Many colleagues and most of my antagonists seem to be unwilling to accept the fact that RNA-directed DNA methylation links the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man. Lack of acceptance appears to be due to the fact that they think mutations and natural selection link evolutionary events to biodiversity. There is no model for that, but they refuse to accept the fact that RNA-mediated events link ecological variation to ecological adaptations.There is a model for that!
The RNA-mediated events are nutrient-dependent because nutrients provide the methly groups required for DNA methylation. In my model, experience dependent odor exposure induces the de novo Creation of receptors that allow nutrients to enter the cell. For example, the Creation of olfactory receptor genes enables nutrient-uptake, which enables DNA methylation. The RNA-mediated events link DNA methylation from nutrient uptake to thermodynamic cycles of protein biosynthesis and degradation. Degradation of proteins links the byproducts of nutrient-dependent RNA-mediated events from DNA methylation and the metabolism of nutrients to the production of species-specific pheromones. Pheromones control the nutrient-dependent physiology of reproduction in species from microbes to man via the conserved molecular mechanisms I just detailed.
The links from physics and chemistry to the thermodynamics of RNA-directed DNA-methylation via RNA-mediated events that link the epigenetic landscape to protein folding that enables increasing organismal complexity via nutrient-dependent pheromone-controlled de novo gene Creation may be impossible to describe to those who are not familiar with physics, chemistry, and the molecular biology of biologically-based cause and effect. However, that is no excuse for anyone to continue to proceed with mathematical models of evolution that do not first address Darwin’s ‘conditions of life.’ Conditions of life are nutrient-dependent, no matter who first suggested they be considered before natural selection of anything else occurred for anything except food. Organisms without enough food due not mature or cannot attract a mate by producing nutrient-dependent pheromones. Thus, the pheromones that control reproduction fit into the context of conditions of life that lead to biodiversity. The fact that RNA-mediated events link nutrient-dependent amino acid substitutions to cell type differentiation in species from microbes to man and that fixation of the amino acid substitutions occurs only in the context of successful nutrient-dependent reproduction seems to be ignored by evolutionary theorists as if that fact — along with physics, chemistry, and molecular biology — could continue to be ignored.
Who is ignoring the facts?
Karl Grammer co-authored our award-winning 2001 review: Human pheromones: integrating neuroendocrinology and ethology He recently mentioned that he would publish a mathematical model of how pheromones influence behavior. This would be a counter-measure that might limit the successful defense of my model. He thinks my attempts to eliminate the theories of evolutionists and human ethologists from consideration are a waste of time. I think it is past time to provide serious scientists with experimental evidence of biologically-based cause and effect and require them to defend their ridiculous theories based on their mathematical models.
However, others have offered a relatively simply mathematical model of RNA-mediated events that links epigenetic effects of pheromones on hormones (neuroendocrinology) to the affects of hormones on behavior (ethology) via feedback loops. See: Mathematical model: microRNA and epigenetic regulation.
Now see: Maternal Methyl Supplemented Diets and Effects on Offspring Health “Lastly, methyl components may lead to tissue/cell-specific effects. Such differences would suggest that these diets might aide in disease prevention in select organs or tissues but also exacerbate disease risk in others.”
Now others can skip the physics, chemistry, and molecular biology. The link from the nutrient-dependent pheromone-controlled physiology of reproduction to tissue/cell-specific effects is clear in the context of what is known about Feedback loops link odor and pheromone signaling with reproduction and what is detailed in the mathematical model: Interplay of microRNA and epigenetic regulation in the human regulatory network.
The maternal methyl supplementation report links epigenetic effects on cell type differentiation in tissues of organs in organ systems of organisms from ecological variation to the nutrient-dependent pheromone-controlled physiology of ecological adaptations via conserved molecular mechanisms of ecological, social, neurogenic, and socio-cognitive niche construction that I detailed in my model.
Ask Karl Grammer and other theorists who think they can mathematically model the complexities of biologically-based cause and effect that lead to tissue/cell-specific effects and affects on behavior in my model these two questions:
1) Why haven’t you told us what biologically-based evolutionary event links DNA methylation to the morphological and behavioral phenotypes you think somehow arose in the context of mutations, natural selection, and the evolution of biodiversity.
2) What makes you think you can mathematically model the interplay of microRNAs and epigenetic regulation of RNA-mediated biodiversity that clearly occurs in the context of amino acid substitutions that differentiate all cell types in all individuals of all species?
Other have claimed: “We cannot conceive of a global external factor that could cause, during this time, parallel evolution of amino acid compositions of proteins in 15 diverse taxa that represent all three domains of life and span a wide range of lifestyles and environments.” Jordan et al., (2005)
RNA-mediated events link nutrient-dependent pheromone-controlled cell type differentiation in every individual of every honeybee colony via conserved molecular mechanisms linked to cell type differentiation in all cells of all organisms of all species. See: Epigenomics and the concept of degeneracy in biological systems
“Feeding a complex diet known as royal jelly to a growing female larva inhibits global DNA methylation, increases levels of juvenile hormone and correlates with changes in gene expression, which result in the queen phenotype. In contrast, larvae fed less-nutritious worker jelly develop into functionally sterile short-lived worker bees. However, there are no specific ‘queen’ or ‘worker’ genes in the Apis genome. During the initial critical 96 h of larval growth, multiple sensory and secretory systems are involved in receiving, processing and conveying the nutritional information to multilevel, interlocked signaling pathways. The contrasting phenotypes result from threshold-based processes driven by metabolic fluxes, hormonal changes and differential methylation and expression of many genes . All these components have the capacity to respond to environmental change, but their combined and coordinated action has evolved in honey bees as a powerful mechanism for reprograming the entire developmental trajectory with profound consequences for cellular and organismal phenotypes [82–85].”
The honeybee is the model organism that links conserved molecular mechanisms of biophysically-constrained biologically based cause and effect in species from microbes to man.
Does anyone seriously think they can mathematically model that, or anything else about RNA-mediated cell type differentiation. Do they think they can continue to make their mathematical models appear to be consistent with the pseudoscientific nonsense of evolutionary theory and human ethology? If so, perhaps Karl will have help in his efforts to continue to keep others from learning about how ecological variation leads to RNA-mediated ecological adaptations in species from microbes to man.
He’s been doing that since 2001, and it has become more difficult to continue doing so when all biological facts continue to attest to the pseudoscientific nonsense population geneticists used to invent and define neo-Darwinian evolutionary theory. But, I think there is little hope for him if he tries to continue to mathematically model anything that has not become established as a biological fact via experimental evidence of biologically-based cause and effect.