Becoming biologically informed (3)

By: James V. Kohl | Published on: July 23, 2015

See also: Becoming biologically informed and Becoming biologically informed (2)
Now available for free: New Perspectives on microRNA in Disease and Therapy (July 22, 2015)
My comments: Perhaps someone will correct me if I am wrong.
The microRNAs do not appear to participate in a direct response to viruses. But, over long periods of time they may fine-tune the microRNA/messenger RNA balance in the organized genomes of all living genera.  If so, the changes are manifested in morphology and in the transcriptome.
Dr. TenOever uses the influenza virus as an example. The addition of less than 45 nucleotides prevents viral replication. Adding to the host microRNA controls DNA viruses and RNA viruses in a tissue-specific species-specific manner. This is probably the best example of how nutrient-dependent energy alters base pairs that lead to the stability of organized genomes via RNA-mediated amino acid substitutions. The example cannot be compared to theories about mutations and evolution without clarification by the presenters who may be unwilling to discuss biologically-based cause and effect.
That may explain why the example of bird flu prevention is not linked to cancer prevention. Only 3 amino acid substitutions lead to gain of function that enabled human to human transmission, which probably scared the masses who were taught to believe in ridiculous theories about evolution. That scare appears to have led to banned research because evolutionary theorists have made ridiculous claims about beneficial (e.g., gain of function) mutations.
The clear threat is nutrient-dependent ecological adaptations by viruses that allow them to cross species by adapting to the supply of nutrients in specific cell types in different species. That threat is minimized by discusssion of the inability to create an escape mutant in the lab. Ecological variation leads to ecological adaptations in viruses that naturally adapt — but the adaptations are placed into the context of mutations.
Placing adaptations into the context of mutations will probably cause a problem with FDA approval. If it does not, it should. The different delivery strategies may “emerge” to kill us all.
SARCASM ALERT: Let’s try coupling a manufactured microRNA to cholesterol and see how it effects the liver. Keep in mind, however, that a single base pair change and one amino acid substitution may be all that links the nutrient-dependent natural body odor that we produce to the odor of mice. Nutrient-dependent/pheromone-controlled adaptive evolution: a model. 

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 that 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.

However, if Eugene Koonin has correctly assessed the impact of viruses on personalized medicine, there will be no epigenetic effect of social odors on hormones that affect the development of species-specific behaviors. Thus, Koonin could support his claim that [T]he entire ideology of personalized medicine should be taken with many grains of salt.
Alternatively, the claims that currently link a single amino acid substitution to human life history transitions is closely linked to the nutrient-dependent pheromone-controlled changes in the context of the honeybee model organism.
See: Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults
Dr. Kasinski is looking at off-target effects, but Dr. TenOever is not concerned about epigenetic regulation of endogenous retroviruses in mammals or human endogenous retroviruses (HERVs). Like George Church, these researchers seem to be limited by their inability to link physics, chemistry, and the conserved molecular mechanisms of virus-driven RNA-mediated adaptations. For example, miR-34 down-regulates protein coating that may sensitize cells for more manageable chemotherapy.
If  knowledge of cell type differentiation were driving this research, their presentations could be linked from cell type differentiation in plants to nutrient-dependent pheromone-controlled RNA-mediated cell type differentiation in animals.
For an example from Arabidopsis (Arabidopsis thaliana) that appears to link RNA-directed DNA methylation and phosphorylation to fixation of RNA-mediated amino acid substitutions and cell type differentiation, see: Stress induced gene expression drives transient DNA methylation changes at adjacent repetitive elements
Examples from plant physiology can be linked via RNA-directed DNA methylation and phosphorylation to fixation of RNA-mediated amino acid substitutions in animals via the conserved molecular epigenetics of biophysically constrained protein folding chemistry. See also: Global Epigenomic Reconfiguration During Mammalian Brain Development.

Here we provide integrated empirical data and analysis of DNA methylation at single base resolution, across entire genomes, with cell-type and developmental specificity.

The question arises: “Do the molecular mechansims of RNA-mediated gene duplication and RNA-amino acid substitutions that differentiate the cell type of plants vary in animals?”

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