John I do not mean to ignore your questions, it’s just a matter of neglect not intent. There so may of you to respond to and only one of me. As I see it evolutionary theory is designed to be a general theory of biology, but it is not. I think that population genetics still is limited to explaining current and recent genetic conditions, and that the coalescent theory is limited to species that share genes. My goal isn’t to make a speculative theory of everything, but rather to show that biological systems are too interconnected and the genetic mechanism of evolution are to limited to paint an accurate picture of biological history. These are the reasons that evolutionary explanations are limited.
Chromosomal changes are not driven by random chance mutations, but the shortened telomeres of old age.
Since chromosome configuration and number vary from species to species, I decided to look into what the known causes of chromosome change are, and this is how I learned about the role of telomere shortening. Here is how one paper explains this connection:
In the well-established tumorigenesis model, telomeres in human somatic cells gradually become shortened with each cell division. After 50 to 60 cell cycles, cells with shortened telomeres provoke replicative senescence by chromosomal instability and p53 activation, which is induced by the DNA damage response according to telomere shortening [76,77,78]. However, some cells that can overcome senescence by the acquisition of genetic mutations in p53 or other checkpoint proteins continue to proliferate; thus, telomeres become critically short, and apoptosis is subsequently induced (crisis) [79,80]. At this point, a minor population of the cells that activate telomerase (or ALT pathway) acquires immortality and proceeds to carcinogenesis [79]…
Given that telomerase-mediated telomere elongation is important for the infinite proliferation of TERT-positive cancer cells, genetic or pharmacological inhibition of telomerase activity in cancer cells induces gradual shortening of telomeres and eventual cell senescence or apoptosis [109,110,111]. Theoretically, the anticancer effect of telomerase inhibition would emerge earlier in cancer cells with shorter telomeres. In fact, short telomere length could be a predictive biomarker of telomerase inhibitors [[112]
To explain the differences in in chromosomal arrangements evolutionary theorists often claim that these changes are due to random mutations, followed by evolutionary bottle necks. There are two problems with this claim. One easiest problem with this model to demonstrate are the claimed bottlenecks need to fixate the number of changes. After reading about the long chain of chance events, followed by a severe population bottleneck needed to claim that human chromosome 2 fusion happened just by chance. I wondered how many bottlenecks would it take to explain the chromosomal differences between humans and gibbons. Which is how I learned about the research of one oncologist who asked the same question. He writes:
How many bottlenecks are required to generate this kind of karyotypical mess between closely related species? a Gibbon (Hylobates lar) karyotype in comparison to b human karyotype based on correspond- ing color code. Every sporadic chromosomal aberration reduces fertility of heterozygotes due to loss of genetically unbalanced offspring.
The above researcher then develops his own hypothesis of convergent evolution based on progressive telomere erosion while I am not endorsing his hypothesis, I think that the if one wants to claim that chromosome differences are all due to chance driven mutations there would need to be some explanation other than countless low probability mutations, which would cause countless population bottlenecks. The researcher above is aware of the second problem of telomere shortening due to his research in cancer, as I read the profiles of evolutionary biologists who think that there broader theory of evolution is not explained by the current theory I noticed that many of theses biologist are cancer researchers, and physiologists. The reason that I think that this is the case is because cancer researchers get to see the causes and effects of evolution up close in humans, and since different organisms have different genetic toolkits they can see that the sort of model organism based evolutionary explanations that are used to structure evolutionary theory, are not actually universal but confined to the species that have those abilities.
I think the true extent of common descent is unknowable from a scientific standpoint.
This is an interesting consequence of intelligent design, designers make choices even today, a human synthetic biologist might decide to print out functional gene sequences made from scratch, or she/ he may decide to modify existing organisms using guided evolution or both. Without knowing what the designer was thinking, one can not use science alone to demonstrate the limits of common decent, because intelligent agents can do things that chance alone can not. This fact is best explained by of all people Richard Dawkins with his Meme theory, a idea can be reproduced, and adapted to many situations just like a gene can be. So from the standpoint of intelligent design proteins, genomes, lipid structures are ideas, that we can best understand in the terms of mathematics and physics.
