Introducing Geremy (and Behe)

Climate change, the oldest eel fossils are 48.5 million years old so the climate has cycled from warm climates to ice ages many times since then. The European ell and the American eel can hybridize and once shared the same environment a little over 3 million years ago when they were the same species, according to biologists. So what separated the two species? I would say climate change. As the ice ages began the two populations were separated and the eels migratory patterns diverged. The American eel migrates 1,000 miles to spawn but it can find all of the environmental cues that it needs to develop much more locally than the European eel which has to follow the convoluted path that was laid out in the video that I posted earlier in order to find the same environmental cues. If we accept that the environment is part of an organisms inheritance then we can explain why it’s migratory patterns change when the environment changes.

I asked for a testable ID explanation and you threw “climate change” at me. This is why scientists don’t take ID seriously anymore. How does climate change confirm ID as being responsible for the complicated life cycle of the european eel?

In other words, evolution happened after both species diverged. The change in migratory patterns resulted from genetic differences which accumulated in both split lineages as time progressed. If you don’t believe me, read:

https://www.researchgate.net/publication/310599113_Evolutionary_Genomics_of_North_Atlantic_Eels_Current_Status_and_Perspectives

I don’t accept that the environment is part of an organism’s inheritance as that is empirically false. Its genome is the unit of inheritance, nothing more, nothing less. If you feel otherwise, provide empirical data to support that claim.

You have ignored the paper I cited which showed the impact of natural selection on different gene groups at different stages of the eels life cycle. The evolutionary signal is very strong in the data. Deal with it.

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Sorry about that.

Both the growth of cilia and the reaction to differences in pressure are all controlled at the genetic level.

It is the gene sequence of the genome that ultimately determines the range of possible gene expression. If you change that genome sequence then you can get different reactions to physiological stimuli.

That’s not what I am reading:

Why would that exclude junk DNA?

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Hi Geremy,

I admire your devotion to your wife and triplets!

You offer a few anecdotes, and most of them are not bistable with respect to stochastic resonance. So I’m confused as to how the anecdotes even support your contention.

More importantly, you would need to show that genetic mechanisms are bistable with respect to stochastic resonance for your hypothesis to be fruitful.

You have interesting ideas. However, interesting is not the same as helpful, it’s not the same as productive, it’s not the same as evidential.

Biology has been obsessed with genetics ever since Gregor Mendel’s experiments with peas showed that variance in pea characters was controlled by genes.

Right now your “admittedly speculative” hypothesis cannot account for the data from the very first biology experiment that every schoolchild learns. Thus your hypothesis does not seem promising to me.

But I’m not a biologist, so I recommend that you listen to everyone in this thread who is a biologist.

Best,
Chris

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I have three testable hypotheses that I think can demonstrate a high degree of physics based fine tuning specific to biology that I think is comparable to what is found in cosmology. The first principle is the role of mechanical pressure in biology. Perhaps I have not done justice to the idea that I intend to convey, so I will try to remedy that situation now. First I need to explain the concept of top down causation, or better yet I will allow the physicist Paul Davies explain it, in his paper “The Algorithmic Origins of Life he wrote:

The algorithm for building an organism is therefore not only stored in a linear digital sequence (tape), but also in the current state of the entire system (e.g. epigenetic factors such as the level of gene expression, post-translational modifications of proteins, methylation patterns, chromatin architecture, nucleosome distribution, cellular phenotype and environmental context). The algorithm itself is therefore highly delocalized, distributed inextricably throughout the very physical system whose dynamics it encodes. Moreover, although the ribosome provides a rough approximation for an UC (see endnote 5), universal construction in living cells requires a host of distributed mechanisms for reproducing an entire cell.

.”

https://royalsocietypublishing.org/doi/10.1098/rsif.2012.0869

I think that Davies algorithmic model is an excellent description of ontogeny, and so that is the model that I am using, which is why I am also including mechanical pressures, hormones and electrical chemical signalling. However for the purpose of clarity and simplicity I am focusing just on mechanical pressures at this time. So in talking about the role of mechanical forces in ontogeny I must emphasize that I am not saying that it is always the most important factor in every single transformation the embryo/ fetus experiences, but rather that it is very often the hidden driving mechanism that is pushing the various developmental processes along.

