Transgenerational biological embedding / imprinting in gametes

Transgenerational biological embedding / imprinting in mammalian male gametes appears to link the conserved molecular mechanisms of speciation in species from microbes to man to subtle differences in Skull 5.

For example, in my model, subtle alterations in the nutrient-dependent thermodynamics of intercellular signaling and stochastic gene expression enable the morphological adaptations across species that include differences in Skull 5. See my comments to the Science Magazine site on the Skull 5 article.

Transgenerational epigenetic effects on these alterations must extend to organism-level thermoregulation to affect species diversity.

In a report published earlier this year, the diversity I attribute to thermodynamics and organism-level thermoregulation appears to originate in male gametes of mice.

Receptors involved in sugar and amino acid sensing in taste cells and in the gastrointestinal tract are also expressed in testis and sperm. The genetic absence of these receptors leads to male-specific sterility in a mammal. However, in the experiment, sterility was quickly reversed after clofibrate was removed from the diet. See: Mosinger et al (2013).

This may be the clearest indicator of how the nutrient-dependent molecular epigenetics of alternative splicings link the epigenetic ‘landscape’ to the physical landscape of DNA. The link now appears to include transgenerational epigenetic effects of diet on the de novo creation of “taste” and “smell” receptors in male gametes.

Predictably, this extends what we detailed in our 1996 Hormones and Behavior review article: “From fertilization to adult sexual behavior” from epigenetic effects in yeast to transgenerational epigenetic effects of olfactory/pheromonal input that alter 1) the physiology of nutrient-dependent pheromone-controlled reproduction, 2) morphological changes in the brain and body, which include skull morphology, and 3)the behavior of a single Homo species (sans mutation-initiated natural selection).

I do not think effects of a “mutation” in a single base pair (suggested elsewhere by David Marjanović) can be compared to epigenetic cause and effect across species. Thus, suggestions that the differences in skull morphology are somehow associated with a “mutation” in a base pair, instead of nutrient-dependent pheromone-controlled changes in a base pair (i.e., biological embedding) should be supported with experimental evidence.

Meanwhile, given the lack of information that might otherwise support mutation-driven evolution, which seems more likely:

1) Mutations in base pairs alter the hydrogen bonds that link sensory input to ecological, social, neurogenic, and socio-cognitive niche construction as is required for adaptive evolution to occur in species from microbes to man.

2) Nutrient uptake and cellular metabolism and organism-wide metabolism of nutrients to species-specific pheromones in unicellular and multicellular organisms control alterations in hydrogen bonds via the nutrient-dependent pheromone-controlled physiology of reproduction in species from microbes to man.

In my model, the nutrient-dependent pheromone-controlled substitution of  the achiral amino acid glycine in the gonadotropin releasing hormone (GnRH) molecule, which is conserved across what appears to be 400 million years of adaptive evolution, appears to link physics and biology. Is there an evolutionary theory that suggests that link is due to mutations in base pairs?


Author: James Kohl

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