Re:  Adaptive Evolution of Multiple Traits Through Multiple Mutations at a Single Gene

My comment to the Science site (submitted 3/14/13 approved 4/513): In the context of adaptive evolution, Linnen et al., reminds us to look at models of genes with large effects for comparison to random mutations theory. For example, using the molecular mechanisms common to all species and exemplified in the mouse, the time from pleiotropy to epistasis in a human population appears to be approximately 30,000 years (Kamberov et al., 2013; Grossman et al., 2013). Perhaps epistasis requires only one nutrient-dependent pheromone-controlled amino acid substitution. That likelihood led me to look at pleiotropy, amino acid substitutions, and epistasis in several different model organisms via the common molecular mechanisms of “Nutrient-dependent / Pheromone-controlled thermodynamics and thermoregulation” (posted to figshare).

 

I moved quickly from microbes to nematodes, insects, and mammals. Receptor-mediated mouse to human examples of how nutrient-dependent amino acid substitutions can be readily linked to pheromone-controlled reproduction via common molecular mechanisms become as clear as they are in the honeybee model organism. What the queen eats determines her pheromone production and everything else about the interactions in the colony, including the development of the worker bees brain. The epigenetic effects occur sans mutations, which tends to refute the multiple mutations approach to adaptive evolution and replace theory with a model. In the model, natural selection is for nutrients that metabolize to pheromones. The pheromones control reproduction and link epigenetic effects on the microRNA/messenger RNA balance from stochastic gene expression to behavior and back.

 

Human Breath Analysis May Support the Existence of Individual Metabolic Phenotypes

My comment to The Scientist site (4/5/13):

 

Disclaimer / Conflict of Interest: I own the domain Pheromones.com

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 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 missense “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 simultaneously happen: 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 missense “mutation” involved in nutrient acquisition and another missense “mutation” that is involved in odor production because two mutations are not likely to simultaneously occur.

In my model, the adaptive evolution of nutrient-dependent pheromones controls reproduction and non-random species divergence. Is there a reason for use of the term “breathprint” in humans, or does “breathprint” intentionally infer that human pheromones do not exist? Would it not be unusual for chemical signals that control reproduction in species from microbes to man, to not exist in the context of human pheromones?

Dolphin, C. T., Janmohamed, A., Smith, R. L., Shephard, E. A., & Phillips, l. R. (1997). Missense mutation in flavin-containing mono-oxygenase 3 gene, FMO3, underlies fish-odour syndrome. Nat Genet, 17(4), 491-494. https://dx.doi.org/10.1038/ng1297-491

Li, Q., Korzan, Wayne J., Ferrero, David M., Chang, Rui B., Roy, Dheeraj S., Buchi, M., et al. (2013). Synchronous Evolution of an Odor Biosynthesis Pathway and Behavioral Response. Curr Biol, 23(1), 11-20. https://www.ncbi.nlm.nih.gov/pubmed/23177478

Author: James Kohl

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