Nutrient-dependent microRNAs control cell types

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Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
Excerpt: “…the epigenetic ‘tweaking’ of the immense gene networks that occurs via exposure to nutrient chemicals and pheromones can now be modeled in the context of the microRNA/messenger RNA balance, receptor-mediated intracellular signaling, and the stochastic gene expression required for nutrient-dependent pheromone-controlled adaptive evolution. The role of the microRNA/messenger RNA balance (Breen, Kemena, Vlasov, Notredame, & Kondrashov, 2012; Duvarci, Nader, & LeDoux, 2008; Griggs et al., 2013; Monahan & Lomvardas, 2012) in adaptive evolution will certainly be discussed in published works that will follow.”
My comment: My 2013 claim about microRNAs showed up last week in this report published in Science.

MicroRNA control of protein expression noise

Excerpt: “Combinatorial miRNA regulation may thus be a potent mechanism to reinforce cellular identity by reducing gene expression fluctuations that are undesirable for the cell.”

reported as: MicroRNAs silence the noisy genome

Excerpt:  “Examining expression for the entire mouse genome, Schmiedel et al. reveal that some 90% of the genes fall within the range of expression that would subject them to such a miRNA-based noise dampening mechanism.”

See for the role of microRNAs in RNA-directed DNA methylation: Reconstructing the DNA Methylation Maps of the Neandertal and the Denisovan

Excerpt: “…massive developmental remodeling of the human cortex, which affects hundreds of genes, might be driven by expression changes of only a few key regulators, such as microRNAs.”
See: My comments to Science Magazine:

See also: All in the (bigger) family

Excerpt: “Jerome Hui of the Chinese University of Hong Kong found that in both insects and crustaceans, the same set of micro RNAs control expression of the genes for those enzymes.”
See: My comment to Science Magazine:
This is the author’s copy of an invited review of nutritional epigenetics that I submitted to the journal “Nutrients”

Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems

Abstract: This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent pheromone-controlled ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity in species from microbes to man. Species diversity is a biologically-based nutrient-dependent morphological fact and species-specific pheromones control the physiology of reproduction. The reciprocal relationships of species-typical nutrient-dependent morphological and behavioral diversity are enabled by pheromone-controlled reproduction. Ecological variations and biophysically constrained natural selection of nutrients cause the behaviors that enable ecological adaptations. Species diversity is ecologically validated proof-of-concept. Ideas from population genetics, which exclude ecological factors, are integrated with an experimental evidence-based approach that establishes what is currently known. This is known: Olfactory/pheromonal input links food odors and social odors from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man during their development.
My comment: Evolutionary theorists know nothing about cell type differentiation. That fact is is not going to become clearer.  It will only become clearer to evolutionary biologists that their assumptions about evolution were based on a ridiculous definition of “mutation” that is now more than 100 years old. Attempts to define terms and link them to biologically-based cause and effect have always been useless, as have assumptions. All serious scientists have always known that. Some have simply been too lazy to examine the facts or to attempt to establish new facts.
Examining the facts has led to new facts such as those reported here:
Natural Selection on the Olfactory Receptor Gene Family in Humans and Chimpanzees (2003)
Loss of Olfactory Receptor Genes Coincides with the Acquisition of Full Trichromatic Vision in Primates (2004)
The Human Condition—A Molecular Approach (2014)
Excerpt: “Another example is the gene EDAR, which encodes the receptor for ectodysplasin, a protein involved in the development of ectodermal organs. An EDAR variant, the 370A allele, causes an amino-acid change in the receptor that is associated with increased hair thickness and shovel-shaped incisors. The 370A allele is present in frequencies close to 100% in many populations in Asia, where it shows signs of having been positively selected (Grossman et al., 2010; Sabeti et al., 2007). Recently, the human 370A allele has been engineered into mice. As expected, hair thickness was increased in the mice. However, the allele was also found to cause a higher density of ducts and smaller fat pads in the mammary glands and to increase the number of eccrine sweat glands. Prompted by this finding, an association study in humans found that individuals homozygous for the 370A allele had more eccrine glands than heterozygous individuals (Kamberov et al., 2013).”
My comment: I am happy to see that Paabo’s group finally discovered the works on the EDAR variant (a single amino acid substitution).  I used the companion reports cited above as the link from nutrient-dependent RNA-directed DNA methylation and RNA-mediated amino acid substitutions to cell type differentiation in species from microbes to man in my 2013 review:

Excerpt: “Two additional recent reports link substitution of the amino acid alanine for the amino acid valine (Grossman et al., 2013) to nutrient-dependent pheromone-controlled adaptive evolution. The alanine substitution for valine does not appear to be under any selection pressure in mice. The cause-and-effect relationship was established in mice by comparing the effects of the alanine, which is under selection pressure in humans, via its substitution for valine in mice (Kamberov et al., 2013).

