Another Memo: Adaptive evolution is nutrient-dependent and pheromone-controlled
September 27, 2013 | James Kohl
Science 27 September 2013: Vol. 341 no. 6153 pp. 1431-1431 DOI:10.1126/science.341.6153.1431-a Editors’ Choice by L. Bryan Ray
Excerpt: “These signaling pathways are highly conserved, and thus these results suggest possible crosstalk between nutrient and energy-sensing pathways and G protein–coupled receptor–regulated processes in higher organisms as well.”
My comment to Science: submitted on Fri, 09/27/2013 – 09:34 and approved at 10:00:
The nutrient-dependent de novo creation of G-protein coupled olfactory receptor genes epigenetically links food ‘odors’ associated with nutrient acquisition to the metabolism of the nutrients and production of species-specific pheromones, which control reproduction in species from microbes -like yeasts- to man. This perspective, from yeasts to mammals, was addressed in our 1996 review article: From Fertilization to Adult Sexual Behavior – especially in the section on molecular epigenetics.
It is now clearer that adaptive evolution requires ecological niche construction supported by pheromone-controlled social niche construction, which enables controlled nutrient-dependent sexual reproduction. The reciprocity that integrates all the feedback loops involved may -at first- seemed to be merely a circular argument for nutrient-dependent adaptive evolution sans mutations theory. But, as we will predictably see in Schmidt (2013), it actually represents a way to establish non-random ecological, social, neurogenic, and socio-cognitive niche construction with across-species examples of how nutrient-dependent alternative splicings link the epigenetic ‘landscape’ to the physical landscape of DNA in the organized genomes of species from microbes to man.
The conserved molecular mechanisms of nutrient-dependent intercellular signaling, intranuclear interactions, stochastic gene expression and alternative splicings in yeast can now be viewed in the context of pheromone-controlled adaptive evolution in all species at a time when there is still no biologically based experimental evidence to support mutation-driven evolution. Thus, we can view “fueling reproduction” in yeasts in the context of nutrient-dependent reproduction in moths. We then find that predator-driven selection was not responsible for evolution in the commonly used example of peppered moth industrial melanism. Instead, the fueled reproduction of adaptive evolution was nutrient-dependent and pheromone-controlled as it is in yeasts and in every other adaptively evolved species on the planet (e.g., from microbes to man). For example, a single nutrient-dependent amino acid substitution is all that’s required for a change in the species-specific production of a pheromone blend in Ostrinia moths. Schmidt appears to be sending a clear message to evolutionary theorists: pay attention to the physiology of reproduction, not mutation-driven evolution. That’s a message we somehow failed to convey in 1996, or perhaps our message was simply ignored.
Addendum: I received the reprint of Schmidt (2013), at 10:21. It included more information of a broader scope than I thought it would. I responded: “Yours is the most comprehensive article to ever succinctly address the molecular mechanisms of nutrient-dependent pheromone-controlled adaptive evolution, which are common to all species. Please comment to me or to the science site on how you think your work will contribute to scientific progress. It is regrettable that a subscription separate from Science magazine, is required to see what’s published in Sci. Signal…. If there is anything that I can do to help with your distribution of your now published work, please tell me. Some authors make “author’s copies” available, for example, from their academic sites, as we did with From Fertilization to Adult Sexual Behavior. In any case, I hope you get the credit you deserve for publishing what will be a very important addition to the knowledge base of many researchers.
What I think is most important for other researchers to know is that Schmidt (2013) noted these facts:
1) “…yeast cells have developed multiple signaling pathways that respond to the availability of sugars…, amino acids, and other nutrients”
2) “…immune complexes showed rapid increases in activity in response to the addition of glucose to cell cultures.”
3) “…Ste2 signaling is dampened in response to nutrient limitation…”
4.) “The mechanism by which one signaling pathway regulates a second provides insight into how cells integrate multiple stimuli to produce a coordinated response.”
In my model, the coordinated response to nutrient availability is enabled by
1) non-random experience-driven
2) receptor-mediated changes in
3) intercellular signaling,
4) intranuclear interactions,
5) stochastic gene expression.
The metabolism of nutrients to species specific pheromones is the mechanism by which one signaling pathway regulates a second because it is clear that
6) pheromones regulate reproduction, which limits stochastic gene expression in species from microbes to man.
Schmidt also includes mention of the differences in morphogenesis “…formation of mating projections.” The mating projections are called “shmoos,” and their increased or reduced formation is nutrient-dependent and pheromone-controlled (see Mating of yeast). The alpha-mating pheromone of yeast that facilitates shmoo formation is similar to the hormone that modulates all of mammalian neuroendocrine function and associated sex differences in the brain and behavior. In its concentrated form, the yeast alpha-mating pheromone elicit a hormone response from the cultured pituitary cells of the rat. That hormone response is also elicited by the species-specific pheromones of the opposite sex in potential mates whose reproductive fitness is nutrient-dependent.
This links nutrient-dependent pheromone-controlled sexual reproduction in yeasts to nutrient-dependent pheromone-controlled sex differences in mammalian brain development and reproduction via molecular mechanisms that appear to have been conserved across 600 million years of nutrient-dependent pheromone-controlled adaptive evolution. After a single substitution of a chiral amino acid 400 million years ago, the coordinated evolutionary selection of amino acids participating in binding GnRH has resulted in such perfection that it is not possible to improve its physiological potency of GnRH using any natural amino acid.
Chemists interested in the synthesis of activated pyrimidine ribonucleotides under potentially prebiotic conditions, elementary chemical structures, and modern biological molecules involved in the plausible prebiotic construction of RNA via evolution of biomlolecular homochirality may wish to examine the emergence of single chirality of sugars and amino acids that enabled the thermodynamic stability of nutrient-dependent pheromone-controlled adaptive evolution of organism-level thermoregulation and thus of adaptively evolved life on earth. However, it currently appears that any small initial imbalance of either sugars by amino acids or amino acid by sugars would alter the chiral pool of others and make the GnRH-dependent adaptive evolution of life on earth improbable, if not impossible. Therefore, mutations would never be fixed in the genome. Thus, for now, suffice it to say that it is more likely that adaptive evolution is nutrient-dependent and pheromone-controlled in species from microbes to man because there is a model for that. Genetically predisposed life is epigenetically effected by olfactory/pheromonal input. That model could be compared to asteroid-effected chirality due to collisions in outer space that led to life on earth, which somehow evolved via random mutations. But so far as it seems, no one can make sense of that nonsense and no biologically based experimental evidence supports such ridiculous theories.