Excerpt: Epialleles are heritable, nongenetic (epigenetic) differences in DNA methylation…. Regions in the genome may undergo spontaneous changes in their epigenetic status, and these differences may be one evolutionary mechanism affecting the evolution of new genes. PLoS Genet.9, e1003437 (2013).
My comment: Does the concept of epialleles in plants extends to animals via the epigenetic effects of plant nutrients (e.g., starch) on the thermodynamically controlled microRNA/messenger RNA balance and organism-level thermoregulation? If so, it might clarify how the molecular mechanisms for de novo gene expression have been conserved across plant and animal species. For example, microRNAs from plants may have facilitated the nutrient-dependent adaptive evolution of species from microbes to man via ecological, social, neurogenic and socio-cognitive niche construction. Indeed, the ecological niche construction of the first animals may have required different plants as sources of various nutrients that led to epigenetically-effected social niche construction and species diversity in animals.
Obviously, the diversity begins in microbes but we’re now beginning to see how important starch metabolism can be to differences in the adult behavior of wolves and dogs. At the same time, we see that starch production in plants and starch metabolism may have contributed to adaptive evolution in a human population. This appears to link the starch diet of humans to dog-human co-evolution in the context of the origins of agriculture. Once again, however, this evidence of nutrient-dependent changes suggests that mutations theory is somewhat ridiculous compared to a model of nutrient-dependent pheromone-controlled adaptive evolution. And here we have an article that compares mutations theory in the context of epialleles and suggests that epialleles have greater explanatory power (see below).
Article excerpt (full text is free) “…given that epigenetic variation enables genes to adjust their expression in a heritable manner much more rapidly than through mutation while preserving the possibility for rapid reversion, it could prove particularly beneficial in the case of genes that are created from scratch. Once the most adaptive expression state is reached, it could then become irreversibly stabilized (i.e. genetically assimilated) through DNA sequence changes.”
My comment: In animals, nutrient-dependent pheromone-controlled epigenetic “switching” enables adaptations to changing environments during development (e.g., exemplified in the honeybee model organism). For contrast, mutations may permanently perturb intracellular signaling and internuclear interactions to result in their typically detrimental effects. Mutations are less likely to be beneficial because epistasis cannot be achieved without their control. Mutations don’t control mutations. Therefore, I think it falls on the theorists and philosophers to explain mutations theory in the context of what is currently known about biological facts that include the concept of nutrient-dependent pheromone-controlled adaptive evolution.
James V. Kohl detailedl how quantized energy-dependent microRNA biogenesis links the pheromone-controlled physiology of reproduction to biophysically constrained viral latency and healthy longevity. Links from what organisms eat to the enzyme-dependent metabolism of food also link metabolic networks to microRNA-mediated genetic networks in the context of RNA interference. Drug therapies alter RNA interference by altering cell type differentiation in all cells of all individuals of all species. For comparison, during the past 26 years, Kohl has detailed how the chemistry of protein folding is biophysically constrained at every level of biological organization by conserved molecular mechanisms.