“As for mutations, some members of this group might have a misunderstanding regarding the role of mutations and evolution. A review of college textbooks on evolution reveal this:
Mutations are any change to the genomic sequence of an organism and mutations ARE REQUIRED for evolution.
Yes, there are a few scientists who argue for such things as “genetic engineering” (e.g., James Shapiro) and “germ line epigenetic inheritance” in mammals (e.g., Eva Jablonka)…but their views are in the minority. They present some interesting arguments (e.g., the CRISPR system in bacteria, which Shapiro notes as an example of “genetic engineering”), but most evolutionary biologists reject a role for these two mechanisms in evolution.”
My comment: I addressed the recently revised ‘definition’ of mutations in my ISHE presentation earlier this month, and predicted that the definition would be revised earlier this year in a blog post. If Williams cited his source, we could compare it to what’s found in the book “Mutation-driven evolution.” The rejection by “…most evolutionary biologists…” that Williams alludes to is addressed by Denis Noble in Physiology is rocking the foundations of evolutionary biology. Like me, Noble rejects the opinions of evolutionary biologists. Like Noble in his published work and in recent presentations, Nei clearly has incorporated my model in the context of what he states in his book: “MicroRNAs (miRNAs) and other small RNAs encoded by the noncoding regions of DNA are known to control the level of protein production by degrading mRNAs. Changes in these small RNAs may then alter the expression of phenotypic characters.” (p. 136)
My translation: The microRNA/messenger RNA balance controls nutrient-dependent protein biosynthesis and protein degradation via the metabolism of nutrients to species-specific pheromones that control reproduction, which is required for adaptive evolution via selection for phenotypic expression sans mutations theory. I wrote: “Thermodynamically controlled cycles of RNA transcription and protein degradation are responsible for organism-level changes in pheromone production, which enable accelerated changes in the miRNA/mRNA balance and thermoregulation of controlled nutrient-dependent adaptive evolution.” These changes rapidly occur, which places them outside the context of statistical analyses attesting to various theories of mutation-driven evolution, which is why the term “mutations’ must be redefined.
Unlike Noble and others who understand the requirements for controlled gene expression during development, which is dependent on physiological changes, Nei states opinionated beliefs that are inconsistent with biological facts. He writes: “(1) Mutation is the source of all genetic variation on which any form of evolution is dependent. Mutation is the change of genomic structure and includes nucleotide substitution, insertion/deletion, segmented gene duplication, changes in gene regulatory systems, transposition of genes, horizontal gene transfer, etc. (2) Natural selection is for saving advantageous mutations and eliminating harmful mutations. Selective advantage of the mutation is determined by the type of DNA change, and therefore natural selection is an evolutionary process initiated by mutation. It does not have any creative power in contrast to the statements made by some authors.” (p 196)
Changes in gene regulatory systems are clearly nutrient-dependent and pheromone-controlled. With no citations to works that might otherwise attest to the de novo “creation” of olfactory receptor genes, Nei’s claims cannot be placed into the context of cell-level or of organism-level physiology exemplified in my model. What “creative power” is he alluding to? I suspect it is the direct link I have detailed in which “Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans (Keller et al., 2007; Kohl, 2007; Villarreal, 2009; Vosshall, Wong, & Axel, 2000).”
Nevertheless, without citations to whatever works Nei dismisses (above) in the context of creative power, we are left with his opinion and the opinions of people like Williams who did not cite his source for the revised definition. There is no way to contrast what is currently neuroscientifically known about the de novo creation of olfactory receptor genes. Thus, citations to works like: Promoter architecture of mouse olfactory receptor genes will not enter the discussion of adaptive evolution (sans mutations).
Commentary “Genetic hitch-hiking prevalence .” I have a copy of the research. If you are among those who meet my ethical standards, send me a private email and ask for Lang et al, 2013.
Providing unsupported commentary on works that so clearly require discernment from a perspective on what is currently known about the biological basis of behavior in species from microbes to man is not something that an ethical person would do. It is, instead, typical of those who would rather continue to tout ridiculous theories of biologically based cause and effect that have never been scientifically supported (e.g., mutation-driven evolution). Watch for more claims by Williams on the ISHE’s human ethology yahoo group, where the moderator blocks most of my responses to claims made by people like Williams because the moderator: Jay R. Feierman also touts “Random mututations as the substrate on which directional natural selection acts.“
More recently, however, even Feierman admits that “…a more accurate statement is “mutations are A substrate upon which natural selection acts.” For someone like Feierman, who has drastically misrepresented everything currently known about mutations to suddenly acknowledge that, at best, “mutations are A substrate…,” is an admission that he has been wrong for many years about cause and effect, but also that he will continue to be wrong about anything he says in the context of mutation-driven evolution.