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By: James V. Kohl | Published on: August 17, 2015

Leaving an Imprint

Among the first to discover epigenetic reprogramming during mammalian development, Wolf Reik has been studying the dynamics of the epigenome for 30 years.

By Anna Azvolinsky | August 1, 2015


In the mammalian field, the imprinting field, together with the X-inactivation field, was the birthplace of epigenetics.

My comment: Researchers like Wolf Reik never mentioned the role viruses play in preventing cell type differentiation. The birthplace of epigenetics became associated with a “still-birth.” The still-birth continued to leave a horrid stain on every aspect of imprinting. Epigenetic effects on imprinting should have been placed into the context of what later came to be known about the RNA-mediated events that link nutrient-dependent RNA-mediated protein folding to the biophysically constrained chemistry of cell type differentiation that is perturbed by viruses.
For more than 30 years, the role of virus-perturbed protein folding has been placed into the context of mutations linked to biodiversity as if epigenetic imprinting attributed to viruses could link viruses from mutations to biodiversity in the context of transgenerational epigenetic inheritance. Epigenetic inheritance requires nutrient-dependent microRNAs that protect organized genomes from virus-driven damage to DNA. The damage to DNA links entropic elasticity to genomic entropy in all living genera.
Re: “X-inactivation field, was the birthplace of epigenetics.”
See also:  Sex differences in the brain: a whole body perspective
Excerpt with my emphasis: (Thanks to Teresa Binstock for calling my attention to this.)

Another example concerns one of the most pervasive sex differences: the inactivation of one X chromosome in every cell of the body in females. Random X inactivation is perhaps the prime example of a sex difference (in this case, a process that happens in all female cells and no male cells) that exists in order to make the sexes more similar (more or less equalizing the dosage of X chromosome genes). For the most part, nature does a great job in covering up the consequences of this. However, the inactivation of an entire chromosome in each female cell utilizes epigenetic machinery, and the inactivation state must be continually maintained[20], [21]. There is evidence that this affects the expression of autosomal genes [22], [23], presumably because there is a limiting supply of the DNA methyltransferases and histone-modifying enzymes required for the epigenetic changes that underlie the inactivation of an entire chromosome. It is not hard to see how this one event (usually thought of in terms of equalizing males and females) may have ripple effects that result in sex differences elsewhere.

My comment: Imprinting cannot automagically affect the expression of genes. Instead, nutrient-dependent RNA-directed DNA methylation links the epigenetic effect of sensory input to hormone-organized and hormone-activated behaviors via the effects of hormones on gene expression. Hormones are linked to affects on behavior.
The “ripple effects” of epigenetically-effected RNA-mediated gene duplication and RNA-mediated amino acid substitutions cause hormones to differentiate all hormone-differentiated cell types, which are linked to behavior during life history transitions. That fact was exemplified in: Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults. 
The single amino acid substitution and human behavior were linked to the honeybee model organism in: Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
Excerpt with my emphasis:

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).

My comment: All other model organisms with hormone-organized and hormone-activated behaviors present a problem to sex researchers. Most of them are among the best examples of human pheromone-deniers.
The pheromone-deniers try to link nutrient-dependent hormone-organized and hormone-activated behaviors without placing the behaviors into the context of feedback loops. All serious scientists know: Feedback Loops Link Odor and Pheromone Signaling with Reproduction.
Not much more can be said about sexologists whose fear of pheromones may lead them to continue touting pseudoscientific nonsense about X inactivation and everything else linked from RNA-mediated events to cell type differentiation in all cells of all individuals of all species.
Similarly, not much more can be said about molecular biologists who have failed to learn or failed to teach others about RNA-mediated events during the past 30 years.

See: Wolf Reik.

He appears to have left a stain on what should have become known to serious scientists about the role that viruses play in cell type differentiation. Viruses link entropic elasticity to genomic entropy. His focus appears to be only on the stability of organized genomes.

