Excerpt (with my emphasis): “The prevalent view of neodarwinism (or better “new” or “modern evolutionary synthesis”) is characterized by the assumption that evolutionary changes are caused by a combination of two major processes, (i) heritable variation of individual genomes within a population by mutation and recombination, and (ii) natural selection, i.e., selective environmental or genomic forces leading to better adaptation of those bearing the mutation and as a consequence to their greater differential reproductive success.”
May the forces above be with you as you read about how you mutated to become the person you are and how a Famous physiologist embarrasses himself by claiming that the modern theory of evolution is in tatters
Excerpt: “…there are no experiments—none—showing that mutations are not indifferent, and plenty showing they are.”
My comment: There are no experiments showing that mutations are fixed in the genome (i.e., none are fixed population-wide). Thus, there is no population-wide evidence they are heritable. That means mutations cannot contribute to population-wide heritable variation. Since they cannot contribute to population-wide heritable variation, no evolutionary forces can lead to better adaptation of those bearing the mutation because the mutation is not fixed in the genome population-wide and cannot contribute to greater differential population-wide reproductive success.
Coyne embarrasses himself by claiming that Noble has done so. Coyne does not yet realize the need for “…the development of more general theoretical models explaining the fate of new alleles across long evolutionary timescales.” Noble realizes there are no general theoretical models waiting to be developed that do not include the nutrient-dependent pheromone-controlled adaptive evolution evidenced across species, which is attributed to the epigenetic effects of olfactory/pheromonal input on de novo creation of olfactory receptor genes in my model.
Since my model details how adaptive evolution occurs via ecological, social, neurogenic, and socio-cognitive niche construction, other theorists will continue to embarrass themselves until they, unlike Coyne, realize why Physiology is rocking the foundations of evolutionary biology. Physiology is rocking the foundations of evolutionary biology because there is no experimental evidence to support mutation-driven evolution (i.e., the prevalent view of neodarwinism), and there is overwhelming experimental evidence that supports the physiology of nutrient-dependent pheromone-controlled reproduction, which is essential to the adaptive evolution prevented by mutations. Because mutations prevent adaptive evolution in species from microbes to man, it would be odd to find them fixed in the genome of any species that has adaptively evolved. That explains why mutations are not fixed in the genome and why continuing to look for fixed mutations in the genome of any species that has adaptively evolved is a ridiculous waste of time. What may be worst for theorists is the fact that neodarwinism was “…characterized by the assumption that evolutionary changes are caused by a combination of two major processes…” (see above). Their assumption was wrong! Not only that, it was a ignorant assumption to make given Darwin’s assertions about the ‘conditions of life’ that must be met before evolution can occur by any means whatsoever.
Theorists might now fare better with attempts to redefine the term “mutation” to make it fit into the context of how cells integrate epigenetic effects from their sensory environment into a mechanism through which one signaling pathway (i.e., olfaction) regulates other pathways via olfactory/pheromonal input that produces a coordinated response in species from microbes to man. However, those attempts will force them to include what is already neuroscientifically known about how the physiology of adaptive evolution is epigenetically effected.
Coyne tells us “What we mean by “random” is that mutations occur regardless of whether they would be good for the organism.’ But wait, regardless of whether they would be good for the organism, the mutations that occur are not fixed in the genome. Thus, it doesn’t matter if we adopt his suggestion to use uses the term “indifferent” instead of “random.” Indifferent mutations would be among those that are not fixed in the genome. Everything else Coyne tells us about Noble embarrassing himself, will remain an embarrassment to anyone who agrees with Coyne and is willing to disagree with the current president of the International Union of Physiological Sciences and to challenge the obvious biological fact that adaptive evolution is nutrient-dependent and pheromone-controlled.
Finally, because Coyne’s arguments are so simple-minded and simply ridiculous that it is probably pointless to address them, I will close by addressing one of the most ridiculous arguments of all. He writes: “If you’re a male, methylate this bit of DNA in your sperm.” That is not environmentally-induced or Lamarckian change of the DNA. It’s based on simple, garden-variety evolution of genes themselves.”
The morphogenesis of ‘males’ in unicellular yeasts is nutrient-dependent and reproduction is pheromone-controlled at the advent of sexual reproduction. Males are not simply mutant females, which is what Coyne inadvertently infers. What he might like others to believe was addressed in the context of our section on molecular epigenetics in a 1996 review: From Fertilization to Adult Sexual Behavior.
“Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes (Saunders, Chue, Goebl, Craig, Clark, Powers, Eissenberg, Elgin, Rothfield, and Earnshaw, 1993; Singh, Miller, Pearce, Kothary, Burton, Paro, James, and Gaunt, 1991; Trofatter, Long, Murrell, Stotler, Gusella, and Buckler, 1995). Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.”
The alternative splicings are epigenetically effected, and nothing I just quoted resembles what Coyne may want others to believe is “…based on simple, garden-variety evolution of genes themselves.” Everything incorporates the conserved molecular mechanisms responsible for the physiology of reproduction in species from microbes to man, and some biologists have known that for several decades. If not for the retarded scientific progress readily attributed to evolutionary theorists, research funding might already have enabled the finding of cures for mutation-caused physical diseases and mental disorders. Instead, we have people like Coyne who want to continue to retard scientific progress because they have a ridiculous theory that they like, and probably never learned or never fully grasped anything about the complexity of biologically based cause and effect, which means they cannot understand anything about the physiology of reproduction in species from microbes to man.
P.S. May the nutrient-dependent pheromone-controlled forces above be with you. Even if you really, really, really believe in scientifically unsubstantiated theories in which the only force that drives evolution is mutations, I do not want the forces of mutation-driven evolution to be with you, since they are so obviously detrimental to us all.