Rather than attempt in a few paragraphs to provide a comprehensive review of this topic, using what is to me and perhaps to me alone, a logical shorthand of expressions that describe various tissue migration processes, I will simply develop the concept of how mechanical pressures can and do control the length of metaphase, and then use that example to provide a detail falsifiable hypothesis about the role of mechanical pressure in controlling metaphase has in nerve cell proliferation in the human neocortex.

To explain in the simplest way possible the reason that metaphase duration can be controlled by changes in mechanical pressure, I will use a simple analogy, please bear in mind it is only an analogy and no analogy is perfect. Imagine that you put a button on a string and tied the string to each of your pointer fingers, and then pulled your hands apart and began to spin it. You would find that the tighter that you held onto the ends the string the faster the button would be able to spin. Well this same principle also applies to the speed in DNA polymerase rotates along the DNA strand, simply reducing the amount of tension in the DNA strand, can slow down its progress prolonging prometaphase. For empirical support of this hypothesis please read the paper below:

This hypothesis is further supported by a separate experiment where researchers prolonged prometaphase by applying mechanical pressure to precise points of a cell during metaphase which I post in an earlier comment, but will repost below:

So let’s think about this quality of DNA from an engineering standpoint, by asking the following question: If you were designing a cell today why would you engineer the DNA, in such a way that the timing of prometaphase could be adjusted by slight changes in mechanical tension? I hypothesize that the answer is linked to the mechanics of tissue migration, here is how one paper describes this process:

Mechanobiology studies have shown that cell–ECM and cell–cell adhesions participate in mechanosensing to transduce mechanical cues into biochemical signals and conversely are responsible for the transmission of intracellular forces to the extracellular environment. As they migrate, cells use these adhesive structures to probe their surroundings, adapt their mechanical properties, and exert the appropriate forces required for their movements
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5541834/

Now that we have this common basis for conversation, I will share with you my hypothesis about the role of mechanical pressures in the differential growth of the neocortex in humans versus chimpanzees and other mammals.

In a paper that I mentioned earlier, the authors found that a significant difference between the development of the chimpanzee neo cortex and the human one is that length of prometaphase is longer in humans than it is in chimpanzees. Now my hypothesis is that the human cells exert more mechanical force against the extracellular matrix while migrating into the neo cortex. This increased force generated during the contraction phase of its movement reduces the amount of tension in the mitotic spindle at just the right angle and just the right amount to slow down prometaphase and promote the proliferation of more neurons into the human neocortex as compared to the amount of proliferation that occurs in the chimpanzee, and all other mammals. to what happens in chimpanzees and every other.

A few days ago my hypothesis was incomplete. I needed a mechanism to increase the amount of torque in just the human cells, and I also could only look into it late at night due to other responsibilities. However after re-reading the original paper I found this sentence:

Genes with the highest specificity score encoded canonical cerebral cortex patterning transcription factors such as PAX6, ID4, and GLI3, as well as proteins involved in cell adhesion and ECM signalling (CDH4, EFNB1/2, COL4A2). Notably, no genes associated with cell cycle, kinetochore, or spindle terms were specific to human APs (Figure 8C, inset)
(Boldness added for emphasis)

Now my hypothesis made a lot more sense, but only if if the human cells had to overcome stronger adhesions to the ECM, than the chimpanzee cells that would require that they would generate more torque, just like a car has to generate higher torque when it’s stuck in the mud. This would also suggest that the human cell should move more slowly than the chimpanzee cells do which led me to discovering this paper:

It supports my hypothesis that the humans cells need to exert more torque to overcome adhesive forces and thus moves slower, by stating:

The distribution of migration speed of cells from the three species differed, with human NPCs moving significantly more slowly than either chimpanzee or bonobo NPCs (mean migration speed: human = 0.46 ± 0.19 μm /min, chimpanzee = 0.70 ± 0.31 μm /min, bonobo = 0.72 ± 0.35 μm /min, [Figure 2F (https://elifesciences.org/articles/37527#fig2)). By contrast, we did not find significant differences in the migration speeds between chimpanzee and bonobo NPCs.

So the hypothesis that higher mechanical forces in human nerve cells regulates the speed of prometaphase, is both consistent with the known properties of the reduced tension mitotic DNA spindle, the role of adhesive proteins in cell migration, the physics of torque, and the relative speeds between species. All it needs is direct empirical validation, something that is beyond my technical expertise, and available equipment, but well within the grasp of any scientist reading this long post, who is willing to accept the possibility that open innovation in science is still a useful proposition. Just imagine if a random inventor or the internet can use his limited knowledge on mechanics to possibly solve a long standing mystery about what makes our human neocortex unique, just imagine what you all can do. Here’s a link that I find fascinating perhaps you will too:

As I mentioned earlier it is essential to my broader hypothesis that the role of mechanical pressure in biology is understood first, before I can tie this principle to ID in post in the near future. Thanks for reading, and feedback is welcome.

