Black Queen trumps the Red Queen
June 14, 2014 | James Kohl
Earlier today, I wondered how best to note that the ridiculous misrepresentations in “Mutation-driven evolution” (2013) appeared in book publication on the same day my review article was published, which was one year ago.
This article, from “The Scientist Magazine” allowed me to vent some of my frustrations via my comments related to different hypotheses “Red Queen” and “Black Queen.”
Only the “Black Queen” hypothesis has been supported by experimental evidence of biologically-based cause and effect. The “Red Queen” hypothesis attests only to the theoretical nonsense that attests to the unwillingness of evolutionary theorists to learn about the basic principles of biology and levels of biological organization required to link sensory cause to behavioral affects via conserved molecular mechanisms in species from microbes to man.
My comment to The Scientist Magazine:
Re: “…none of us can actually tell how our experimental observations really relate to human disease, but we’re getting, all of us, closer to mechanistic insights…”
These mechanistic insights eliminate the “Red Queen” hypothesis and substitute biological facts about the molecular epigenetics of cause and effect, which can be accurately linked to the “Black Queen” hypothesis linked here. “The most likely explanation for the fitness advantage conferred by genomic and metabolic “streamlining” in both natural and experimental populations is that it reduces the amount of carbon and other limiting nutrients required to produce a new cell (12, 15, 16).”
This “Black Queen” explanation of cell type differentiation and organization of the genome links the conserved molecular mechansims of sensing and signaling in species from microbes to man via the sensing of nutrients and their metabolism to pheromones that control the physiology of reproduction.
Nutrient-dependent base pair changes and amino acid substitutions link the microRNA/messenger RNA balance from alternative splicings of pre-mRNA to the de novo creation of olfactory receptor genes in invertebrates and vertebrates. The de novo creation of olfactory receptor genes enables the required receptor-mediated changes in behavior that link food acquisition and mate acquisition to biodiversity manifested in the morphological and behavioral phenotypes, which are life-support systems for their microbiomes.
Microbiome-dependent phenotypic expression shows how readily ecological variation enables the epigenetic landscape to become the physical landscape of DNA in the organized genome. (Nutrient-dependent pheromone-controlled phenotypic expression explains what is called the Cambrian “explosion” via the same model that explains the more recently reported differences in 500 species of fish in 15,000 years.)
In the mouse-to-human example of cell type differentiation and biodiversity of mammals, chemical ecology and one nutrient-dependent amino acid substitution link differences in hair, sweat glands, teeth, and mammary tissue from ecological variation to ecological adaptations associated with the microbiome-dependent loss of olfactory receptors in human populations. (One modern human population supposedly arose in what is now central China during the past ~30K years.)
In modern human populations, some human olfactory receptor genes are no longer needed because our gut microbes modulate the sensing of food and our skin microbes modulate the signaling of reproductive fitness that enables our biodiversity. (Also,microbiome- and nutrient-dependent ecological, social, neurogenic, and socio-cognitive niche construction enabled brain development and processing power associated with the unconscious affects of odors on behavior.)
Fixation of the nutrient-dependent amino acid substitutions that stabilize the DNA in the cell types of the organized genome is obviously required. Otherwise nutrient-dependent DNA repair mechanisms would fail as they clearly do with nutrient stress and with social stress associated with mutations and pathology. Stress perturbs the thermodynamics of protein folding and organism-level thermoregulation required for ecological speciation to occur via the natural genetic engineering of protein biosynthesis and degradation.
Unfortunately, most people cannot think in terms of “Black Queen” biological facts known to molecular biologists because they have been taught to believe in the “Red Queen” hypothesis and in mutation-driven evolution. Thankfully, ideas associated with the invention of neo-Darwinism by population geneticists are being replaced with the facts about Darwin’s ‘conditions of life,’ which he insisted must receive first consideration.
Obviously natural selection of food must occur before anything else can somehow be naturally selected, and the natural selection that was subsequently more loosely associated with mutations and evolution was a horrid misrepresentation of cause and effect. It should not have been added to Darwin’s theory, especially given his protests.
Whatever motivated population geneticists to bastardize Darwin’s theory and also motivated social scientists to continue the bastardization has confused some of the serious scientists who might otherwise have told us how their experimental observations relate to human disease via what is currently known about the physics, chemistry, and molecular biology of their mechanistic insights. These mechanistic insights eliminate the “Red Queen” hypothesis and substitute biological facts about the molecular epigenetics of cause and effect, which can be accurately linked to the “Black Queen” hypothesis.