To illustrate this point let’s look at the theory of endosymbiosis, which explains that both chloroplasts and mitochondria are remarkably similar to bacteria, and so hypothesizes that their ancestors were bacteria. From an ID perspective bacteria, archaea and eukaryotes all began as ideas in a mind, so the hypothesis that an intelligent agent could combine elements of each to make something new is simple and easy to understand from an engineering standpoint. Now lets look at it from a blind chance perspective. A eukaryotic cell is much more than a just an archaeal cell with mitochondria, so even assuming that an ancient eukaryote engulfed bacteria long ago wouldn’t in itself explain the origins of eukaryotes. So the more common speculation is that an ancient archaea host cell engulfed a bacterial cell and developed a symbiotic relationship. Of course there is one huge problem neither archaean nor bacteria are capable of phagocytosis, so how did this happen in the past? Despite the claims of some researchers there are no demonstrably transitional organisms between archaean and eukaryotes, the claims about Lokiarchaea such claims are contradicted by available data, such as the paper that I linked below:
As I mentioned in an earlier post mutations are caused by physics, so some genetic sequences are simply more stable than others. As explained in Koonin’s common descent paper that I mentioned earlier it would absurd to credit all of this similarity to convergent evolution, however it is not absurd to think that an intelligent agent would use the most stable genetic sequences over and over again to prevent the destruction of these sequences by evolution. This is why I do not agree that phylogenetic trees are genealogical unless common ancestry can be demonstrated by other evidence.
Genome interconnectivity makes gene driven evolution impossible
As I mentioned in an earlier paper most complex traits are spread throughout the entire genome, this design feature is a good way of inhibiting the impact of gene evolution. Another way would be to place the global regulation of genes outside of the reach of physics driven gene evolution. I think that mechanobiologists who think that gene regulation is regulated by mechanical pressures have it right, and that the biologist here who don’t see how such a system of mechanical pressure regulation of the genome can inherited across the theoretical evolutionary tree of life, see the exact same problem that I see and if the above can be demonstrated to be true, the only real solution will be ID, because it is simply a brute fact that intelligent agents can do things that blind natural forces cannot.
So how could mechanobiology regulate gene transcription? This is a long conversation already so I will only provide one example taken from a mechanobiology paper, it explains:
Like twist, tension in the substrate DNA can be critical to this sort of long-range regulatory function. DNA loop formation is driven by thermal fluctuations and intracellular interactions that randomly bend and twist the DNA. When two binding sites come in close proximity to one another, a regulatory protein may form a bridge between the operators to generate a loop in the intervening DNA. The force associated with thermal fluctuations, needed to form such a loop, can be estimated from the persistence length of the DNA at around 0.1 pN—only a fraction of the scale of forces exerted on the DNA during normal cell functioning, like those discussed in §1. It was, therefore, predicted that forces as small as a few hundred femtonewtons could supersede the thermal fluctuations and easily suppress the rate of formation of protein-mediated DNA loops [43,44], effectively preventing all loop formation and, in turn, dramatically altering transcription levels…
In a separate experiment, Chen et al . [46] found that by applying a fluctuating level of tension to the DNA they could greatly enhance the rate of loop formation. The experiment was meant to simulate the fluctuating micromechanical environment of the cellular interior, where fluctuating forces arise from a wide range of intracellular processes. The introduced fluctuations were formally equivalent to increasing the effective temperature of the system and it was found that the loop formation rate could be more than doubled by adding an effective temperature of only 10 per cent of the thermal background. This rate enhancement, owing to force fluctuations, might explain why DNA loops result in a several 100-fold level of repression in vivo [47] despite the observation of equal lifetimes in the looped and unloooped states in vitro . Moreover, the sensitivity of the loop formation rate to the additive fluctuations was shown to be independent of the baseline static tension in the substrate DNA. This led the authors to suggest that schemes which employ mechanical tension as a regulatory switch can be surprisingly robust even in a mechanically noisy environment.
So this is why I consider evolutionary tree of life to be speculative.