DNA repair via junk DNA (1)

By: James V. Kohl | Published on: September 12, 2016

Initiating DNA repair

To communicate stress signals within cells, JNKs add phosphate groups to proteins, and the Rochester study found the amino acid residue on SIRT6 that is modified by JNK.

They found an energy-dependent RNA-mediated amino acid substitution linked to the physiology of reproduction. It makes DNA repair and transgenerational epigentic inheritance of biologically-based cause and effect possible. The innate immune system, links RNA-mediated amino acid substitutions to supercoiled DNA and protection of organized genomes from virus-driven entropy. The chemistry of biophysically constrained RNA-mediated protein folding is detailed in the context of the amino acid substitutions and cell type stability in:


Our results define the pathway leading from oxidative stress to activation of DSB repair by SIRT6.

My comment: Pathways that initiate DNA repair are exemplified. They are not defined.  Examples of the pathways link ecological variation to energy-dependent ecological adaptations. Alternatively, they link virus-driven energy theft to all pathology.

The most recent reported results on the detailed pathway link RNA amino acid substitutions from energy-dependent changes in the microRNA/messenger RNA balance to supercoiled DNA via phosphorylation. Phosphorylation links everything known about biophysically constrained protein folding chemistry from fixation of RNA-mediated amino acid substitutions to all biodiversity via the physiology of reproduction and transgenerational epigenetic inheritance.

See: Socially responsive effects of brain oxidative metabolism on aggression


Aerobic glycolysis is commonly observed in cancer cells, where it is known as the Warburg effect. In this context, high rates of glycolysis relative to OX provide an efficient route to generate amino acids and nucleotides necessary for rapid growth (69)

Reported as: Angry bees: Insect aggression boosted by altering brain metabolism

These genes play a key role in the most efficient type of energy generation in cells, a process called oxidative phosphorylation.

My comment: Cell type differentiation is nutrient energy-dependent. The claim that genes play a key role is misleading. The energy, not the genes, must be linked to oxidative phosphorylation in the context of RNA-mediated protein folding chemistry. Natural selection for energy-efficient codon usage obviously links the energy from phosphorylation to cell type differentiation via codon optimality.

Evolutionary conservation of codon optimality reveals hidden signatures of cotranslational folding (2013)

 …the choice of the coding sequence emerges as finely tuned to the action of the ribosome.

A Nutrient-Driven tRNA Modification Alters Translational Fidelity and Genome-wide Protein Coding across an Animal Genus (2014) reported as Nutrient availability can cause whole-genome recoding and Researchers find hidden meaning and ‘speed limits’ within genetic code

The code not only dictates what amino acids are incorporated into proteins, it also tells the cell how fast they should be incorporated.

Codon Optimality Is a Major Determinant of mRNA Stability (2015)

…codon optimization exists as a mechanism to finely tune levels of mRNAs and, ultimately, proteins.

Codon identity regulates mRNA stability and translation efficiency during the maternal-to-zygotic transition (2016)

The amino acid optimality code (Fig 6) provides an alternative perspective on sequence changes between paralogs in evolution and human disease.

Simply put, the optimality code links virus-driven energy theft to all pathology and nutrient energy-dependent RNA-mediated amino acid substitutions to all healthy longevity. No definitions and no assumptions are required. Serious scientists have known that for at least 20 years.

See also: Wrangling Retrotransposons


Several studies have indicated that SIRT6 helps catalyze repair of the damage at numerous types of DNA lesions, including single- and double-strand breaks. A characteristic feature of aging cells is an increase in the amount of DNA damage. It is possible that, under basal conditions, SIRT6 is bound to the L1 promoter, enforcing silencing of the genomic parasite, but upon DNA damage, the enzyme vacates the L1 sequence to facilitate repair at the damage site. This creates a window of opportunity for L1 elements to escape repression and replicate themselves. Consistent with this model, when cells are treated with DNA-damaging agents, such as hydrogen peroxide and paraquat, SIRT6 leaves L1 sites and becomes enriched at damage sites.1

More than a year later, the three co-authors from this March 1, 2015 article have linked an energy-dependent RNA-mediated amino acid substitution to cell type differentiation and healthy longevity, but they refer to lysine as a residue linked to DNA repair.

See for comparison: Histone H3K36 mutations promote sarcomagenesis through altered histone methylation landscape
The authors link virus-driven energy theft from failed RNA-directed DNA methylation to loss of function histone mutations via these amino acid substitutions.
1) lysine 27–to–methionine (K27M)
2) glycine 34–to–arginine/valine (G34R/V)
3) glycine 34–to–tryptophan/leucine (G34W/L)
4) lysine 36–to–methionine (K36M)
They call the cancer-associated mutations “oncohistones.” Their word-play may confuse others who know how to link the virus-caused mutations from the sites of histone posttranslational modifications and RNA-directed DNA methylation or histone acetylation in H3K27 and H3K36 to creationism.
Creationism, for comparison, can be linked to nutrient energy-dependent healthy longevity, and young earth creationists have linked virus-driven energy theft to all pathology.
See: Did God Make Pathogenic Viruses? (1999)

A review of the structure, function, and role of viruses in ecology is presented. It is concluded that viruses are non-living entities, similar to seeds and spores whose functions include carrying genes from one plant or animal to another. Viruses are a part of a system that helps to produce the variety that is critical for life and, importantly, they carry resistance to disease from one organism to another. Most viruses live in their host without causing problems. Pathogenesis is evidence of something gone wrong, a mutation or the accidental movement of genes, and not evidence of a system deliberately designed to cause human disease and suffering.

See also: Viral Genome Junk Is Bunk (2015)

So, where do viruses come from that essentially share the same sequences as those found in their host genomes? Perhaps the evolutionists have placed the cart before the horse on this issue, as proposed by several creationist scientists.4,6 In fact, in an ironic twist, the evidence mentioned above indicates that viruses likely arose from their hosts and not the other way around. As molecular biologist and biochemist Peter Borger notes, “The most parsimonious answer is: the RNA viruses got their genes from their hosts.”6

Deliberate attempts to confuse others have been made for at least 17 years. I suspect that others are trying to support neo-Darwinian theories about genes that pop into existence. Confusing others about how energy-dependent de novo gene creation occurs may cause the failure to recognize the link from virus-driven energy theft and loss of function mutations, which has been linked to all pathology via what would otherwise be the organized genomes of all living genera.
Organized genomes do not pop into existence. De novo gene creation is nutrient energy-dependent. Top-down causation links the theft of energy manifested in a tornado like this one to it destructive power. Functional stuctures, which are destroyed by the energy theft, do not pop back into existence. Even if they did, someone would need to explain the first instance of genes or houses popping into existence.

Summary: The concept of evolved genes can be compared to the evolution of a house from the debris carried and/or deposited by a tornado.

See for comparison: Two fatty acyl reductases involved in moth pheromone biosynthesis

Studies over the last two decades have pinpointed that the epigenetic effect of pheromone-driven adaptive evolution is one of the major factors driving the successful diversification of Lepidopteran insects10. In moths, a few substitutions in critical amino acids in the key pheromone biosynthetic enzymes are sufficient to create a novel pheromone component11,12.

10 is a citation to my 2013 review of RNA-mediated amino acid substitutions and cell type differentiation in species from microbes to humans.
Nutrient-dependent/pheromone-controlled adaptive evolution: a model

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