https://phys.org/news/2023-10-thousands-programmable-dna-cutters-algae-snails.html

"A diverse set of species, from snails to algae to amoebas, make programmable DNA-cutting enzymes called Fanzors—and a new study from scientists at MIT's McGovern Institute for Brain Research has identified thousands of them. Fanzors are RNA-guided enzymes that can be programmed to cut DNA at specific sites, much like the bacterial enzymes that power the widely used gene-editing system known as CRISPR.

***

"Researchers have since uncovered other RNA-guide enzymes throughout the bacterial world, many with features that make them valuable in the lab. The discovery of Fanzors, whose ability to cut DNA in an RNA-guided manner was reported by Zhang's group earlier this year, opens a new frontier of RNA-guided biology. Fanzors were the first such enzymes to be found in eukaryotic organisms—a wide group of lifeforms, including plants, animals, and fungi, defined by the membrane-bound nucleus that holds each cell's genetic material. (Bacteria, which lack nuclei, belong to a group known as prokaryotes.)

***

"Among the more than 3,600 Fanzors that the team found in eukaryotes and the viruses that infect them, the researchers were able to identify five different families of the enzymes. By comparing these enzymes' precise makeup, they found evidence of a long evolutionary history.

"Fanzors likely evolved from RNA-guided DNA-cutting bacterial enzymes called TnpBs. In fact, it was Fanzors' genetic similarities to these bacterial enzymes that first caught the attention of both Zhang's group and Gootenberg and Abudayyeh's team.

"The evolutionary connections that Gootenberg and Abudayyeh traced suggest that these bacterial predecessors of Fanzors probably entered eukaryotic cells, initiating their evolution, more than once. Some were likely transmitted by viruses, while others may have been introduced by symbiotic bacteria. The research also suggests that after they were taken up by eukaryotes, the enzymes evolved features suited to their new environment, such as a signal that allows them to enter a cell nucleus, where they have access to DNA.

"Through genetic and biochemical experiments led by biological engineering graduate student Kaiyi Jiang, the team determined that Fanzors have evolved a DNA-cutting active site that is distinct from that of their bacterial predecessors. This seems to allow the enzyme to cut its target sequence more precisely the ancestors of TnpB, when targeted to a sequence of DNA in a test tube, become activated and cut other sequences in the tube; Fanzors lack this promiscuous activity. When they used an RNA guide to direct the enzymes to cut specific sites in the genome of human cells, they found that certain Fanzors were able to cut these target sequences with about 10 to 20 percent efficiency."

Comment: in all this research we must use existing living mechanisms as we still have no idea how to make life. Luckily, these mechanisms are quite efficient in what they do, which is kill an invader by slicing and dicing the enemies' DNA.

https://www.sciencemag.org/news/2021/07/deadly-viruses-help-moths-and-butterflies-fight...

"Moths and butterflies have long fallen victim to two deadly threats: parasitic wasps and viruses, which battle each other over their lepidopteran hosts. Now, a new study shows some viruses transfer their weapons to infected moths and butterflies, arming them with the genes to make parasite-killing proteins.

"Many species of wasps and flies lay their eggs inside other insects, giving their young a source of food and a safe place to develop—and killing the host in the process. But even though moths and butterflies are favored hosts, some species, including armyworms, cutworms, and cabbage butterflies, have shown a strange resistance to a plethora of wasp parasites, such as Cotesia vanessae and C. kariyai.

***

"To find out what was going on, entomologist Madoka Nakai and her team at the Tokyo University of Agriculture and Technology infected northern armyworm larvae with a common pox virus before introducing the immature insects to various parasitic wasp species. Whereas uninfected larvae succumbed to the parasites, the infected larvae—and their plasma—killed almost every parasite, aside from the basket-cocoon parasitoid Meteorus pulchricornis. Researchers then identified two proteins in the infected armyworms, which they called parasitoid killing factor (PKF), that they thought might be toxic to the parasites.

***

“'We all arrived at these genes from slightly different directions. Putting our research together created this very interesting story about the biological arms race occurring on a very large scale between multiple pathogens, wasps, and hosts, which we now know are also fighting back,” Theilmann says.

"But the researchers also found an interesting twist—at least one of the PKF-harboring viruses is transmitted to moths and butterflies by the basket-cocoon parasitoid, protecting the very wasp whose larvae can survive its assaults. That suggests that even though PKFs can help the lepidopterans, they may also give an advantage to some parasitic wasps.

"The new work should help researchers understand why moths and butterflies often resist parasitoids used as pesticides for crops and forests, Herrero says. But when it comes to fully understanding the complexity of this evolutionary arms race, many questions are unanswered, Theilmann says. For example, his team still doesn’t know why some viruses have genes for PKF and others don’t. They also don’t know whether all PKFs function in the same manner."

Comment: horizontal gene transfer can come from being infected, which then provides protection in other ways!!! Work in progress. All part of protective designs.

https://medicalxpress.com/news/2020-09-immune-cells-sculpt-circuits-brain.html

"Immune cells play an unexpected role in fine-tuning the brain's neural circuits, according to research published in September, 2020 in Neuron. The immune cells that reside there, known as microglia, not only protect the brain from infection and inflammation, they also help physically sculpt circuits in the developing brain. The new work demonstrates that microglia also direct neurons to modify their own connectivity in response to sensory cues.