If such a feature is beneficial, why couldn’t it evolve?

Why does mechanical tension change the rate of DNA replication? Again, it has to do with genetics. Change the sequence of different genes and genetic features and you get a different outcome.

Why does that happen? From everything I am reading, it is due to sequence differences between the two species.

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I’m left wondering what this has to do with evolution and your assumption that changes in the physical pressures exerted on different tissues can’t have a genetic influence.

15 posts were split to a new topic: Is Information Only Present in the Genome

So I have been asked about the genetic evidence for common descent, and so I decided to share my thoughts on this topic. First as far as universal common descent I find that hypothesis to be untenable because it implies that biological life predates cells, although it provides no plausible mechanism to explain how that could be the case. What’s more it can not be formally tested, as was explained quite clearly by an author who thinks that it is true, but is aware that the evidence doesn’t perfectly align with that assumption. In the article below:

At the same time hybridization, is direct evidence that common descent goes beyond the species level so the real question for me is how much common decent can be demonstrated to exist? Well the first thing that I thought of is that mutations must be driven by physics, since the DNA is held together with hydrogen bonds, and different nucleotides have different ionization potentials. This is not controversial and well explained in one paper in the following way:

Mutations occur in a highly non-random fashion along a DNA molecule. Although natural selection helps shape the DNA’s mutation spectrum—the variant frequency vs. nucleotide position—its sequence-dependent physical properties have also been found to locally influence mutation rates1,2,3. Electron holes, in particular, are common targets of base-pair substitutions in cancer and other diseases1. A hole is a site of positive charge created when an electron is removed, e.g., by ionizing radiation or contact with an oxidizing compound. The newly created hole then migrates4,5 until it localizes6,7,8 and potentially triggers a base-pair mismatch during replication1.

https://www.nature.com/articles/srep13571#Tab1

As all of you are all well aware of this property of DNA results in hotspots, where mutations are more likely to occur. When I learned about hotspots I looked for evidence that the physics driven hotspots are well correlated within the same species, genera and family. So I looked to see how well it aligns with the expectation of evolutionary theory that mutational hotspots among mammals would not be independent, but would display covariance. That is how I learned about another paper which explains:

One surprising finding of this study is the high apparent rate of evolution of site-specific mutation rates. As little as 10%-12% sequence divergence between congeneric species is enough to generate a detectable shortage of polymorphism co-occurrence. At the family level, virtually all the co-occurrence signal vanishes: Knowing that site i is polymorphic in species 1 does not increase the probability that it is found polymorphic in species 2.

The process of site-specific variation of evolutionary rate, known as covarion or heterotachy (Fitch 1971; Galtier 2001; Lopez et al. 2002), is usually considered as the consequence of changes in the selective constraints applying to specific sites (see Gu 1999; Pupko and Galtier 2002). Our results suggest that, at least for mammalian mitochondrial DNA, such patterns can also occur neutrally as the consequence of mutational effects…

From an empirical point of view, this “mutational covarion” means that one can hardly learn from one species which mitochondrial sites are going to be variable in another one. It would be worth knowing whether this statement also applies at the level of the gene or genome fragment. It is tempting, when starting a molecular biodiversity project in a new species, to target markers known to be polymorphic in related species. The current study suggests that this practice might be of little relevance in many cases.

So when I thought about the observation that hybridization also seems to be limited to animals from the same Genera in mammals I concluded that population genetics is only applicable to inter-fertile populations. This would actually make the capabilities of population genetics consistent with the capabilities of genetic ancestry tests which also become less accurate the further one goes back in time. When I combined the above genetic evidence with what I consider to be good evidence that many of the arboreal apes that are hypothesized to be human ancestors are actually closer to orangutans than chimpanzees, I decided that the evidence for recent chimpanzee and human ancestor is more speculative than I had been led to believe, although I can not direct rule it out. I would be willing to accept Joshua’s argument that whether or not one believes it to be true it certainly looks like God made human’s from chimpanzee parts if I hadn’t read so much about how similar proposed human ancestor are to orangutans, here are some examples:

https://anatomypubs.onlinelibrary.wiley.com/doi/pdfdirect/10.1002/ar.b.20107

https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2699.2009.02141.x

This only reinforced my thinking that all of these phylogenetic relationships are highly speculative.

