Epigenesis vs mutagenesis: Who’s a mutant?
February 10, 2014 | James Kohl
Epigenetics is about how DNA determines development, not the contrary.
Published on February 8, 2014 by Christopher Badcock, Ph.D. in The Imprinted Brain
Excerpt: The alterntive to preformation is epigenesis. We owe the term to Aristotle, who used the example of making a net as an analogy of how epigenesisgenerates organisms rather than preforming them. Indeed, with the benefit of hindsight we can now see that this was a wonderfully apt analogy, given the fact that DNA spells out instructions for stringing together amino acids, whose patterns of folding determine many of the characteristics of the proteins they form. Looked at this way, you could indeed see the organism as a tightly woven net of proteins. Certainly, this view is much more accurate than that of seeing it as material which has been printed from a ready-made template as preformationism did. Think of the difference between a woven tartan and a printed one: the former corresponds to epigenesis, the latter to preformation.
My comment: According to Clarence “Sonny” Williams on 2/10/13: “Anyone with a college freshman-level understanding of genetics knows that the term “epigenetic” literally means “above the gene” and broadly refers to ALL gene regulatory mechanisms. So, saying “epigenetically effected” says nothing of importance.”
Williams, who is one of the most ignorant people I have ever encountered is consistently allowed to attack me on the International Society for Human Ethology yahoo group moderated by Jay R. Feierman. In this case he attacked because I wrote: “I think most of you have already realized that ER stress-related protein folding is epigenetically effected, which is why it may show up in behavioral phenotypes as readily as nutrient stress shows up in morphological phenotypes. Social stress and nutrient stress epigenetically effect the same signaling pathway.”
I was responding to publication of this article: Elevated systemic expression of ER stress related genes is associated with stress-related mental disorders in the Detroit Neighborhood Health Study. Allowing the attacks by Williams helps to ensure there will be no discussion of facts about ER stress related gene activation and behavioral disorders, or epigenetically effected gene activation and any affects on behavior. By allowing attacks that limit discussion, Jay R. Feierman promotes his pet theory that “Random mutations are the substrate upon which directional natural selection acts“.
Williams supports that ridiculous theory because he does not understand the fact that the term epigenetics is derived from epigenesis. Epi — i.e., above — is not added to genetics to arrive at epigenetics. That fact makes it clearer that epigenesis can be compared to mutagenesis in the context of what is known about how the epigenetic landscape is linked to the physical landscape of DNA in the orgnaized genomes of species from microbes to man via epigenetic effects of the sensory environment on the de novo creation of genes. Mutagenesis links nothing to nothing since mutations perturb the protein folding that is required for increased organismal complexity to arise via epigenetically effected nutrient-dependent pheromone-controlled ecological, social, neurogenic, and socio-cognitive niche construction.
Christopher Badcock, Ph.D. in The Imprinted Brain also comments on the fact that “…single genes can and do determine complex features of entire organisms.” If not for ridiculous ideas about mutagenesis, which is neither a biologically plausible nor ecologically validated approach to species diversity, it would be perfectly clear the ER stress related genes are manifested in epigenetically effected morphological and behavioral phenotypes.
For example, there are 1182 hemoglobin variants that differentiate human cell types. Single nucleotide substitutions lead to amino acid substitutions and hemoglobin variants in the α-like and β-like globin gene clusters. That’s why nutrient-dependent pheromone-controlled hemoglobinopathies are the most common single-gene genetic disorders in humans.
Reporting the hemoglobinopathies, such as sickle cell anemia, as if they were caused by mutations exemplifies racism because it attributes ecological variations in some human population to mutations, which infers other populations are “normal” when it is clear that all populations of all extant organisms are ecologically adapted. If some modern human populations with hemoglobin variants are mutants, and some are not — someone better start explaining who the mutants are, and why they mutated into existence instead of adapting to ecological variants like every other species on the planet.