***

"'To a large extent, the general architecture and wiring of the brain is accomplished by birth," he says. "But it really requires this robust feedback from the environment to continue that maturation." As an animal interacts with its surroundings, some neuronal connections are eliminated while others are strengthened, he explains. It's a process that, in humans, continues for decades after birth. Cheadle says:

"'What's really important's that during development, the right neurons connect with one another in the right way. We want to have tight control over how many connections there are and how strong the connections are. So that's actually something that sensory experience is important for."

"Cheadle and colleagues monitored the connections between neurons, or synapses, in a visual processing circuit in the brains of mice. Young mice need visual input at the right time to develop brain pathways related to vision. But if the mice lack visual input for a critical period, the circuits sprout too many synapses and the mice end up with abnormal connections. The team found that the circuits relied on microglia, which, with the right visual stimuli, signaled nearby neurons to prune some of the synapses.

"This impact on neural connectivity represents a new role for microglia in the healthy brain, and could help explain why the cells have been implicated in autism and other neurodevelopmental disorders. "I think this study will be seen as a big breakthrough in our mechanistic understanding of how sensory experience and microglia coordinate the process of synaptic pruning that is critical for brain maturation in early life," Greenberg says."

Comment: this means the complexification mechanism is actually under immune control and involves synapse pruning. How some areas thicken is related to regions of the hippocampus adding neurons as in London cabbies memorizing London. In humans adding neurons is very limited to this region.

https://medicalxpress.com/news/2020-09-immune-affects-mind-body.html

"What we've found here is that an immune molecule—IL-17—is produced by immune cells residing in areas around the brain, and it could affect brain function through interactions with neurons to influence anxiety-like behaviors in mice. We are now looking into whether too much or too little of IL-17 could be linked to anxiety in people."

"IL-17 is a cytokine, a signaling molecule that orchestrates the immune response to infection by activating and directing immune cells. IL-17 also has been linked to autism in animal studies and depression in people.

"How an immune molecule like IL-17 might influence brain disorders, however, is something of a mystery since there isn't much of an immune system in the brain and the few immune cells that do reside there don't produce IL-17. But Kipnis, along with first author and postdoctoral researcher Kalil Alves de Lima, Ph.D., realized that the tissues that surround the brain are teeming with immune cells, among them, a small population known as gamma delta T cells that produce IL-17. They set out to determine whether gamma-delta T cells near the brain have an impact on behavior.

***

"Using mice, they discovered that the meninges are rich in gamma-delta T cells and that such cells, under normal conditions, continually produce IL-17, filling the tissues surrounding the brain with IL-17.

"To determine whether gamma-delta T cells or IL-17 affect behavior, Alves de Lima put mice through established tests of memory, social behavior, foraging and anxiety. Mice that lacked gamma-delta T cells or IL-17 were indistinguishable from mice with normal immune systems on all measures but anxiety. In the wild, open fields leave mice exposed to predators such as owls and hawks, so they've evolved a fear of open spaces. The researchers conducted two separate tests that involved giving mice the option of entering exposed areas. While the mice with normal amounts of gamma-delta T cells and levels of IL-17 kept themselves mostly to the more protective edges and enclosed areas during the tests, mice without gamma-delta T cells or IL-17 ventured into the open areas, a lapse of vigilance that the researchers interpreted as decreased anxiety.

"Moreover, the scientists discovered that neurons in the brain have receptors on their surfaces that respond to IL-17. When the scientists removed those receptors so that the neurons could not detect the presence of IL-17, the mice showed less vigilance. The researchers say the findings suggest that behavioral changes are not a byproduct but an integral part of neuro-immune communication.

***

"To determine whether gamma-delta T cells or IL-17 affect behavior, Alves de Lima put mice through established tests of memory, social behavior, foraging and anxiety. Mice that lacked gamma-delta T cells or IL-17 were indistinguishable from mice with normal immune systems on all measures but anxiety. In the wild, open fields leave mice exposed to predators such as owls and hawks, so they've evolved a fear of open spaces. The researchers conducted two separate tests that involved giving mice the option of entering exposed areas. While the mice with normal amounts of gamma-delta T cells and levels of IL-17 kept themselves mostly to the more protective edges and enclosed areas during the tests, mice without gamma-delta T cells or IL-17 ventured into the open areas, a lapse of vigilance that the researchers interpreted as decreased anxiety.

"Moreover, the scientists discovered that neurons in the brain have receptors on their surfaces that respond to IL-17. When the scientists removed those receptors so that the neurons could not detect the presence of IL-17, the mice showed less vigilance. The researchers say the findings suggest that behavioral changes are not a byproduct but an integral part of neuro-immune communication.

***

"'The immune system and the brain have most likely co-evolved," Alves de Lima said. "Selecting special molecules to protect us immunologically and behaviorally at the same time is a smart way to protect against infection. This is a good example of how cytokines, which basically evolved to fight against pathogens, also are acting on the brain and modulating behavior."

"The researchers now are studying how gamma-delta T cells in the meninges detect bacterial signals from other parts of the body. They also are investigating how IL-17 signaling in neurons translates into behavioral changes."

Comment: My comment would be God evolved this system. A specific protein is not likely a result of chance.

https://www.sciencemagazinedigital.org/sciencemagazine/28_august_2020/MobilePagedArticl...