Ok so I need to answer this question seriously. The first thing I have to say is that there are different levels of evidence of common descent, direct indirect and theoretical. A direct evidence of common descent is inter-fertility including hybridization, while genetic evidence of past inter fertility such as evidence of a past genetic introgression, while the theoretical evidence of common descent is evolutionary homology. So I will explain why I don’t find the evidence of genetic evolutionary homology to be convincing in a longer answer addressed to everyone.

If you could remind me of the exact time I stated that, I will be happy to say that is not the thought that I intended to convey. What I think I said was that if one is explaining the origins of the phenotype then genetics has a limited explanatory power, or something to that effect. Perhaps I should explain what I meant. As you no doubt know some traits are simple traits where a simple genetic mutation could reshape it easily, while many complex traits are spread over much of the genome. So it’s not so simple to claim that any particular genes are the cause of any particular phenotype instead they are associated with them.

I think that mechanical forces are one of the most unexplored but obviously important factors in development, and and another level of system interconnectivity to biology.

As far as the environment is concerned, what I am saying is that the phenotype is the result of the interaction of the whole cell and its environment, which during development is mostly other cells, although in some cases abiotic factors are just as important. Two examples I can quickly think of are ambient CO2 levels in termite mounds, and water temperature, pH, and salinity in the case of fish represent important developmental cues that guide development. Termites can and do build, and remodel their mounds in such a way that CO2 levels are exactly what they need them to be, but fish have to migrate to the right sort of environment.

That sentence is referring to genes that are specific to apical progenitor cells, not specifically human apical progenitor cells. Here’s the quote again, including the next couple of sentences.

Genes with the highest specificity score encoded canonical cerebral cortex patterning transcription factors such as PAX6, ID4, and GLI3, as well as proteins involved in cell adhesion and ECM signalling (CDH4, EFNB1/2, COL4A2). Notably, no genes associated with cell cycle, kinetochore, or spindle terms were specific to human APs (Figure 8C, inset). Of genes specific to APs, a subset were also differentially expressed between human and chimpanzee cerebral organoids (APOLD1, BICC1, EFNB1, GSTM1, IFI44L, ITGB8, SDK2, SEMA5A, SLC35F1, ZNF516), which makes them candidates for the unique regulation of AP proliferation in humans (Figure 8D)

I’ve highlighted in bold the relevant part - those are the genes that you should be interested in.

Even if your hypothesis is correct, it’s far from “solving” the whole story. It would be one component of a much larger systemic change. I think you’re overstating quite a few things, including how simple this idea would be to test. I doubt any of the scientists here have the facilities and expertise to empirically test your hypothesis, and it would take scientists that do actualy work in this kind of field months or years to test. This kind of biomechanical developmental biology work isn’t overlooked or neclected, it’s just extremely challenging.

I’ve read this thread quite quickly, perhaps too quickly, but where is the connection between all this and ID/evolution? Are you under the impression that evolution is incompatible with mechanical forces influencing development? Genetic changes can obviously differential mechanical forces that can in turn influence development. This is no different from the genetic changes that directly influence development - both are selectable.

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Please justify this division you have created between “direct, indirect and theoretical evidence.” Is it a principle of science that indirect evidence is weaker than direct? What differentiates “indirect” from “theoretical” evidence? We need to be on the same page on these basic issues before you go and elaborate at length on the basis of these assertions of yours. If it turns out these assertions are unjustified, then it will save a lot of time, yours included.

Also, are you under the impression that the evidence for common descent is limited to inter-fertility, introgression and homology? Have you not overlooked some other very important evidences? This might help you answer that:

http://www.talkorigins.org/faqs/comdesc/

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Without a basis in observable phenomena what would be the difference between science and philosophy? So let’s take the theory of a static universe for example. Much like, evolutionary theory the idea of an eternal universe is one that is rooted in the philosophy of the ancient Greeks. Since it eliminated a priori any need to explain the origin of the universe, it was a favorite theory of those who believe that the philosophy of materialism is the only logical basis for science. However, its plausibility was based on ignorance about how the physics of the universe worked. Despite being based on false presuppositions the static universe model was able to accommodate most evidences from modern physics including relativity all that was needed were a few post hoc adjustments to it such the universal constant. Similarly common descent can explain everything so long as one is willing to make few post hoc adjustments to align ones results to the “known” phylogenies.

