Introducing Geremy (and Behe)

I have no disagreement with anything in that article. But how does it relate to evolution? How does it relate to inheritance and to the differences between species?

Right, situs inversus. Notice that in the system you cited, there’s genetic control both above and below the mechanical stimulus. It in no way supports your hypothesis that mechanical forces dominate.

I’m not speaking for the other John, but I’m well aware of all of this, having studied unconventional myosins for decades and knowing the players. As one example, I’ve known Dan Kiehart and his Drosophila work, the focus of one section of that review, for decades.

There’s evidence that mechanical forces are involved, but no evidence that they dominate except in a few very interesting systems.

Thanks. Your response comes across as insulting (maybe not intentionally), because I’m quite aware of the field; I know people in it. I’m saying that I don’t understand your point because it was not expressed coherently, but I was trying to be polite.

No, it does not even come close to demonstrating that.

No, they did not control it, they merely influenced it, which itself is interesting. This is shown most vividly in Fig 3 panels E-H. You are grossly overstating the data, but in your defense, the title does too.

I don’t see the slightest indication in the eLife paper that the researchers were confused. I also know the senior editor who approved the eLife paper (K VijayRaghavan) very well. I’m pretty steeped in this stuff, Geremy.

Hypotheses by definition are speculative, so there’s no need to qualify yours that way. But hypotheses are science, so that’s good!

Unless there is evidence for differential directional pressures in the embryonic brain, there’s no reason to hypothesize that. The eLife paper shows that this species difference is independent of pressure, since they saw the difference in culture!

I think that you are conflating the fact that force can influence mitosis and gene expression in an artificial system as force controlling it in vivo. It’s one factor among many.

Biologists do not ignore these physiological factors and it comes across as arrogant for you to posture as though they do. You might want to look up situs inversus caused by ciliary dyskinesia for a vivid example of this–a genetic change produces a mechanical change (fluid flow in the early embryo) that produces a reversal of left/right polarity of everything in the body. So we still have the allegedly limited explanatory power of genetics at the top of the hierarchy explaining the physiology.

TL;DR: there’s excellent evidence that mechanical pressure is important in some cases, but zero evidence that it dominates.


I did not mean to be insulting John, when I am presenting an idea I usually have a presentation and an outline of what I am trying to say which helps me to organize my thoughts in a way that is easy to understand. So I am accustomed to saying to those interest in one of my ideas something like: “Let me draw your attention to Fig. 3b where we have a longitudinal view of the preferred embodiment” etc., when discussing my own technical designs, so no arrogance or condescension was intended, so I apologize for giving you that impression. As far as being incoherent that is probably due to trying to cover too many topics in a short paragraph, I promise to stick to one topic and develop it using a linear progression of the same theme from this point forward.

Now as far as my hypothesis, it is well known that a great majority of animal life on earth begins life in an egg external to the body. Many animals also pass through a larval stage, where they hatch early and pass through various stages analogous to our fetal development in an environment that wasn’t created by their parents. In these cases the environment above is not the result of genetics, and such creatures often have to migrate thousands of miles to encounter the right environment in which to continue their growth and development. A excellent example of this phenomenon is the European eel which has to migrate thousands of miles to complete it’s life cycle as shown in the short video below:

Now if we accept that inheritance is strictly based on genetics and that all of the cues needed to develop are genetic in origin then the life cycle seems absurd. Why travel thousands of mile to undergo sex differentiation and grow only to end back up where it began to spawn. This is why I think that inheritance includes three basic features:

  1. A cell nucleus from our father.
  2. An ova cell (nucleus, cytoplasm, osmotic sensors, molecular machines etc.) from our mother.
  3. A very specific environment in which to grow.

Now for mammals we inherit all of the above in a enclosed biological system, but we are by no means the rule. This is why I think of the environmental cues provided by the womb as part of our inheritance. There is actually much more to my hypothesis than I have explained so far, so I will explain the rest very soon. Have a great Sunday.

Because there’s some advantage to spending larval life in one place and spawning in another. It has nothing to do with necessary developmental cues. You would appear to be wearing blinders that force you into one preferred explanation for everything. But I would bet that an eel raised in a laboratory would develop normally, contra your hypothesis.