These two reports (Grossman et al., 2013; Kamberov et al., 2013) tell a new short story of adaptive evolution. The story begins with what was probably a nutrient-dependent variant allele that arose in central China approximately 30,000 years ago. The effect of the allele is adaptive and it is manifested in the context of an effect on sweat, skin, hair, and teeth. In other mammals, like the mouse, the effect on sweat, skin, hair, and teeth is due to an epigenetic effect of nutrients on hormones responsible for the tweaking of immense gene networks that metabolize nutrients to pheromones. The pheromones control the nutrient-dependent hormone-dependent organization and activation of reproductive sexual behavior in mammals such as mice and humans, but also in invertebrates as previously indicated. That means the adaptive evolution of the human population, which is detailed in these two reports, is also likely to be nutrient-dependent and pheromone-controlled, since there is no other model for that.”

My comment: The links from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man are nutrient-dependent and pheromone-controlled. We established that fact in 1996. See the molecular epigenetic section of From Fertilization to Adult Sexual Behavior.

Although the role of the pre-mRNAs, which now seem to be called microRNAs, has become perfectly clear, the role of viral microRNAs also has become perfectly clear. The viral microRNAs are linked to perturbed protein folding and physiopathology, which is controlled by nutrient-dependent microRNAs. The nutrient-dependent microRNAs typically repair the damage to DNA caused by viruses. Only with the uncontrolled proliferation of viruses does the increased load of viral microRNAs adversely effect the microRNA/messenger RNA balance. The effect of too many viral microRNAs and the altered microRNA/messenger RNA balance prevents nutrient-dependent RNA-mediated amino acid substitutions from stabilizing organized genomes.  The genomic instability is manifested in morphological phenotypes and behavioral phenotypes that are linked to limited reproductive fitness in individuals and in species.  The honeybee model organism may be the best example of that. However, examples of nutrient-dependent pheromone-controlled RNA-directed DNA methylation and RNA-mediated amino acid substitutions that stabilize the metabolic and genetic networks of organized genomes can be examined in all animal models.

Also, the basis of top-down causation manifested in the nutrient-dependent pheromone-controlled cell type differentiation in animals is linked to what is known about links from physics and chemistry to the conserved molecular mechanisms of reproduction in plants. The light-induced de novo creation of amino acids links the sun’s biological energy from RNA-mediated cell type differences in plants to RNA-mediated amino acid substitutions and cell type differentiation in animals via spectral energy.

See: Let There Be Life (2014) and Common origins of RNA, protein and lipid precursors in a cyanosulfidic protometabolism (2015), which was reported as: On the Origins of Life. The origins of life are linked from plants and animals in the context of Single-residue insertion switches the quaternary structure and exciton states of cryptophyte light-harvesting proteins.

The origins of pathophysiology are presciently linked from viruses and viral microRNAs to perturbed protein folding in this book Review in Nature

Excerpt: “He has mustered a cadre of facts, loosely connected and ill understood. There are little happenings at the periphery of Mendelian genetics, at the edge of neo-Darwinian theory, and what used to be beyond the realm of molecular biology. We know that bacteria contain extrachromosomal elements that transmit traits, such as drug resistance, between individuals and between species. We know that elements exist which insert in and excise from the genome, sometimes in response to environmental signals or stresses.  Most of us believe that simple, incremental changes in allele frequencies, driven by the forces of genetic drift, mutation, recombination, migration and natural selection, are enough to explain evolution from adaptation to speciation, to the origin of higher taxa. There is no compelling evidence to the contrary, but neither is there compelling evidence in favour of the idea; we simply haven’t observed or catalogued the forces and changes that create new species. Bear fills this void in our understanding with the notion that radical changes in the genome, brought about by mobilization of transposable elements such as human endogenous retroviruses, result in rapid change at the subspecies or species level.

See: Endogenous retroviruses function as species-specific enhancer elements in the placenta, which was cited in Viral Genome Junk Is Bunk

See also: Is there a role for endogenous retroviruses to mediate long-term adaptive phenotypic response upon environmental inputs? It was cited in: DNA Methylation Is Dispensable for Suppression of the Agouti viable yellow Controlling Element in Murine Embryonic Stem Cells

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