"Bacteria and archaea are frequently attacked by viruses and other mobile genetic elements and rely on dedicated antiviral defense systems, such as restriction endonucleases and CRISPR, to survive. The enormous diversity of viruses suggests that more types of defense systems exist than are currently known. By systematic defense gene prediction and heterologous reconstitution, here we discover 29 widespread antiviral gene cassettes, collectively present in 32% of all sequenced bacterial and archaeal genomes, that mediate protection against specific bacteriophages. These systems incorporate enzymatic activities not previously implicated in antiviral defense, including RNA editing and retron satellite DNA synthesis. In addition, we computationally predict a diverse set of other putative defense genes that remain to be characterized. These results highlight an immense array of molecular functions that microbes use against viruses."

Comment: we use bacterial CRISPR enzyme to edit DNA, a perversion of its use in life, in which it is used to chop up enemy DNA's. But the real consideration is when does this type of immunity appear in relation to the origin of the organism? And it obviously has to be designed simultaneously into the first appearance of each new species..

https://medicalxpress.com/news/2019-03-mechanism-inflammation.html

"UT Southwestern researchers have identified two proteins that act as gatekeepers to dampen a potentially life-threatening immune response to chronic infection.

"The proteins—the transcription factors SIX1 and SIX2—activate cellular pathways required for fetal development and later switch to a new role in which they repress these pathways in adult immune system cells.

***

"Transcription factors are proteins that bind to special regions of DNA to turn genes on (activate them) or off (repress them). "One of the surprising findings was that a transcription activator that is essential for the development of tissues and organs has been repurposed as a transcriptional repressor in the immune system. While transcription factors can be used differently in various stages of life, a switch from a transcriptional activator in the fetus to a suppressor in adult immune cells is infrequent," said Dr. Alto,

***

"The researchers found that the two proteins showed inhibitory activities when bound to genes involved in inflammation. Specifically, SIX1 and SIX2 appeared to dampen the body's immune response to prevent damage associated with a potentially life-threatening condition called a cytokine storm, which can occur in chronic inflammatory conditions. "A cytokine storm can occur when the body's immune cells and activators (cytokines) show an overresponse to a health threat such as the flu," he explained.

"An experiment with transgenic mice found that expression of SIX1 in adulthood conferred near-complete recovery following exposure to a toxin released by gram-negative bacteria that can set off a cytokine storm. The two SIX proteins seem to dampen the response of the so-called noncanonical NF-κB pathway, a signaling cascade that is instrumental in the development of the lymph organs, the maturation of the immune system's antibody-producing B cells, and the development of bone cells. The same pathway is involved in the body's immune defense in adulthood.

***

"'In summary, we have established that SIX family transcription factors function as immunological gatekeepers, regulating the activity of inflammatory genes in response to noncanonical NF-κB pathway activation," he said. "These findings indicate that disruption of this pathway could have important consequences for the pathogenesis of human disease, including cancer.'"

Comment: Once again precise controls. This system is another one that had to be designed all at once since the parts are so integrated. Note a cyto kine

https://www.sciencedaily.com/releases/2019/02/190207142153.htm

"During infection, T-cells of the immune system synthesize acetylcholine, explains Dr. Mak. In the brain, acetylcholine functions as a neurotransmitter and controls learning and memory. In the immune system, T-cells making this classical brain chemical are able to jump out of the blood circulation and take action in the tissues to fight infection.

"First author Maureen Cox summarizes the study findings this way: "The neurotransmitter acetylcholine is produced by T-cells during viral infection to facilitate their entry into tissues under attack, where these cells then kill the virus-infected cells."

***

"'We now have absolute genetic proof that immune cells need this brain chemical," says Dr. Mak. "We believe it's an entirely new lens though which to look at numerous diseases including cancer, viral infections and autoimmune conditions."

"With respect to cancers, a tumour is often surrounded by immune cells that can't break through its defences, perhaps because the immune cells are not producing sufficient amounts of acetylcholine. In this case, strategies to increase immune neurotransmitter production may be beneficial. The flip side is at play in autoimmune diseases such as rheumatoid arthritis or multiple sclerosis, where the autoimmune T-cells attack self tissues. In this case, a reduction in neurotransmitter signaling may quell the hordes of immune cells invading joints or the central nervous system.

"The research builds on the findings of a 2011 study also published in Science in which Dr. Mak participated. That study demonstrated for the first time that immune cells can make acetylcholine.

"Dr. Mak says the next research goal is to identify and target the key receptors that facilitate the signalling crosstalk between immune cells and diseased organs."

Comment: Acetylcholine can be produced by more than one cell type, probably following the same instructions as in neurons, which means the T cells must have same receptors as neurons.

https://medicalxpress.com/news/2019-01-secret-sepsis-rare-cell.html

"'As one of the rarest cell types in the body, basophils make up less than 1% of a person's white blood cells," said Piliponsky, an associate professor of pediatrics at the University of Washington School of Medicine. "Scientists have long suspected that basophils can enhance the immune defense against a bacterial infection although there was no scientific proof of this role prior to our study."

"To examine the basophils' contribution to the immune response, the researchers used a model of bacterial infection and sepsis that closely resembles the progression and characteristics of human sepsis in genetically-modified mice.

