Natural selection and sexual selection for thermoregulation
Posted on February 19, 2013 by James Kohl.
Variety is the spice of life, but diversity is controlled by natural selection and sexual selection for thermoregulation
Article Excerpt: “As systems-level research, which integrates multiple types and levels of biological information, becomes more necessary to understand complex diseases, there is an urgent need to find principles that extend across all models…”
Article Excerpt: “Dr. Sabeti said the extra sweat glands could have been the feature favored by natural selection, with all the other effects being dragged along in its train.”
My comment: Reproduction is nutrient-dependent and pheromone-controlled in species from microbes to man. That suggests the molecular mechanisms are the same. Thus, after a thorough review of the extant literature, we can readily conclude that “Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans (Kohl, 2012).”
That fact is demonstrable. Substitution of alanine for valine in a human population results in alterations of skin, sweat, and hair (Grossman et al., 2013). The hypothesis supported is that the enhanced thermoregulation required for evolution at the molecular level fuels adaptive mitochodrial-nuclear interactions (Brunstein, 2013; Meiklejohn et al., 2013). This includes the mitochodrial-nuclear interactions of the microbiome (McFall-Ngai et al., 2013). The intranuclear interactions are manifested in phenotypical changes that enable sexual selection for nutrient-dependent reproductive fitness.
Adaptively evolved reproductive fitness is signaled by pheromones via the alterations in skin, eccrine sweat, apocrine secretions, and hair in mammals. The microbiome is largely responsible for digestion and for conversion of nutrient metabolites to pheromones. The problem for some people is the complexity of the systems biology. There is a requirement to get from nutrient fueled energy driven protein synthesis in cells to ecological, social, neurogenic, and socio-cognitive niche construction (Kohl, 2013). That requirement exists to link the sensory environment to protein synthesis via changes in gene expression. The changes in gene expression lead to changes in behavior. The changes in behavior must lead back to changes in gene expression via reproduction for adaptive evolution to occur.
If not for animal models of that complexity, all hope for understanding would be lost. The honeybee model organism incorporates what is known about nutrient-dependent pheromone-controlled social behavior. The mouse model extends what is known to sexual selection in mammals. The physics of thermoregulated DNA strand pairing extends common molecular mechanisms from microbes to man (Brunstein, 2013).
Extending the concept of nutrient-dependent pheromone-controlled reproduction from microbes to humans may not be possible in the current climate of animal model specializations and what are believed to be mutations that somehow cause adaptive evolution. In Drosophila, for example, an experimentally induced valine-alanine point “mutation” reduces fecundity as is consistent with starvation. But “fixation” of the mutation is used to explain adaptive evolution (Meiklejohn et al., 2013). Drosophila is a commonly used animal model of diversity. Note the sharp contrast of “mutations” theory compared to nutrient-dependent thermoregulatory mechanisms that clearly are pheromone-controlled in microbes (McFall-Ngai et al., 2013).
In my opinion, adaptive mutations theory should not be used as a substitute for explanations of the epigenetic effects of nutrients and pheromones on thermoregulated epigenesis, epistasis, and adaptive evolution. Instead, differences in perspectives on the valine / alanine variants (Kamberov et al., 2013; Meiklejohn et al., 2013) should be compared to determine if or how “adaptive mutations” enable nutrient-dependent pheromone-controlled species diversity. What if all adaptations are nutrient-driven and pheromone-controlled as is consistent with a model of adaptive evolution (Kohl, 2013)?
Let’s first get the physics and the biology correct, before we mathematically model what may be impossible. Is it possible that mutations are adaptive at the level of population genetics? If there is a model for that, the first priority is to get the model right.
Brunstein, J. (2013). DNA and RNA structure: nucleic acids as genetic material. Medical Laboratory Observer, January 26(22). Jan 2013 http://www.mlo-online.com/articles/201301/dna-and-rna-structure-nucleic-acids-as-genetic-material.php
Grossman, Sharon R., Andersen, Kristian G., Shlyakhter, I., Tabrizi, S., Winnicki, S., Yen, A., et al. (2013). Identifying Recent Adaptations in Large-Scale Genomic Data. Cell, 152(4), 703-713. http://linkinghub.elsevier.com/retrieve/pii/S0092867413000871 (see link to video on adaptive mutations that result in more sweat glands)
Kamberov, Yana G., Wang, S., Tan, J., Gerbault, P., Wark, A., Tan, L., et al. (2013). Modeling Recent Human Evolution in Mice by Expression of a Selected EDAR Variant. Cell, 152(4), 691-702. http://linkinghub.elsevier.com/retrieve/pii/S0092867413000676
Kohl, J. V. (2012). Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2(17338). http://www.socioaffectiveneuroscipsychol.net/index.php/snp/article/view/17338
Kohl, J. V. (2013). Nutrient-dependent / Pheromone-controlled Adaptive Evolution. figshare, Retrieved 04:36, Feb 18, 2013 (GMT), http://dx.doi.org/10.6084/m9.figshare.155672
McFall-Ngai, M., Hadfield, M. G., Bosch, T. C. G., Carey, H. V., Domazet-Loso, T., Douglas, A. E., et al. (2013). Animals in a bacterial world, a new imperative for the life sciences. Proc. Natl. Acad. Sci. USA. http://www.pnas.org/content/early/2013/02/06/1218525110.abstract
Meiklejohn, C. D., Holmbeck, M. A., Siddiq, M. A., Abt, D. N., Rand, D. M., & Montooth, K. L. (2013). An Incompatibility between a Mitochondrial tRNA and Its Nuclear-Encoded tRNA Synthetase Compromises Development and Fitness in Drosophila. PLoS Genet, 9(1), e1003238. http://dx.doi.org/10.1371%2Fjournal.pgen.1003238
Retired medical laboratory scientist
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