Nothing you have posted is relevant to anything I’ve asked about. Nobody is saying that mechanical signals don’t affect gene expression. But these mechanical signals are not inherited by gametes or zygotes. They can’t explain the differences among species.
The biggest misconception that I am pushing up against here is that evolutionary theory has ever had a real explanation for phenotypic differences as opposed to anecdotes, analogies and just so stories. This narrative that the theory is pushing that genotypic evolution is somehow creating new phenotypes, and the constraints of ontogeny are irrelevant is both very old and demonstrably false. What is more it is a result of how evolutionary theory was originally designed, here is how one source that is very friendly to the current theory explains it:
The founders of the modern synthesis treated embryology as a ‘black box’, the details of which could be ignored for the purposes of evolutionary theory; their focus was on the transmission of genes across generations, not the process by which genes make organisms. This strategy was perfectly reasonable, given how little was understood about development at the time.
So what about evolutionary theory today, does it actually address the feasibility of evolving actual organisms, complete with the known soft matter physics based constraints on ontogeny? Or does it still only create complicated speculations about how genes can be transmitted from taxa to taxa, while ignoring the very real constraints on such processes? The answer seems to be that modern evolutionary theory tries to incorporate developmental biology but is simply unable to for reasons that I will now explain.
Any theory of common descent will be constrained by the mechanisms of biological descent. So there is no rational basis to believe that evolutionary theory can ignore the constraints of most developmental processes or simply cherry pick a few elements of ontogeny such as the role of HOX genes, while ignoring how the overall process works and still explain how such development processes can change to create new phenotypes. Unlike what occurs on the organismal level where predators and environmental changes can be accurately described by the metaphor of natural selection, the constraints on developmental processes are imposed by physiology and soft matter physics. Physiological adaptations can dramatically change the phenotype of animals as a result of plasticity, but on the genetic level it most constrains genetic variation (I will talk more about this point later). Soft matter physics simply is a property of the universe, as is all physics and does not change in response to the needs of organisms. So when I describe processes by which emergent mechanical forces regulate both gene expression and phenotype shape, I am describing the role of soft matter physics in development as demonstrated by empirical evidence from developmental biology, mechanobiology and tissue engineering. Unlike genetics where information is contained in nucleotide sequences, the constraints imposed by physics under a given circumstance, do not need to be encoded anywhere in particular because they exist everywhere in the entire visible universe, so simply recreating the exact same circumstances recreates the same physical constraints.
Understanding how mechanical pressures caused by cell movements create predictable differences in the shape of the cell, their nuclei and chromosomes arrangement in different cell types helps us to understand both the role of non coding DNA in making such arrangements and the importance of genome topography in gene regulation. So what I have been explaining is that it is the topography of the entire genome that varies slightly even between individuals of the same species, and varies much more between different species that is causing most the differences in phenotype. What is more it is these differences in whole genome shape and positioning that causes the distribution of mechanical forces within cells to change, resulting in differential transcription in different organs of the same organism, different members of the same species and different species. This physic based understanding of gene regulation is the result of advances in technology, not theoretical considerations. Here is how one study explains it:
Most studies examining three-dimensional structure genome-wide are limited to a single species. In this study, we compared three-dimensional structure in the genomes of induced pluripotent stem cells from humans and chimpanzees. We collected gene expression data from the same samples, which allowed us to assess the contribution of three-dimensional chromatin conformation to gene regulatory evolution in primates. Our results demonstrate that gene expression differences between the species may often be mediated by differences in three-dimensional genomic interactions. Our data also suggest that large-scale chromatin structures (i.e. topologically associating domains, TADs) are not well conserved in their placement across species. We hope the analytical paradigms we present here could serve as a basis for future comparative studies of three-dimensional genome organization, elucidating the putative functional regulatory loci driving speciation.
So there is plenty of evidence that is consistent with the hypothesis that mechanical pressure that arises during development regulating gene expression. This hypothesis is made stronger when we look carefully at the alternative hypothesis that gene controlled genetic regulatory networks are globally regulating gene expression.