"Their studies showed that basophils were one of the first types of immune cell to appear at the infection site. The presence of basophils not only enhanced inflammation at the early stages of an immune response to infection and improved survival in mice, but did this in part by releasing a protein known as tumor necrosis factor (TNF).

"As a major player in the immune response to an infection, TNF sends the signal to other cells causing them to switch into high gear and generate the inflammatory response that is vital to protecting and healing damaged tissue. Its presence in this research adds to mounting evidence that basophil-derived TNF plays a major role in the first stages of the immune system's defense against an infection, and indicates that a reduced basophil presence or a deficiency in factors regulated by basophils can lead to sepsis.

"'These findings show that basophils, despite their low numbers, can trigger a cascade of events that both helps them to initiate an immune response against infection and enhances the effectiveness of this response," wrote Piliponsky and his co-authors in the paper. "Together, these findings provide novel insights into how basophils, and basophil-derived TNF, might have key roles in the early stages following bacterial infections and in resisting the progression of such infections to sepsis."

Comment: The basal cells automatically release TNF to call in the rest of the cells that cause inflammation. The term inflammation comes from the red appearance of tissue caused by a delivery of more blood to the area by dilation of vessels. The basal cells act as scouts. This shows that different white cells are designed for different jobs. Since infectious organisms have existed since the beginning of life (think bacteria) an immune mechanism had to designed into some of those bacteria and also into multicellular organisms when they first appeared. Uncontrolled killing infections would have ended life.

https://www.nature.com/articles/d41586-019-00175-0?utm_source=Nature+Briefing&utm_c...

"A fever fights infection by helping immune cells to crawl along blood-vessel walls to attack invading microbes.

"JianFeng Chen at the Shanghai Institute of Biochemistry and Cell Biology in China and his colleagues grew immune cells called T cells from mice, and raised the temperature of these cells from the normal mouse body temperature of 37 °C to 40 °C — the equivalent of a high fever. This heat triggered the T cells to start producing heat-shock proteins (Hsps), which protect cells against stress.

"The Hsps travelled to the inner surface of cells’ outer membranes, where they bound to the tails of membrane proteins known as integrins. This process pulled integrins together, and the integrin sections jutting from the cells’ outer surfaces formed complexes that stuck to blood-vessel walls. The formation of integrin complexes also triggered the migration of T cells to infection sites.

"The researchers then engineered mice to have a mutated form of integrin that couldn’t bind to Hsps. When the team infected these animals with a diarrhoea-causing bacterium (Salmonella typhimurium), the mice died quickly from fever and infection. The findings suggest that therapies designed to raise levels of Hsps could help to fight infection."

Comment: A typical chain reaction by specified molecules. Certainly looks designed. All the process had to be integrated. The T cells responded to a signal stimulus.

https://www.the-scientist.com/the-literature/mitochondria-play-an-unexpected-role-in-ki...

"One piece of evidence for mitochondria’s role surfaced in 2011, when researchers curtailed the production of reactive oxygen species (ROS)—highly destructive molecules that are byproducts of metabolism—in mouse macrophage mitochondria, and found that the immune cells became less effective at killing bacteria. Four years later, immunologist Mary O’Riordan of the University of Michigan Medical School uncovered another piece of the puzzle when she exposed mouse macrophages to the bacterium Staphylococcus aureus. This appeared to activate a particular stress pathway in the cells’ endoplasmic reticulum, which in turn revved up production of ROS.

"To find out where the ROS were coming from, O’Riordan and her colleagues recently extracted macrophages from mice and used CRISPR-Cas9 to cut out the gene encoding IRE1α, a stress-sensing protein in the endoplasmic reticulum. When the researchers exposed these cells to S. aureus, they observed markedly decreased production of ROS in the macrophages’ mitochondria, and the cells were much less effective at killing the bacteria than were unaltered macrophages. The team then used fluorescent probes to visualize the ROS hydrogen peroxide in normally functioning macrophages and observed the compound travelling from mitochondria to the phagosome. Additional experiments showed that this transport occurs through vesicles that bud off from mitochondria and are shuttled to the phagosome. Macrophages deficient in Parkin, a gene involved in generating mitochondria-derived vesicles, proved less able to kill S. aureus and two other types of microbes.“

"What I think happens is the bacteria [get] engulfed, the signal is sent to turn on ER stress, that turns on mitochondrial ROS, and they quickly send out these packages to the phagosome,” where they are lobbed into bacteria, O’Riordan explains. Researchers tend to think of mitochondria primarily as power plants, she adds, “but in fact, the cell has evolved to use these organelles and many of their constituent parts in lots of different ways,” such as in peroxisome formation and for mediating programmed cell death.

"For Greg Fairn, a cell biologist at the University of Toronto who was not involved in the study, the results represent “a new twist” on macrophage antimicrobial defenses. Phagosomes have their own toxins and ROS-producing machinery to kill bacteria, he notes, so the newly discovered mechanism may destroy the tougher, more resistant strains. Repurposing mitochondrial ROS to kill pathogens is an elegant mechanism, he adds. “It’s almost taking advantage of something that’s an unwanted byproduct,” Fairn says, adding one more tool to macrophages’ arsenal against invading bacteria."

