Predictable Evolution Trumps Randomness of Mutations
Separate bacteria populations may respond to environmental changes in identical ways
By Lucas Laursen and Nature magazine Feb 20, 2013
Excerpt: “Coyne adds, however, that it may not be practical to extrapolate very much from an asexually reproducing species such as E. coli to organisms that reproduce sexually.”
My comment: Of course it’s practical, and it’s required unless you propose an alternative model using an organism that demonstrates predictable evolution via random mutations. Is Coyne willing to start us off with a demonstration in a model organism that shows sexual reproduction is due to a random mutation? In my model, the advent of sexual reproduction in yeasts is nutrient-dependent and pheromone-controlled.
My comment to the Scientific American site:
I may be the only participant here who has published on nutrient-dependent pheromone-controlled adaptive evolution and modeled it based on what is currently known about molecular epigenetics with the use of animal models of epigenetic effects in species from microbes to man. See, for example, “Nutrient-dependent / Pheromone-controlled Adaptive Evolution.”
There are links from the model to my peer-reviewed publications.
Despite the claims, no scientific evidence suggests that mutations cause adaptive evolution. Adaptive evolution obviously occurs via 4-stages of niche construction: 1) ecological 2) social 3) neurogenic and 4) socio-cognitive. Is is not possible for any mutation to cause fixation/epistasis via step 1 (the ecological niche is nutrient-dependent). Step 2 is required for control of nutrient-dependent adaptive evolution. Ecological niche construction is controlled by the metabolism of nutrients to species-specific pheromones in species from microbes to man. Pheromones establish the constraints of the social niche.
Those who are trapped in the statistics of population genetics where selection somehow occurs for phenotype may need to start with the basic principles of biology and levels of biological organization that link olfaction and odor receptors to the epigenetic tweaking of immense gene networks portrayed in my model of systems biology. But because that’s the only way to understand adaptive evolution it may be worth it to learn. Minimally, you won’t be caught discussing mutation-driven adaptations, or redefining your terms to make it appear that a theory represents the biological facts. It never has, and we can see now that it never will. Adaptive evolution has always been nutrient-dependent and pheromone-controlled, and always will! That’s probably as predictable as anything that’s ever been believed, which makes it somewhat unbelievable that so many people believe in mutations theory.
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.