So sticking with my comparison between cosmology and biology, inter fertility is equivalent to trigonometric parallax, both are examples of direct measurement, or observations, and without any scientific theory having an empirical basis either direct measurements or observations then we are discussing philosophy not science. Similarly, much as astronomers and astrophysicists were able to create by directly measuring nearby Cepheid variables and using those measurements to create brightness scales by using red shift to indirectly measure how far away nearby galaxies are, biologists are able to use evidence of past genetic introgressions to indirectly demonstrate common descent in organisms where there is currently no known active gene exchange.

Beyond the point of direct and indirect measurement the accuracy of any theory is dependent on the how close the presuppositions that it is based on accurately reflect reality. Since presuppositions are by definition philosophical, they are speculative and maybe overturned by contrary data at any time, so we should not have confidence in their accuracy, only in their explanatory power or lack thereof. Just as the null theory of the static universe was Big Bang cosmology, the null theory of universal common decent, is limited common descent.

Even if evolutionary biologists reject such a null theory in practice and decide to call it something else such as convergent evolution, the inability of evolutionary theory to falsify the null theory that something other than common descent is responsible for certain aspects of biology still, weakens the premise that the theory is based on because it raises the possibility that other aspects of biology currently attributed to common descent are in fact caused by something else as well. So in my humble opinion, the goal of ID should not be to replace one speculative philosophy of science with another one, but rather to discover what causes the appearance to some of common descent where there is none.

Thanks for writing a bunch of words that did not answer my questions. I hope you had more fun writing them than I did reading them.

I suggest you stop trying to convince the members of this forum that you are a brilliant unschooled genius regarding evolutionary biology, and just pay attention to the corrections and explanations you are receiving from people who actually understand this subject.

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Cart before horse. You haven’t established that there is none. You haven’t even presented an alternative to common descent, though you may think you have. Perhaps you might try clearly articulating this alternative, and you might also articulate where you think common descent ends. What parts of the tree of life are not actually due to descent?

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Actually, just the opposite. The proposed universal common ancestor would have existed well after the first life emerged.

Where do the authors state that universal common ancestry can not be tested at all? The authors are arguing that it is difficult to impossible to determine if protein sequences are convergent or inherited.

Common descent among vertebrates would seem to be rather easy to demonstrate.

No scientists are claiming that any living ape is a human ancestor. You are using ladder thinking instead of tree thinking.

You should also realize that chimps share more DNA with humans than they do any other ape species.

image
" We estimated nucleotide divergence in unique gap-free sequence, indicated at each node, from the alignment of rhesus macaque (yellow), gibbon (purple), orang-utan (orange), gorilla (aqua), chimpanzee (green) and human (blue) whole genome shotgun reads to the human reference (Hs.35; Supplementary Information section 3). Note that the Bornean ( P. pygmaeus ) and Sumatran ( P. abelii ) orang-utan species showed nucleotide identity comparable to that of bonobo ( Pan paniscus ) and chimpanzee ( Pan troglodytes ). Estimates of divergence time based on sequence identity are indicated at each node, ∼1 Myr implies approximately 1 Myr or less. Values taken from refs 29 and 30 where indicated."
https://www.nature.com/articles/nature09687

The phylogenetic relationships are based on DNA sequence which isn’t speculative at all.

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Then how is it that you have been able to find so many reports by people who study mechanical forces?

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Why would it imply that? It just says all known life is genealogically related, which by itself says nothing about the relationship between what life is and the origins of cells.

Also, leaving aside the subject of universal common descent, the relationship between the origin of life and the origin of cells appears to be a matter of definition. If you simply define life such that it would have to be cellular(if you were to say that in your view, if itsn’t cellular then it doesn’t count as a form of life), then life originated at the origin of the first cell regardless of how that occurred exactly.

By insisting on such a definition of life you do not really argue that life could not originate by some sort of evolutionary process, as it is entirely possible there was a substantial period of pre-cellular evolution (a sort of chemical evolution) that eventually gave rise to the first cells.

Non-life —> chemical evolution —> origin of cellular life —> more evolution —> last universal common ancestor —> diversification of all known cellular life into it’s extant forms.

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