Comment: As dangerous as oxygen molecular species can be and we are filled with antioxidant defenses, this is a clever adaptation of the defense mechanisms against oxygen to repurpose them to add to defense. Another layer of immune system complexity not an antibody, but a killer chemical byproduct.

https://phys.org/news/2018-12-image-atomic-important-immune.html

"A new study by investigators from Brigham and Women's Hospital provides a biophysical and structural assessment of a critical immune regulating protein called human T-cell immunoglobulin and mucin domain containing protein-3 (hTIM-3). Understanding the atomic structure of hTIM-3 provides new insights for targeting this protein for numerous cancer and autoimmune therapeutics currently under clinical development.

***

"'The hTIM-3 protein is an important immune regulator, yet it has been difficult to target for drug development as high-resolution structure conformational details have been elusive," said senior author Richard Blumberg, MD, chief of the Division of Gastroenterology, Hepatology and Endoscopy in the Department of Medicine at the Brigham. "We resolved the structure of hTIM-3 and established a novel biochemical assay to define its functionality, which will be useful for understanding the role of hTIM-3 in the immune system."

"The team captured a high-resolution X-ray crystal structure and nuclear magnetic resonance (NMR) image of the hTIM-3 IgV domain that is involved in functional interactions with CEACAM1, which is a crucial immune escape mechanism for many cancers. Importantly, the team determined the precise location of a calcium atom, an essential co-factor, bound to the hTIM-3 IgV domain.

"This is the first NMR analysis of any immune-related TIM molecule and the first high resolution structural report of the hTIM-3 IgV domain with association of critical co-factors such as calcium," said author Amit Gandhi, Ph.D., a researcher in Blumberg's laboratory in the Department of Medicine. "No one has been able to do this before. Hopefully this will help with the targeting of human hTIM-3 and the development of useful therapeutics.'"

Comment: The point as usual is how did evolution as s process find this highly specific shape with an exact position of a calcium atom to produced an exact function?

DAVID: Innovations are not minor adaptations.

I know. That is why I keep repeating that we have no proof that the mechanism for adaptation is also capable of innovation. We have no proven explanation for innovation, which is why we hypothesize.

DAVID: My belief is unchanged. God is in control even if an inventive mechanism exists. I have no idea why you want God to give up full control. I realize as an agnostic, you can invent any kind of God you want. I'll stick with religion's view of Him as a Supreme Being.

dhw: Theists like yourself can and do invent any kind of God they want. If he exists, I have no quarrel with the concept of your God as a Supreme Being. That does not mean he does not have any characteristics in common with ourselves – who according to the bible are made in his image. I do not “want” him to give up full control. My theistic hypothesis is that he deliberately gave up full control (as below), and this explains the higgledy-piggledy history of life on Earth. Your own reading of his mind – that he created 50,000 spider webs etc. etc. in order to produce humans – makes no sense even to you, which is why you keep telling us his logic is different from ours.

Why would I keep repeating the same idea? I make sense to me. Stop denigrating my thought processes. Again slighting my view: the diversity provides econiche supplies of food so life can survive for all the time evolution took. You illogically want HIM to view spectacles. You've constantly downgraded God to a human level. Of course God is logical in His own purposeful way.

DAVID: Innovations are not minor adaptations.

I know. That is why I keep repeating that we have no proof that the mechanism for adaptation is also capable of innovation. We have no proven explanation for innovation, which is why we hypothesize.

DAVID: My belief is unchanged. God is in control even if an inventive mechanism exists. I have no idea why you want God to give up full control. I realize as an agnostic, you can invent any kind of God you want. I'll stick with religion's view of Him as a Supreme Being.

Theists like yourself can and do invent any kind of God they want. If he exists, I have no quarrel with the concept of your God as a Supreme Being. That does not mean he does not have any characteristics in common with ourselves – who according to the bible are made in his image. I do not “want” him to give up full control. My theistic hypothesis is that he deliberately gave up full control (as below), and this explains the higgledy-piggledy history of life on Earth. Your own reading of his mind – that he created 50,000 spider webs etc. etc. in order to produce humans – makes no sense even to you, which is why you keep telling us his logic is different from ours.

DAVID: I've agreed that is possible, but all it does is keep God in control if he mechanisms have guidelines.

dhw: Why the if clause with "guidelines"? My theistic proposal is that he did not WANT to keep control, which is why he allowed his mechanism to do its own autonomous designing. Much more interesting than watching billions of automatons do exactly what you want them to do.

DAVID: "Much more interesting" is again humanizing Him which you can't resist doing.

That does not make my hypothesis illogical, and in any case you have frequently told us you think your God is watching us with interest. (See also under "Neanderthal".)

DAVID: My objection, as always, is that it takes mental planning to create advanced designs as required by the gaps in the fossil record.

dhw: Gaps in the fossil record may be the result of saltations, but in any case they do not require your God to have designed every innovation, lifestyle and natural wonder in advance of the changing conditions in which each new organism lives.

DAVID: A non-answer, Popping in the word 'saltations' applies a label to gaps. But what makes the saltation (which by definition is a new design) happen. What is the agency that causes saltation?

Nobody knows. You propose a divine 3.8-billion-year computer programme or direct divine dabbling. I propose a possibly God-given, autonomous intelligence.

dhw: Your one step further is to say that only your God can design innovations, lifestyles and natural wonders, including such items as 50,000 different spider webs, different stages of whale, and the weaverbird’s nest. My theistic proposal is that your God may have designed the mechanism that enables organisms to do their own designing, but I keep agreeing that there is no proof that this mechanism may be responsible for major changes.