Actually, the father contributes only the genome, not the entire nucleus.

Would you go so far as to claim that a cat embryo implanted in a dog womb would grow up to be a dog? Note also that wombs are not inherited, but develop from a single-celled zygote. No inheritance there, any more than legs or gall bladders are inherited.

So far your hypothesis is either trivial (there are physical factors in development) or trivially untrue.


All you need for inheritance is a genome, DNA or RNA. Sperm cells and ova are carriers of those genomes in sexually reproducing organisms. Transcription factors and other molecules only modulate gene expression patterns.

We don’t inherit all of that, we only inherit information needed to recreate those features in new organisms. That information is stored and transmitted through a genome. That’s why certain mutations to genes which control morphology can produce deformed kids, even though this kids get the same womb, sperm and egg cells healthy kids get.

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I know of no biologist who says everything that affects development(or any kind of gene-regulation, really) is strictly based on genetics and that environment plays no role. It simply wouldn’t make sense to say that.
The first thing I was taught about gene-regulation was the lac-operon, and it immediately becomes obvious that gene expression can be tied to external stimuli through other genes. The expression of carbohydrate metabolizing enzymes are regulated by the detection of carbohydrates in the environment. A DNA-binding repressor protein responds to the presence the carbohydrate, changing it’s conformation so it lets go of the DNA, enabling transcription-initiators to bind and initiate transcription of the downstream enzymes that metabolizes the carbohydrate.

lac operon

Now here’s the question. Is the regulation of lactose metabolism environmentally or genetically controlled? The repressor protein that blocks transcription of the enzyme-encoding genes is itself the product of transcription of some other gene. And the RNA polymerase binding spot is a promoter sequence. And RNA polymerase is itself a protein that is expressed and regulated from genes elsewhere in the genome. That means the genes encoding the enzyme, are under control of the protein product of some other gene. But that repressor protein won’t let go the DNA before lactose binds to it. And RNA polymerase won’t bind and transcribe the beta-galactosidase enzymes without a transcriptional promoter sequence.

To say it is either the environment, or the genes, that control expression of lactose metabolism is then a false dichotomy. They both are necessary components of the regulation. The mere existence of lactose in the environment won’t magically force RNA polymerase to bind and transcribe the enzyme genes, the promoter region is still required for efficient transcription. Similarly the repressor protein requires lactose to be present to stop blocking the promoter(and requires the promoter region to bind and repress expression). Neither thing by itself is the cause of why the operon is expressed or not, they must all be considered together to understand why the genes are or are not transcribed at any given moment.

The fundamentals of gene expression during development in multicellular eukaryotes are based, ultimately, on similar principles. DNA binding proteins respond to environmental cues causing them either to repress or enable transcription of genes. The expression of genes is always some sort of interplay between DNA and the inter-and-or-intracellular environment.


No problem. I’m just trying to give you feedback.

But you are switching topics.

We do know that, but let’s go back and focus on your previous hypothesis more precisely:

I am saying that the mechanical forces with which you are so enamored are not the primary factor in the regulation of gene expression. Mechanical forces only come into play in a few, very interesting, cases to date.

The cytoplasmic environment of the egg is indeed the result of genetics. There are many known maternal-effect genes that demonstrate this.

  1. That doesn’t address the importance of genetics.
  2. Please, please don’t cite videos. There are far better ways to convey evidence and ideas.

But we don’t accept that it is strictly based on genetics. It’s almost entirely based on genetics. You are positing a patently false dichotomy.

But it doesn’t. Parthenogenesis is fairly common, so the paternal nucleus is not universally necessary. Many lizards, turtles, and (IIRC) frogs have sex controlled by the incubation temperature of the eggs. Others can change sex after hatching.

I see two problems: you think dichotomously and you ignore evidence that doesn’t support your hypothesis.

That’s not a good sign. Simpler hypotheses are better. Overly complex ones can be a sign that you’re just going through the motions and are too invested in your hypothesis to employ it as a tool to gain knowledge.

Enjoy your Sunday.


Short answer: adaptive decoupling. See paper below for more details.

What testable ID explanation can you offer for the life cycle of the European eel?


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:

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.


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.



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.


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

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 ( 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.


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.

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:

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.