Olfactory Receptor Patterning in a Higher Primate
Excerpt: We found that TAARs are also expressed in the macaque OE, suggesting that these receptors may also function as chemosensory receptors in the human nose.
My comment: The article links the senior author’s prior works from nutrient-dependent RNA-mediated events and the de novo Creation of odorant receptor (OR) genes to her 2005 co-authored work on the hormone-organized control of these RNA-mediated events:
Feedback loops link odor and pheromone signaling with reproduction.
Excerpt:”At least 10,000 neurons in 26 different brain areas appear to transmit signals directly to GnRH neurons. Among these are areas involved in odor and pheromone processing, sexual behavior, arousal, reward, and other functions. This suggests that GnRH neurons are poised to modulate reproductive physiology and behavior in accordance with the overall state of the animal.”
Nobel Laureate, Linda Buck has now linked the experience-dependent de novo Creation of another class of OR genes to primate behavior. But her most recent article does not mention the RNA-mediated events that are required to link nutrient uptake associated with food odors to amino acid substitutions that differentiate cell types in all the cells of all different species. Given what is known about these RNA-mediated events, I hope that others will make their refutations of evolutionary theory clearer.
Perhaps serious scientists don’t even consider the evolutionary theorist’s claims because the theorists have not described any biologically-based evolutionary events. Although that means their ridiculous claims can be compared to what is known, there may be no need for serious scientists to address the biologically-based RNA-mediated events that link nutrient-dependent amino acid substitutions to cell type differentiation in all cells of all individuals via conserved molecular mechanisms in species from microbes to man. Unless they are attempting to discuss biologically-based facts with a theorist, there isn’t much need to tell the theorist that evolutionary theory was invented and defined by population geneticists.
Sooner or later, the theorists will learn that conserved molecular mechanisms are responsible for the nutrient-dependent microRNA/messenger RNA-mediated events that differentiate cell types via amino acid substitutions. The differentiation of all other cell types appears to begin with food odor-induced epigenetic effects on the de novo Creation of olfactory receptor genes. However, unless a serious scientist like Linda Buck comments on the obvious refutations of theories touted by those who try to link mutations and natural selection to the evolution of biodiversity, the evolutionary theorists may not realize that the only evidence of biodiversity links ecological variation to ecological adaptations that occur in the absence of mutations and natural selection.
For example, in my 2013 review I noted that:
“The recently detailed mouse model (Li et al., 2013) builds on what is known about olfactory/pheromonal communication in species from microbes to man and incorporates works from mammals that elucidate the molecular mechanisms that are clearly involved. Sex-dependent production of a mouse ‘chemosignal’ with incentive salience appears to have arisen de novo via coincident adaptive evolution that involves an obvious two-step synergy between commensal bacteria and a sex-dependent liver enzyme that metabolizes the nutrient chemical choline.
The result of this synergy is (1) a liver enzyme that oxidizes trimethylamine to (2) an odor that causes (3) species-specific behaviors. Thus, the complex systems that biology required to get from nutrient acquisition and nutrient metabolism to species-specific odor-controlled behavior is exemplified by adaptive evolution of an attractive odor to mice that repels rats (see for review Li et al., 2013).
The mouse odor also repels humans. High excretion rates of trimethylamine-associated odor in humans cause ‘fish odor syndrome’. The aversive body odor has been attributed to a mutation (Dolphin, Janmohamed, Smith, Shephard, & Phillips, 1997). This attribution is not consistent with the portrayal of synergy in the mouse model, which enables both the production of the odor and the response to the odor.
This synergy requires at least two things to happen simultaneously: for example, (1) natural selection for nutrient chemicals and (2) sexual selection for odor production. Sexual selection for nutrient-dependent odor production is not likely to be achieved via one mutation involved in nutrient acquisition and another mutation that is involved in odor production because two mutations are not likely to simultaneously occur.”
We now can read about findings in Horowitz et al (2014) that “…raise the possibility that TAARs have been evolutionarily conserved due to a specialized ability to elicit innate responses, such as avoidance. The functional significance of these responses could vary among animals. For example, aversive responses of mice to 2-beta-phenylethylamine, a mouse TAAR4 ligand present in some carnivore urines, could aid in predator avoidance (Ferrero et al., 2011; Dewan et al., 2013). In contrast, the activation of human TAAR5 by spoiled fish might discourage the ingestion of foods that could harbor pathogenic microorganisms that pose a danger to health.”
In my model, the fish odor links sex differences in species-specific pheromone production from mice to primates via differences in the production of dehydroepiandrosterone (DHEA) in primates. DHEA is the most abundantly produced steroid hormone. The fact that Testosterone increases circulating dehydroepiandrosterone sulfate levels in the male rhesus macaque links its metabolism to sexually dimorphic species-specific ratios of androsterone and etiocholanolone, which were reported to vary with sexual orientation in human males.
Excerpt: “The finding that DHEA/S differs dramatically between males and females is highly consistent and is maintained throughout the lifespan in both humans and rhesus macaques (7, 20–22), but to date no theories as to the mechanism of this difference have been adequately investigated.”
My comment: I have suggested that the androsterone/etiocholanolone ratio is integrated into a blend of sex specific and individual specific indicators of nutrient-dependent reproductive fitness based on links from nutrient-stress and social stress that predictably might be manifested in the testosterone-dependent pheromone-signature of human males and females — along with other indicators of reproductive fitness like those associated with amine-like odors of chemicals called copulins in rhesus macaques. TAARs in the human nose appear to complete the model, which appears to solve “… the “binding problem” of sexual attraction. By that I mean the problem of why all the different features of men or women (visual appearance and feel of face, body, and genitals; voice quality, smell; personality and behavior, etc.) attract people as a more or less coherent package representing one sex, rather than as an arbitrary collage of male and female characteristics. If all these characteristics come to be attractive because they were experienced in association with a male- or female-specific pheromone, then they will naturally go together even in the absence of complex genetically coded instructions.” (LeVay, 2011). See also: D’Scent of Man: A Comparative Survey of Primate Chemosignaling in Relation to Sex.
The latest from Nobel Laureate, Linda Buck, continues to support extension of what is known about nutrient-dependent RNA-mediated events from the pheromone-controlled reproduction of microbes to the nutrient-dependent pheromone-controlled behavioral development of man. Note, I did not claim that pheromones control human behavior or that food odors control human behavior because they obviously do not. If they did, we would always act like other primates or other animals in which Feedback loops link odor and pheromone signaling with reproduction.
However, the fact that most of us do not always act like other animals says nothing about the epigenetic effects of food odors and human pheromones on the hormones that affect our behavior. It would be odd if our species was the only one in which behavior was not conditioned to occur in the context of odor-induced de novo Creation of OR genes that link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to elephants via RNA-mediated events and species specific pheromones that control the nutrient-dependent physiology of reproduction. Besides, there’s no model for differences in the molecular epigenetics of species diversity, only for the similarities.
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