Innovations are not minor adaptations. My belief is unchanged. God is in control even if an inventive mechanism exists. I have no idea why you want God to give up full control. I realize as an agnostic, you can invent any kind of God you want. I'll stick with religion's view of Him as a Supreme Being.

DAVID: I've agreed that is possible, but all it does is keep God in control if he mechanisms have guidelines.

dhw: Why the if clause with "guidelines"? My theistic proposal is that he did not WANT to keep control, which is why he allowed his mechanism to do its own autonomous designing. Much more interesting than watching billions of automatons do exactly what you want them to do.

"Much more interesting" is again humanizing Him which you can't resist doing.

DAVID: My objection, as always, is that it takes mental planning to create advanced designs as required by the gaps in the fossil record.

dhw: Gaps in the fossil record may be the result of saltations, but in any case they do not require your God to have designed every innovation, lifestyle and natural wonder in advance of the changing conditions in which each new organism lives.

A non-answer, Popping in the word 'saltations' applies a label to gaps. But what makes the saltation (which by definition is a new design) happen. What is the agency that causes saltation? .

dhw: Under “microbiome of coral”:
DAVID: Bacteria and other organisms are everywhere and obviously play a role in evolution as microbiomes:
https://phys.org/news/2018-11-corals-microbiomes-evolved.html

dhw: The term “phylosymbiosis” sent me scurrying back to Lynn Margulis, who pioneered the whole idea that symbiosis and cooperation were every bit as crucial to evolution as competition. I found this in a Wikipedia article: https://en.wikipedia.org/wiki/Lynn_Margulis

“…her theory that cell organelles such as mitochondria and chloroplasts were once independent bacteria was largely ignored for another decade, becoming widely accepted only after it was powerfully substantiated through genetic evidence.” The pattern of symbiosis and cooperation becomes clearer and clearer with all these examples, for which many thanks. Incidentally, Margulis was one of “my” scientists who believed in cellular intelligence.

I know. The cells are designed to make intelligent responses to stimuli.

DAVID: Yes, both unproven, but I take it one logical step further: complex designs to cross the gaps in the fossil record require the mentation given by a designing mind. Adaptation produces small steps, nothing more, and these are seen, but nothing more on the way to new species.

Your one step further is to say that only your God can design innovations, lifestyles and natural wonders, including such items as 50,000 different spider webs, different stages of whale, and the weaverbird’s nest. My theistic proposal is that your God may have designed the mechanism that enables organisms to do their own designing, but I keep agreeing that there is no proof that this mechanism may be responsible for major changes.

DAVID: I've agreed that is possible, but all it does is keep God in control if he mechanisms have guidelines.

Why the if clause with "guidelines"? My theistic proposal is that he did not WANT to keep control, which is why he allowed his mechanism to do its own autonomous designing. Much more interesting than watching billions of automatons do exactly what you want them to do.

QUOTE: "[…] if there is a fidelity across generations between hosts and microbes, then the holobiont embodies a coming together of numerous, disparate evolutionary lineages into a singular being, a coalition of many that contributes to the functional integrity of the whole.” (dhw’s bold)

DAVID: […] They create immediate adaptations, for example, in digestion, but it is certainly obvious they do not design giant changes.

dhw: The section I have bolded seems to emphasize the process of emergence, whereby the whole is greater than the sum of its parts. […] This essentially is the basis of my proposal that cells pool their intelligence, but I had never thought of bacteria as members of the same team. It makes perfect sense, though. As to whether these teams are or are not capable of designing giant changes, that is the hypothesis you refuse to consider, but to my mind it is certainly not “certainly obvious” that such “coalitions” cannot design giant changes as well as minor adaptations. (I have retrospectively changed my own wording here, as what I wrote originally meant the opposite of what I intended! My apologies.)

DAVID: My objection, as always, is that it takes mental planning to create advanced designs as required by the gaps in the fossil record.

Gaps in the fossil record may be the result of saltations, but in any case they do not require your God to have designed every innovation, lifestyle and natural wonder in advance of the changing conditions in which each new organism lives. My proposal is that as conditions change, organisms RESPOND to them by using their possibly God-given intelligence. Intelligence is “mental”, but it is not confined to self-awareness or the ability to plan for the future.

Under “microbiome of coral”:
DAVID: Bacteria and other organisms are everywhere and obviously play a role in evolution as microbiomes:
https://phys.org/news/2018-11-corals-microbiomes-evolved.html

The term “phylosymbiosis” sent me scurrying back to Lynn Margulis, who pioneered the whole idea that symbiosis and cooperation were every bit as crucial to evolution as competition. I found this in a Wikipedia article: https://en.wikipedia.org/wiki/Lynn_Margulis

“…her theory that cell organelles such as mitochondria and chloroplasts were once independent bacteria was largely ignored for another decade, becoming widely accepted only after it was powerfully substantiated through genetic evidence.” The pattern of symbiosis and cooperation becomes clearer and clearer with all these examples, for which many thanks. Incidentally, Margulis was one of “my” scientists who believed in cellular intelligence.

If anyone is still interested in this discussion, please reread my post from yesterday, which answers all the points David has raised below. I’ll try to keep today’s answers shorter.

