The maintenance of sex: Ronald Fisher meets the Red Queen by David Green and Chris Mason. OPEN ACCESS
BMC Evolutionary Biology 2013, 13:174 doi:10.1186/1471-2148-13-174 Published: 21 August 2013
Excerpt: “Evolution in both populations is primarily through adoption of novel advantageous mutations within a large allele space.”
My comment: It is scientifically unsubstantiated statements like the one above that should be eliminated from consideration in the study design to also eliminate meaningful interpretation of meaningless results. The results are meaningless due to the bias incorporated into the study design. You simply cannot start with a theory that involves uncontrolled “mutations” and arrive at a model unless somewhere along the way you incorporate biological facts in the context of evolution. Touting the primacy of “adoption of novel advantageous mutations” when that primacy has never been scientifically established enables only a “garbage in” approach that must lead to “garbage out” conclusions.
For contrast, “…the Black Queen Hypothesis offers a new way of looking at complicated, inter-dependent communities of microorganisms.” Adaptive evolution, which includes the advent of sexual reproduction in yeasts, is nutrient-dependent (Kondrashov, 2012) and pheromone-controlled (Weissman and Singer, 1991; Oliva, 2002). There’s a model for that! It can be compared to mutation-driven evolution, but it has not been.
Obviously, however, the emergence of males requires both morphogenesis and signals that convey “maleness” to a potential mate. The morphogenesis and sex differences in species-specific pheromones are nutrient-dependent. Pheromones control reproduction, and thus they control adaptive evolution. Evolution simply cannot occur via “adoption of novel advantageous mutations” because adoption requires selection and there is no model for selection of mutations that enable 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.