Co-evolved genetically integrated mitonuclear communication?

By: James V. Kohl | Published on: July 9, 2018

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MOTS-c, mitonuclear communication, mitochondria, mitochondrial DNA, short open reading frames (sORF), peptide, mitochondrial-derived peptide (MDP), stress response, metabolic stress, homeostasis
Published Date: Apr 18, 2018 Nutrient-dependent Pheromone-Controlled Ecological Adaptations: From Angstroms to Ecosystems
Summary: Nutrient stress and social stress force organisms to ecologically adapt to the virus-driven degradation of their messenger RNA via natural selection for energy-dependent codon optimality in the context of the physiology of reproduction.
See for comparison: The Mitochondrial-Encoded Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress

…MOTS-c, a peptide encoded in the mitochondrial genome, translocates to the nucleus and regulates nuclear gene expression following metabolic stress…

Conclusion:

…mitochondrial and nuclear genomes co-evolved to independently encode for factors to cross-regulate each other, suggesting that mitonuclear communication is genetically integrated.

See for comparison: Psychological Stress and Mitochondria: A Conceptual Framework (Part 1) reported as: Cellular ‘powerhouses’ may explain health effects of stress
Top-down quantized energy-dependent causation and biophysically constrained viral latency are consistently removed from consideration by pseudoscientists who tout co-evolution, independent encoding, cross-regulation and the genetically integrated structure and function of supercoiled DNA.
Serious scientists start with quantized energy-dependent changes in base pairs and link them to fixation of RNA-mediated amino acid substitutions that stabilize the organized genomes of all living genera. The fixation of RNA-mediated amino acid substitutions occurs in the context of the physiology of pheromone-controlled reproduction in species from microbes to humans. That fact is missing from many reports that link nutrient stress and/or social stress to a poor quality of life.
See for comparison: A Role for the Fifth G-Track in G-Quadruplex Forming Oncogene Promoter Sequences during Oxidative Stress: Do These “Spare Tires” Have an Evolved Function? (2015)
Functional structures do not automagically evolve and/or co-evolve. See: It’s all about that base (12/10/14) and/or Structural diversity of supercoiled DNA 10/12/15
Nothing Evolves. All ecological adaptations are quantized energy-dependent and RNA-mediated.
See:
Dependence of RNA synthesis in isolated thymus nuclei on glycolysis, oxidative carbohydrate catabolism and a type of “oxidative phosphorylation” (1964)
Redefining neuroendocrinology: Epigenetics of brain-body communication over the life course (2017)
Psychological Stress and Mitochondria: A Systematic Review (Part 2) (2018)

Studies meeting the inclusion criteria for this systematic review collectively demonstrate four main points. First, chronic stress paradigms cause significant effects on mitochondrial energy production capacity and mitochondrial morphology. Second, acute and chronic stress may have different and possibly opposite effects on mitochondrial functions. Third, specific elements of mitochondrial function may be differentially affected by stress, such as mtDNA-encoded complex IV (COX). Fourth, behavioral, genetic, and dietary factors may influence mitochondrial vulnerability to stress. Collectively, available evidence supports the hypothesis that psychological stress causes MAL and calls for the need for more research investigating this question particularly in humans.

Evidence from metabolomic, proteomic, and transcriptomic studies also suggest additional layers of regulation by which stressful experiences may alter mitochondrial components among rodents. Although these metabolites, protein composition, and gene expression outcomes do not reflect the functionality of mitochondria, when assessed in parallel with functional outcomes, they will help explain and refine our understanding of the mechanisms by which stress influences mitochondrial function and health. In addition, whereas functional changes should be regarded as primary indicators of MAL (21), stress-induced molecular changes within mitochondria may also reflect compensatory mechanisms or recalibrations that contribute to long-term changes in mitochondrial function and to the accumulation of MAL. [mitochondrial allostatic load]

Only biologically uninformed science idiots continue to put what is known to serious scientists about stress back into the context of their ridiculous theories about the co-evolved functional structure of supercoiled DNA. The functional structure of supercoiled DNA is quantized energy-dependent and microRNA-mediated. The future of biology is the future of precision medicine. If the end of the pseudoscientific nonsense touted by theorists is not in the foreseeable future, more unnecessary suffering and premature death will include your suffering and premature death.
See for comparison: Polyamino acid layer-by-layer (LbL) constructed silica-supported mesoporous titania nanocarriers for stimuli-responsive delivery of microRNA 708 and paclitaxel for combined chemotherapy (2018)
Association study of frameshift and splice variant polymorphisms with risk of idiopathic recurrent pregnancy loss (2018)
From Fertilization to Adult Sexual Behavior (1996)