DAVID: What you have again ignored is the obvious requirement for complex design to make the required changes. We know organisms can initiate their own minor adaptations.

dhw: From yesterday, referring back to the day before: Again you have ignored what I bolded last time: I have always accepted that my hypothesis, like your own, is unproven: nobody knows the extent to which adaptation to new conditions may lead to the major, more complex changes required for speciation. That is why, like your own, my hypothesis remains a hypothesis.
Yes, the changes require complex design, and nobody knows how this takes place. We only have unproven hypotheses, including yours and mine.

Yes, both unproven, but I take it one logical step further: complex designs to cross the gaps in the fossil record require the mentation given by a designing mind. Adaptation produces small steps, nothing more, and these are seen, but nothing more on the way to new species

DAVID: The fossil gaps in the records support only punctuated equilibrium with major advances which require design. Logically only a mind can design to that required degree.

dhw: You know that I accept punctuated equilibrium and the need for design. You have no evidence that “logically only a mind can do the designing” if by “a mind” you mean your God. Look at your many ant articles. “Logically” – I’ll keep my theist hat on – it is perfectly possible that your God designed the mechanisms that enable ants and all other organisms to do their own designing, whether external or internal.

I've agreed that is possible, but all it does is keep God in control if he mechanisms hav e guidelines.

dhw: Under “The newly found bacterial role”:
QUOTE: "Proponents of this hologenomic concept of evolution argue that if there is a fidelity across generations between hosts and microbes, then the holobiont embodies a coming together of numerous, disparate evolutionary lineages into a singular being, a coalition of many that contributes to the functional integrity of the whole.” (dhw’s bold)

DAVID: […] They create immediate adaptations, for example, in digestion, but it is certainly obvious they do not design giant changes.

dhw: The section I have bolded seems to emphasize the process of emergence, whereby the whole is greater than the sum of its parts. (See also my post concerning ants and corvids). This essentially is the basis of my proposal that cells pool their intelligence, but I had never thought of bacteria as members of the same team. It makes perfect sense, though. As to whether these teams are or are not capable of designing giant changes, that is the hypothesis you refuse to consider, but to my mind it is certainly not “certainly obvious” that such “coalitions” might explain innovations (giant changes) as well as adaptations (minor changes).

My objection, as always, is that it takes mental planning to create advanced designs as required by the gaps in the fossil record.

DAVID: What you have again ignored is the obvious requirement for complex design to make the required changes. We know organisms can initiate their own minor adaptations.

From yesterday, referring back to the day before: Again you have ignored what I bolded last time: I have always accepted that my hypothesis, like your own, is unproven: nobody knows the extent to which adaptation to new conditions may lead to the major, more complex changes required for speciation. That is why, like your own, my hypothesis remains a hypothesis.
Yes, the changes require complex design, and nobody knows how this takes place. We only have unproven hypotheses, including yours and mine.

DAVID: The fossil gaps in the records support only punctuated equilibrium with major advances which require design. Logically only a mind can design to that required degree.

You know that I accept punctuated equilibrium and the need for design. You have no evidence that “logically only a mind can do the designing” if by “a mind” you mean your God. Look at your many ant articles. “Logically” – I’ll keep my theist hat on – it is perfectly possible that your God designed the mechanisms that enable ants and all other organisms to do their own designing, whether external or internal.

DAVID: Your stretched hypothesis that somehow minor adaptations can reach major adaptations has no evidence of support…

Which is why it remains an unproven hypothesis, just like your own hypothesis that your God designed every single innovation, lifestyle and natural wonder extant and extinct in advance of changing conditions and as stepping stones to humans.

DAVID: What you describe is a hypothesis which has little likelihood of being correct, based on existing evidence.

Based on your personal judgement and your fixed belief in a hypothesis for which likewise there is no existing evidence.

Under “The newly found bacterial role”:
QUOTE: "Proponents of this hologenomic concept of evolution argue that if there is a fidelity across generations between hosts and microbes, then the holobiont embodies a coming together of numerous, disparate evolutionary lineages into a singular being, a coalition of many that contributes to the functional integrity of the whole.” (dhw’s bold)

DAVID: […] They create immediate adaptations, for example, in digestion, but it is certainly obvious they do not design giant changes.

The section I have bolded seems to emphasize the process of emergence, whereby the whole is greater than the sum of its parts. (See also my post concerning ants and corvids). This essentially is the basis of my proposal that cells pool their intelligence, but I had never thought of bacteria as members of the same team. It makes perfect sense, though. As to whether these teams are or are not capable of designing giant changes, that is the hypothesis you refuse to consider, but to my mind it is certainly not “certainly obvious” that such “coalitions” cannot design giant changes as well as minor adaptations.

dhw: […] And it is you who insist that the anatomy of the whale has to be changed before it can enter the water. As repeated over and over again, my proposal is that organisms change IN RESPONSE to changing conditions, as vividly illustrated by minor adaptations. NOT “aforehand”. I use the term “design” as a counter to “chance” (I suggest that the cell communities deliberately change their structure), but I have always accepted that my hypothesis, like your own, is unproven: nobody knows the extent to which adaptation to new conditions may lead to the major, more complex changes required for speciation. That is why, like your own, my hypothesis remains a hypothesis.

