNA, and these cells would be expected to lose genome integrity and die or become cancerous."
***
"The work revealed that a well-known licensing factor, CDT1, not only licenses a segment of DNA to become a replication origin, but also acts as a brake for DNA replication, preventing an essential replication enzyme called CMG helicase from functioning. To start synthesizing DNA, the cell's enzymes must first break down CDT1. "Previously proposed mechanisms for coordinating this transition from the licensing phase of the cell cycle to the firing phase of the cell cycle have depended on inhibiting licensing factors," said Ratnayeke, adding that "the mechanism that we identified here is actually the opposite … the licensing factor CDT1 itself is preventing the progression of DNA synthesis."
"To confirm their results, the scientists collaborated with colleagues at the Medical Research Council in Cambridge, UK, who found that the inhibitory mechanism can be recapitulated in a simplified system that reproduces the entire DNA synthesis process with purified components in a test tube. "That allowed us to reconstitute all the components for DNA synthesis, and to prove that CMG helicase is directly inhibited by CDT1," said Dr. Meyer, who is also a professor of biochemistry and a member of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine."
Comment: another obviously deigned system requiring specific giant enzymes in place.
Genome complexity; lncRNA
by David Turell , Friday, April 05, 2013, 18:34 (4251 days ago) @ David Turell
Much rising interest in lncRNA.- "At the time, modifying gene expression using lncRNA was not a common goal. In the early 2000s, most molecular biologists were interested in the 1...2% of the human genome that encodes proteins, which were presumed to be the brokers of biological functions. But with the rise of high-throughput sequencing, researchers learned that far from being without function, much of the rest of the genome was transcribed into non-coding RNA, including 20-nucleotide microRNAs, which suppress genes, and lncRNAs of 100 nucleotides or more.-"Last September, the multi-institution ENCODE project to catalogue human DNA elements (see Nature 489, 46...48; 2012) revealed that three-quarters of the human genome is transcribed into non-coding RNA, and that there may be between 10,000 and 200,000 lncRNAs. Scientists have shown that these can activate gene expression and silence genes, and links with disease have begun to emerge.-"Enthusiasm for lncRNA has replaced much of the science community's scepticism. Molecular biology and biochemistry departments have taken note of a flurry of high-impact manuscripts, and some are hiring scientists to work in the emerging field. Funding is becoming easier to find. And the first biotechnology companies focused on lncRNA have taken root."-http://www.nature.com/naturejobs/science/articles/10.1038/nj7443-127a
Genome complexity; lncRNA
by David Turell , Thursday, April 25, 2013, 16:11 (4231 days ago) @ David Turell
Best article yet on lncRNA and Lamarkism suggestions:-http://www.the-scientist.com/?articles.view/articleNo/32637/title/Lamarck-and-the-Missing-Lnc/
Genome complexity; lncRNA
by David Turell , Wednesday, July 10, 2013, 02:51 (4156 days ago) @ David Turell
The lncRNA's seem to work in 3 dimensions. How they arose in such specific locations, and they are preciselty positioned, is theorized but really unknown.:-http://www.darwins-god.blogspot.com/2013/07/heres-new-paper-on-long-non-coding-rna.html