Abstract Excerpt: This review serves to integrate studies of the animal in vivo with human epidemiological data pertaining to nutritional regulation of DNA methylation and to further identify areas in which current knowledge is limited.
My comment: The molecular mechanisms of learning and memory in mammals are ecologically adapted from those in yeasts (see for review: From Fertilization to Adult Sexual Behavior). Thus, all articles ever published attest to the fact that conserved molecular mechanisms link ecological variation to ecological adaptations via olfactory/pheromonal input, which epigenetically effects the conserved molecular mechanisms.
Problems arise when theorists attempt to link cause and effect via mutations, natural selection, and evolution. That’s why I object to ‘evolutionary’ approaches that include no explanatory power but attempt to explain biophysically constrained cause and effect. Serious scientists need look no further than our 1996 review (full text linked above) for comparison to the latest research to link epigenetically effected interactions among genes to cell type differentiation and phenotype in species from microbes to mammals.
See for comparison
Excerpt: “BY has a premature stop mutation in FLO8 that prevents it from undergoing many forms of multicellular growth . As for END3, a missense polymorphism in this gene contributes to variability in high temperature growth…”
My comment: The authors of the latest research on yeasts failed to include what is known about conserved molecular mechanisms and conclude that: “…characterizing the larger-scale contribution of [epigenetically effected] higher-order interactions to phenotypic variation is a necessary step in improving our basic understanding of the [epigenetically effected] genotype-phenotype map.” Their conclusion represents how much scientific progress has been retarded by evolutionary theorists and those who have never learned anything about the basic principles of biology or levels of biological organization that are required to link sensory cause to behavioral affect (e.g., via epigenetic effects on hormones in invertebrates and vertebrates).
The difference between a mutation that perturbs protein folding and prevents unicellular or multicellular growth and a nutrient-dependent pheromone-controlled polymorphism that contributes to organism level thermoregulation is that only one represents an ecological adaptation that is beneficial. That adaptation is nutrient-dependent. It does not occur after a beneficial mutation has somehow resulted from something that is somehow naturally selected to automagically then result in either individual differences in cell type or in species diversity.
Minimally, if the scientific facts about how ecological variation in nutrient availability leads to ecological adaptations are too difficult for others to comprehend, social scientists and serious scientists should not continue to mislead others by reporting works in terms that at first may seem to have some explanatory power, but inadvertently state in their conclusions things like “we really have no clue about what causes the interactions” or alternatively claim things like “this effect was hitherto unsuspected.” See for example: Chemosensory Communication of Gender through Two Human Steroids in a Sexually Dimorphic Manner.
In our 1996 review we (TB) wrote: “Parenthetically it is interesting to note even the yeast Saccharomyces cerevisiae has a gene-based equivalent of sexual orientation (i.e., a-factor and alpha-factor physiologies). These differences arise from different epigenetic modifications of an otherwise identical MAT locus (Runge and Zakian, 1996; Wu and Haber, 1995).” The differences are nutrient-dependent and pheromone-controlled in yeasts and mammals, which is why two human steroids have been linked to chemosensory communication of gender. The steroids are metabolites of food via the pathway from one-carbon metabolism that links ecological variation to the physiology of reproduction and ecological adaptation in species from microbes to man.