DAVID: What you blithely constantly overlook is the complexity of design required by my prime example of mammals entering a watery environment and changing both physically and physiologically to enter the new situation. Somehow your brilliant cells can figure out how to change themselves to handle the new way of living. It cannot be step by step, as you should believe by accepting design, but then you do invent the idea that since cells/ animals do minor adaptations, they can somehow create giant changes. I find your concept totally illogical. And the fossil record only shows giant jumps in form and function. The fossil record at this point only supports my view. Beware the gaps. Your idea does not cover them.

dhw: "What you blithely constantly overlook" is what I have bolded at the end of the response you have quoted above. Nobody knows how the major changes take place, but I don’t know why you think the fossil record supports the view that an unknown, sourceless, immaterial mind personally dabbled with a set of prewhales to give them fins before they entered the water, and then over millions of years did more dabbles to create the other features that distinguish modern whales from the known series of ancestors – each modification somehow but inexplicably being a stepping stone to Homo sapiens. The hypothesis that organisms have a mechanism that enables them to change their own structure in response to changing conditions is not illogical, because we know that is precisely what they do when they adapt (unless you now wish to tell us that your God personally dabbles every minor adaptation). But there is no evidence that the same mechanism is capable of the major changes necessary for speciation, and so it remains a logical HYPOTHESIS. The fact that you reject it while I regard it as possible does not make it illogical. A hypothesis is an idea that is suggested as an explanation for something, but has not been proved to be true. To give another example, I would describe the idea that the complexities of life have been designed by an unknown mind we call God as a logical hypothesis.

What you have again ignored is the obvious requirement for complex design to make the required changes. We know organisms can initiate their own minor adaptations. The fossil gaps in the records support only punctuated equilibrium with major advances which require design. Logically only a mind can design to that required degree. Your stretched hypothesis that somehow minor adaptations can reach major adaptations has no evidence of support , by which minor changes in the fossil record show the advance to a major change. What is logical is major gaps require major design. What you describe is a hypothesis which has little likelihood of being correct , based on existing evidence.

DAVID: What you blithely constantly overlook is the complexity of design required by my prime example of mammals entering a watery environment and changing both physically and physiologically to enter the new situation. Somehow your brilliant cells can figure out how to change themselves to handle the new way of living. It cannot be step by step, as you should believe by accepting design, but then you do invent the idea that since cells/ animals do minor adaptations, they can somehow create giant changes. I find your concept totally illogical. And the fossil record only shows giant jumps in form and function. The fossil record at this point only supports my view. Beware the gaps. Your idea does not cover them.

"What you blithely constantly overlook" is what I have bolded at the end of the response you have quoted above. Nobody knows how the major changes take place, but I don’t know why you think the fossil record supports the view that an unknown, sourceless, immaterial mind personally dabbled with a set of prewhales to give them fins before they entered the water, and then over millions of years did more dabbles to create the other features that distinguish modern whales from the known series of ancestors – each modification somehow but inexplicably being a stepping stone to Homo sapiens. The hypothesis that organisms have a mechanism that enables them to change their own structure in response to changing conditions is not illogical, because we know that is precisely what they do when they adapt (unless you now wish to tell us that your God personally dabbles every minor adaptation). But there is no evidence that the same mechanism is capable of the major changes necessary for speciation, and so it remains a logical HYPOTHESIS. The fact that you reject it while I regard it as possible does not make it illogical. A hypothesis is an idea that is suggested as an explanation for something, but has not been proved to be true. To give another example, I would describe the idea that the complexities of life have been designed by an unknown mind we call God as a logical hypothesis.

dhw: And you know perfectly well that this disagreement is NOT over intelligent design, and I accept the logic of the design argument. The disagreement is whether, if your God exists, he designed cells with or without the autonomous intelligence which forms the basis of my hypothetical evolutionary alternative to your God-designed-it-all-as-stepping-stones-to-humans hypothesis.

DAVID: You have dragged God back into the picture with an invented hypothesis that organisms can evolve themselves, even though the definition of design requires an ability to foresee future needs to which to fit the design. For example, the mammal who enters into a watery life knows how to change the physiology and anatomy aforehand!

dhw: I have not dragged God back into the picture. He has always been in this particular picture as the possible inventor of the intelligent cell. (You keep forgetting that I am an agnostic, not an atheist.) Why do you call it an “invented” hypothesis? It is no more and no less “invented” than your own view that 50,000 spider webs are “stepping stones” to humans (though at least the concept of cellular intelligence has the backing of some experts in the field). And it is you who insist that the anatomy of the whale has to be changed before it can enter the water. As repeated over and over again, my proposal is that organisms change IN RESPONSE to changing conditions, as vividly illustrated by minor adaptations. NOT “aforehand”. I use the term “design” as a counter to “chance” (I suggest that the cell communities deliberately change their structure), but I have always accepted that my hypothesis, like your own, is unproven: nobody knows the extent to which adaptation to new conditions may lead to the major, more complex changes required for speciation. That is why, like your own, my hypothesis remains a hypothesis.

What you blithely constantly overlook is the complexity of design required by my prime example of mammals entering a watery environment and changing both physically and physiologically to enter the new situation. Somehow your brilliant cells can figure out how to change themselves to handle the new way of living. It cannot be step by step, as you should believe by accepting design, but then you do invent the idea that since cells/ animals do minor adaptations, they can somehow create giant changes. I find your concept totally illogical. And the fossil record only shows giant jumps in form and function. The fossil record at this point only supports my view. Beware the gaps. Your idea does not cover them.