Stress-induced energy-dependent DNA repair

Predicting 3D Structure, Flexibility, and Stability of RNA Hairpins in Monovalent and Divalent Ion Solutions
Abstract excerpt: 

A full understanding of RNA-mediated biology would require the knowledge of three-dimensional (3D) structures, structural flexibility, and stability of RNAs.

My comment: The stability of RNAs is nutrient energy-dependent. Nutrient-dependent microRNAs and adhesion proteins link RNA-mediated amino acid substitutions in the histones of supercoiled DNA to protection from virus-driven entropy in all living genera.  Energy does not “emerge” and energy stress does not lead to the stability of organized genomes.

AMP-activated protein kinase mediates mitochondrial fission in response to energy stress


…AMPK emerges as a master regulator of mitochondrial homeostasis…

My comment: They seem to be claiming that the emergence of an energy-dependent molecular mechanism makes mitochondrial homeostasis possible in the context of RNA-mediated toxicity.

Reported as: How the cell’s power station survives attacks


…scientists at the Salk Institute have uncovered an unexpected way in which cells trigger this critical response to threats, offering insight into disorders such as mitochondrial disease, cancer, diabetes and neurodegenerative disease—particularly Parkinson’s disease, which is linked to dysfunctional mitochondria.

My comment: This links the emergence of an energy-dependent molecular mechanism, which makes mitochondrial homeostasis possible, to mitochondrial disease.  I cannot follow the logic from emergence and homeostasis in the report published in “Science” to the report on mitochondrial disease published on MedicalXpress.

It’s as if they deliberately avoid the link from energy-dependent RNA-mediated DNA repair to homeostasis by claiming that the energy emerges and is somehow subsequently linked to both homeostasis and disease.

See for comparison:

Study connects mitochondria to psychological stress response and species resilience

Our study demonstrates how mitochondria can shape the major stress–response pathways, thereby recalibrating the multisystemic response to psychological stress (Fig. 6G). Further studies are needed in humans to determine if inherited interpersonal polymorphic differences in mtDNA (i.e., haplogroups) and other common mtDNA mutations (42, 69) are sufficient to modify physiological responses to psychosocial stressors and thus mediate the association between stress exposure and later mental and somatic (i.e., psychosomatic) illness. Allostatic load driven by mitochondrial dysfunction could contribute to mitochondrial disease pathogenesis and clinical variability.

Reported as: Newly discovered windows of brain plasticity may help with treatment of stress-related disorders

The authors note further that based on this model, it seems that mitochondria lie at the interface of genetic and environmental factors that shape an organism’s evolution. They suggest that future research targeting mitochondria can contribute to biological resilience, psychological health, and response to environmental stressors.

My comment: They linked the emergence of an energy-dependent molecular mechanism that makes mitochondrial homeostasis possible from the epigenetic landscape to the physical landscape of DNA.
See also: Stress dynamically regulates behavior and glutamatergic gene expression in hippocampus by opening a window of epigenetic plasticity

Excitatory amino acids play a key role in both adaptive and deleterious effects of stressors on the brain, and dysregulated glutamate homeostasis has been associated with psychiatric and neurological disorders.

My comment: Fixation of RNA-mediated amino acid substitutions in the organized genomes of all living genera appears to be the link to homeostasis. Fixation occurs in the context of the nutrient energy-dependent physiology of reproduction.
Reported as: Newly discovered windows of brain plasticity may help with treatment of stress-related disorders

In other experiments, they looked at mice genetically engineered to carry a genetic variant associated with development of depression and other stress-related disorders in humans, and present in 33 percent of the population.

My comment: In mice, the genetic variant is the RNA-mediated amino acid substitution BDNF Val66Met, which is fixed in 33 percent of the population and linked to the treatment of stress-related disorders.
For comparison, see: Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults

Prefrontal dopamine levels are relatively increased in adolescence compared to adulthood. Genetic variation of COMT (COMT Val158Met) results in lower enzymatic activity and higher dopamine availability in Met carriers. Given the dramatic changes of synaptic dopamine during adolescence, it has been suggested that effects of COMT Val158Met genotypes might have oppositional effects in adolescents and adults.

My comment: Fixation of the COMT Val158Met amino acid substitution in the organized genomes of adults is linked to the honeybee model of nutrient-dependent pheromone-controlled life history transitions in morphological and behavioral phenotypes in species from microbes to humans.
See: Nutrient-dependent/pheromone-controlled adaptive evolution: a model

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).

See also: NORAD Gene Could Aid Cancer Research

Evidently, maintaining the normal chromosome number in a cell is the critical function the NORAD RNA provides.

My comment: The folks at ICR seem to be following my reports on biologically-based cause and effect, and they also are a resource for information on other aspects of YEC. The fact that they are now only two weeks behind me is interesting, since many of their recent articles seem to incorporate my model, albeit without citing any of my published works.
See for example: NORAD: air defense and defense against genomic entropy

All organisms appear to use nutrient uptake to support their innate immune system function, which enables NORAD to link the sun’s anti-entropic virucidal energy from UV light to absorbances in bacteria and the response of bacteria to stresses and nutrient conditions that enable their ecological adaptation instead of virus-induced genomic entropy.

My comment: You will continue to see reports that make claims about the need to link NORAD RNA, chromosomal number, and nutrient-dependent pheromone-controlled chromosomal rearrangements. The reports will be linked to implications in cancer biology until all serious scientists link nutrient-dependent RNA-mediated cell type differentiation from atoms to ecosystems. A model of atoms to ecosystems is the only way to link cell type differentiation in all genera via the conserved molecular mechanisms of genomic stability/homeostasis. My model allows other serious scientists to compare what is known about biophysically constrained protein folding chemistry and link mutations to the genomic instability that is a a hallmark of tumor cells.
See for example: Kohl, James V. (2014): Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems
My comment: I think what we are seeing is that all factions “jockey for positions” and hope that they will be the first to reveal the scientific truth. At the same time, they actively or passive/aggressively suppress any information from those who are no longer racing to find the truth because the information about cell type differentiation has been known to them all along.
But information does not sell their metaphorical newspapers. Headlines do!

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