Some problems with the current model of gene regulatory networks were delineated in a paper entitled “Rethinking gene regulatory networks in light of alternative splicing, intrinsically disordered protein domains, and post-translational modifications”, the author explains:
Models for genetic regulation and cell fate specification characteristically assume that gene regulatory networks (GRNs) are essentially deterministic and exhibit multiple stable states specifying alternative, but pre-figured cell fates. Mounting evidence shows, however, that most eukaryotic precursor RNAs undergo alternative splicing (AS) and that the majority of transcription factors contain intrinsically disordered protein (IDP) domains whose functionalities are context dependent as well as subject to post-translational modification (PTM). Consequently, many transcription factors do not have fixed cis-acting regulatory targets, and developmental determination by GRNs alone is untenable. Modeling these phenomena requires a multi-scale approach to explain how GRNs operationally interact with the intra- and intercellular environments.
If we combine both the evidence that the genetic elements of GRNs are characterized by indeterminacy, with the observations that originally inspired the GRN hypothesis, namely the that there was a bi-stable genetic switch that activated the lytic cycle bacteriophages that had previously been in the lysogenic phase, it seems obvious at least to me, that the stochastic regulatory elements of the genome are being organized, by a highly structured outside force not the intrinsic genetic elements. The mechanical pressures that arise from cell movements are a natural consequence of the soft matter physics that universally constrains intracellular, and intercellular organization of all multicelluar organisms on earth.
The evidence that gene regulation is a result of physics, has implications for evolutionary theory:
- It removes natural selection as a flexible factor of gene regulation evolution. Natural selection is a metaphor for environmental constraints that change with time. There is no evidence that soft matter physics has changed, since the initial appearance of water in the universe about 11 billion years ago.
- As some biologists knew decades ago, repetitive gene elements are not junk DNA, but rather create the sequence dependent structural context for gene expression. The well know rule of, form equals function applies to DNA, just as much as it applies to protein.
Word salad too. Whether sequence similarities are caused by common descent has nothing to do with cell movements but with the structure of the comparative data, a consistent nested hierarchy. We know what causes changes in DNA sequences: various sorts of mutations whose mechanisms are fairly well understood. You have to answer this simple question: why a nested hierarchy?
The nested hierarchies of evolutionary theory are strictly conceptual models used to make biological complexity comprehensible to most people who are linear thinkers. What I am saying is that the actual variables that the nested hierarchy model is used to explain, do not change in the manner predicted by neutral theory they fail at their principle objective of demonstrating that the evidence is consistent with common decent as opposed to common physiological constraints. A good example of this is rRNA sequences used in some phylogenetic trees, there is good evidence going back several decades that rRNA differences between eukaryotic species is not explainable by the neutral theory while that of bacteria and archaea superficially appears to be. That simple observation was made in the paper below:
If we go look at the evidence for why rRNA in prokaryotes appears to evolve in line with the neutral theory, it gradually becomes clear that the appearance of neutral evolution is deceptive. The real answer seems to be that the variation rRNA gene sequences are determined by shared physiological constraints. Here is how one paper explains it:
We discovered that rRNA alleles are differentially expressed in response to nutrient limitation-induced stress and that the rRNA allele most upregulated on a relative basis is distinguished by conserved sequence variants clustered in the small subunit head domain of the assembled ribosome (Kurylo et al. 2018). These findings revealed for the first time that the rRNA allele composition of the actively translating ribosome pool is indeed regulated in response to physiological stimuli. Remarkably, we further showed that ribosomes bearing these sequence variations causally affected stress-response gene expression and phenotype, including biofilm formation, cell motility, and antibiotic sensitivity. Consistent with the sequence variants modulating the so-called ribo-interactome (Simsek et al. 2017), we further identified rRNA allele-dependent genetic interactions with stress-related proteins that transiently interact with the ribosome in the proximity of the sequence variants during protein synthesis. The varied expression of this operon alters the mechanisms of ribosome-interacting factor engagement during translation to affect gene expression and cell physiology during stress. Interestingly, the exact same sequence variations were found to be conserved in many Enterobacteriaceae, including Salmonella enterica, which diverged from E. coli more than 120 million years ago.
Now if we compare the above example to humans we can say that it there is strong evidence all of us carry many rRNA s that have coding sequences that diverge from the standard human rRNA sequences used in phylogenetic trees. For example human chromosome 21 has 101 different rRNA coding sequence variants as explained in the paper below:
So I think that there are probably rRNA gene variants in one animal species that are identical to the dominant rRNA gene sequence of another species, but that the dominant rRNA gene variant of given species is dependent on the constraints that the physiology of a given species places on rRNA gene sequence variation . So what this would mean for phylogenetic trees that use rRNAs to represent genetic distance, is that the researchers are likely to be simply comparing how similar the physiological constraints on ribosomes gene sequences of selected species are to each other, not their genetic distance from each other due to common descent.