That must include the stability of organized genomes in heterosexuals and homosexuals during their epigenetically-effected life history transitions. If you don’t teach that fact to sexologists, they might think they can get away with touting their ridiculous theories about the sexual differentiation of cell types while linking their ridiculous theories to the expression of autosomal genes.

See: Global reorganization of the nuclear landscape in senescent cells.


Comparison of embryonic stem cells (ESCs), somatic cells, and senescent cells shows a unidirectional loss in local chromatin connectivity, suggesting that senescence is an endpoint of the continuous nuclear remodelling process during differentiation.

See also: Selective impairment of methylation maintenance is the major cause of DNA methylation reprogramming in the early embryo.


The dispersed patterns of CpG dyads in the early-cleavage embryo suggest a continuous partial (and to a low extent active) loss of methylation apparently compensated for by selective de novo methylation. We conclude that a combination of passive and active demethylation events counteracted by de novo methylation are involved in the distinct reprogramming dynamics of DNA methylomes in the zygote, the early embryo, and PGCs.

My comment: The concept of de novo methylation appears to lie outside the context of nutrient-dependent RNA-directed DNA methylation that links RNA-mediated amino acid substitutions to the stability of organized genomes in all genera via the protection of damage from viruses when proliferation of viral microRNAs overwhelms the thermodynamic stability of organisms, which is nutrient-dependent and controlled by the physiology of reproduction.

See also: Genome-wide bisulfite sequencing in zygotes identifies demethylation targets and maps the contribution of TET3 oxidation.


Unexpectedly, we demonstrate that TET3 activity also protects certain CpG islands against methylation buildup.

My comment: Why was that unexpected? See:

Alteration of genic 5-hydroxymethylcytosine patterning in olfactory neurons correlates with changes in gene expression and cell identity


Tet3 overexpression disrupts olfactory receptor expression and the targeting of axons to the olfactory bulb, key molecular and anatomical features of the olfactory system. Our results suggest a physiologically significant role for gene-body 5hmC in transcriptional facilitation and the maintenance of cellular identity independent of its function as an intermediate to demethylation.

My comment: This report inadvertently linked viral microRNAs to Tet3 overexpression and nutrient-dependent microRNAs to protection of organized genomes via the respective roles of viruses and nutrients in cell type differentiation. Nutrient-dependent RNA-directed DNA methylation differentiates the cells of all individuals in all species from microbes to man via their receptor-mediated biophysically constrained chemistry of nutrient-dependent protein folding and amino acid substitutions that are fixed in organized genomes via the physiology of reproduction.

See for comparison: From Fertilization to Adult Sexual Behavior

Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes…

See also: Unmasking Secret Identities


Epigeneticists don’t know yet how important it is to describe methylation at single-base resolution…

If they learn how important that is, they may also learn how important it is to include the links from viral microRNAs to energy-dependent changes at the atomic level of single-base resolution. They could then place the changes into a model that links atoms to ecosystems via the sun’s biological energy and the epigenetic traps that are perturbed by viruses.
See also: Signalling

The study of the proteins that control communication within and between cells


For cells to grow there must be both available nutrients and positive signals from proteins responding to environmental stimuli.
Suppression of a single protein, mTOR, which acts as a quality control step activity can result in increased lifespan through an unknown mechanism and we will attempt to reveal this.

My comment: Are they pretending that they will reveal an unknown mechanism of signaling and suppression that already links the nutrient-dependent RNA-mediated cell type differentiation of nematodes from the pheromone-controlled physiology of their reproduction to the biodiversity of all species via this report: System-wide Rewiring Underlies Behavioral Differences in Predatory and Bacterial-Feeding Nematodes
See also: The neurobiological consequence of predating or grazing

“The patterns of synaptic connections perfectly mirror the fundamental differences in the feeding behaviours of P. pacificus and C. elegans”, Ralf Sommer concludes.

My comment: If you know what naturally occurs to alter feeding behaviors you can link viruses and the proliferation of viral microRNAs to entropic elasticity that leads to genomic entropy — unless the entropy is biophysically constrained by ecological variation that leads organisms to find an alternative source of food and to reproduce in the context of Darwin’s “condition of life.”

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