Epigenetic (re)programming of behavior

By: James V. Kohl | Published on: January 1, 2016

Epigenetic (re)programming of caste-specific behavior in the ant Camponotus floridanus


Our results suggest that behavioral plasticity in animals may be regulated in an epigenetic manner via histone modification.

My comment: Experimental manipulation of a single gene changed behavior. The evidence suggests all invertebrate and all vertebrate morphological and behavioral phenotypes can be linked via nutrient-dependent changes in microRNAs, adhesion proteins, and supercoiled DNA.

See: The phylogenetic utility and functional constraint of microRNA flanking sequences
My comment: Nutrient-dependent RNA methylation, RNA-directed DNA methylation, and RNA-mediated amino acid substitutions in the histones link microRNAs and adhesion proteins to supercoiled DNA in the context of chromosomal rearrangements and the physiology of species-specific reproduction linked to the stability of organized genomes in all living genera via protection from virus-driven entropy.
The results from ants extend what is known about how nutrient-dependent pheromone-controlled weekend evolution of the bacterial flagellum occurred via two amino acid substitutions.
See: Evolutionary resurrection of flagellar motility via rewiring of the nitrogen regulation system

Genome resequencing revealed a single-nucleotide point mutation in ntrB in strain AR2S, causing an amino acid substitution within the PAS domain of the histidine kinase sensor NtrB [Thr97→Pro97 (T97P)] (13). The fast-spreading strain AR2F had acquired an additional point mutation in the σ54-dependent EBP gene ntrC, which alters an amino acid (R442C) within the DNA binding domain (Table 1 and table S2).

My comment: Neo-Darwinian theorists do not seem to know the difference between the definition of mutation, which is linked to pathology, and how nutrient energy-dependent amino acid substitutions are typically linked to healthy longevity. They bastardized Darwin’s “conditions of life” by placing de Vries “jump-like” changes in energy (i.e., mutations) into the context of natural selection and evolved biodiversity.
Serious scientists have linked atoms to ecosystems within the biophysical constraints of Darwin’s “conditions of life” and everything known about nutrient-dependent pheromone-controlled biodiversity in species from microbes to humans.
See: Structural diversity of supercoiled DNA

Our data provide relative comparisons of supercoiling-dependent twisted, writhed, curved, and kinked conformations and associated base exposure. Each of these structural features may be deferentially recognized by the proteins, nucleic acids, and small molecules that modulate DNA metabolic processes.

My comment: I cannot put that conclusion into the context of neo-Darwinian theories. And, neo-Darwinists do not seem willing to address the speed at which weekend evolution of the bacterial flagellum occurred.
As more examples from other species show that experimental manipulation of a single gene changes behavior, other model organisms can be linked to human behavior via as little as a single base pair substitution and single RNA-mediated amino acid substitution. Changes that would typically only occur during life history transitions can be linked from animal models, which are often used to model human physical and mental disorders.
For example: 

The honeybee already serves as a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, the development of the brain and behavior, mental health, longevity, diseases of the X chromosome, learning and memory, as well as conditioned responses to sensory stimuli (Kohl, 2012).

The molecular mechanisms continue to be detailed in disparate reports that make evolutionary theorists seem to become more desperate to change their theories each week. They have run out of “wiggle room.”
See also: An Illuminated State of Mind

“A subsequent study demonstrated that scientists can even implant — we call it ‘incept’ — false memory in the mouse brain,” added Tonegawa. “The challenge is how to extend the information obtained in animal models to human models. The invention of revolutionary noninvasive or low-invasive technologies will be needed, and God knows when that will happen.”

My comment: I wonder how many minds need to be illuminated before everyone accepts the extension of information obtained in animal models to human behavior.
Additional illumination comes from several other articles published today in Science.
Sperm RNA fragments modify offspring metabolism (subscription required)
…two new studies highlight a different class of RNAs, transfer RNAs, carried by sperm.
The effects of the RNA fragments don’t have to be harmful, Chen notes. “If a bad diet can influence us, I think a healthy diet can do it in the same way,” he predicts.
Seeing mTORC1 specificity (subscription required)

On page 48 of this issue, Aylett et al. (1) help uncover the molecular underpinnings of mTORC1, while on pages 43 and 53, Wolfson et al. (2) and Saxton et al. (3), respectively, make strides in determining how mTORC1 is regulated by the amino acid leucine.

My comment: Nutrient-dependent immune system function is regulated by one amino acid substitution. Researchers seem to have difficulty placing that fact into the context of how ecological variations are linked to ecological adaptations manifested in supercoiled DNA that protects organized genomes from virus-driven entropy.
There seems to be a disconnect between theories and what is know about the theft of nutrient energy by viruses.
For example, I keep reminding people of this claim: The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.
It replaced this comment, which I fortunately had also posted to The Atlantic before it was removed by Science

See also: “Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution”
The idea of biophysical constraints seems antithetical to the idea of nature somehow selecting mutations that cause amino acid substitutions. However, I am not a biophysicist or evolutionary theorist.
The problem may be my focus on nutrient-dependent receptor-mediated amino acid substitutions in species from bacteria to humans (non-viral organisms). Since I am not a virologist or physicist, I’m not sure that the laws of physics apply to viruses and their replication.
If they do, natural selection for random mutations is not likely to result in amino acid substitutions because the thermodynamics of changes in organism-level thermoregulation preclude such randomness. Stability of protein biosynthesis and degradation that probably depends on protein folding must somehow be controlled. Besides, I don’t know how random mutations in viruses could be naturally selected for inclusion in the human virome (or in the virome of any organism capable of thermoregulating its thermodynamic intercellular signaling).
If the Second Law of Thermodynamics does not apply to viruses, which means the chemical bonds that enable the amino acid substitutions can form at random and somehow be naturally selected, the details of biophysical constraints in this article seems out of place, since I do not think in terms of constrained random mutations and natural selection in mutation-driven evolution.
Hopefully, someone with a background in biophysics will address my confusion in case others are confused. In addition, I wonder if the consequences of understanding the evolutionary mechanisms that govern viruses extend to consequences important to understanding the evolution of species from bacteria to humans via constrained random mutations and natural selection?



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