The decay of mRNA plays a vital role in modulating mRNA abundance, which, in turn, influences cellular and organismal processes. In plants and metazoans, three distinct pathways carry out the decay of most cytoplasmic mRNAs: The mRNA decapping complex, which requires the scaffold protein VARICOSE (VCS), removes a protective 5′ cap, allowing for 5′ to 3′ decay via EXORIBONUCLEASE4 (XRN4, XRN1 in metazoans and yeast), and both the exosome and SUPPRESSOR OF VCS (SOV)/DIS3L2 degrade RNAs in the 3′ to 5′ direction. However, the unique biological contributions of these three pathways, and whether they degrade specialized sets of transcripts, are unknown.
A claim like this could be used as cannon-fodder for any serious scientist who wanted to target a neo-Darwinian theorist. I will do what Daniel Dennet suggested and re-express my target’s position.
Ready… Aim… Fire
Simply put, the target claims that the molecular mechanisms of energy-dependent microRNA-mediated cell type differentiation remove a protective 5′ cap, allowing for 5′ to 3′ decay. But, they place their claim into something that supposedly is unknown about how the biological contributions of three pathways prevent mRNA decay.
The problem with the target’s position: A one-sided attack on Schroedinger’s claims fails to link the epigenetic landscape to the physical landscape of supercoiled DNA in the context of energy-dependent feedback loops. The feedback loops link the physiology of reproduction from the creation of RNA to prevention of the decapping.
The energy-dependent creation of RNA is required to prevent the virus-driven theft of quantized energy that causes the decapping of the mRNA complex and link mutations to all pathology. For contrast, the food energy-dependent creation of microRNAs has repeatedly been linked from RNA-mediated DNA repair and the fixation of amino acid substitutions to the stability of supercoiled DNA in the organized genomes of all living genera.
…we believe that this remarkable type of amino acid sequence variation reflects in part the mechanism by which specificity is conferred.
Note: The co-author, Lee E. Hood is scheduled to present at Schrödinger at 75 – The Future of Biology – September 2018
Supercoiled DNA protects organized genomes from the virus-driven degradation of messenger RNA that the authors of the article on mRNA link to specialized RNA decay substrates, decapping-mediated feedback, and redundancy without linking the energy-dependent feedback to healthy longevity via the fixation of RNA-mediated amino acid substitutions and DNA repair.
The article is paywalled, so you may need to take my word for the fact that they seem to be deliberately deceptive. The level of their obfuscation became clear to me in the context of their Figure 6. They placed the role of energy-dependent RNA-mediated amino acid substitutions into the proper perspective of everything known to serious scientists about biophysically constrained viral latency.
Also, in the article text, they conclude that studies of oxidative phosphorylation attest to facts about prevention of mRNA decay components in response to nutrient stress or social stress, which they refer to as “osmotic stress.” They link the stress from changes in the mRNA half-life and suggest that energy-dependent regulation of the half-life could arise in the context of the direct modulation of mRNA decapping machinery.
The direct modulation is obviously energy-dependent but they place the modulation into some other context that seemingly involves upstream pathways and the creation of proteins. Simply put, they are swimming upstream at a time when all serious scientists are starting with energy-dependent top-down creation of microRNAs.
They conclude with a plea for funding of more pseudoscientific nonsense that fails to link the creation of the sun’s anti-entropic virucidal energy to healthy longevity via the creation of microRNAs that prevent the virus-driven degradation of messenger RNA, which serious scientist have linked from mutations to all pathology. They claim that an important area of future research includes research that might lead to a better understanding of how stress is linked to pathology via conserved molecular mechanisms. I claim they are using correlations from the bottom-up to replace top-down causation and biophysically contrained cause and effect.
See for comparison: ORACLE: Options to Read in the Archive: Churchland Lab’s Experience
They highlight 7 comp/systems neuro papers to help others keep up with the amount of information that is being published in bioRxiv Neuroscience preprints.
Human obesity can result from the aberrant production or processing of proopiomelanocortin (POMC) in hypothalamic neurons, but it is unclear which human POMC-derived peptides are most relevant to body weight regulation.
In a living cohort, carriers of the minor allele of a SNP associated with increased LINC01268 expression in brain scored higher on a lifetime aggression questionnaire and show diminished engagement of prefrontal cortex (BA10) when viewing angry faces during fMRI. WGCNA highlighted the immune response. Conclusions: These results suggest that LINC01268 influences emotional regulation, aggressive behavior and suicide by violent means; the underlying biological dynamics may include modulation of genes potentially engaged in the immune response.
See also: The behavioral and neurobiological effects of reduced Brd1 expression in mice are sex-biased and implicate gender dependent dysregulation of nuclear receptor mediated signaling in mental disorders
…we provide in vitro evidence that BRD1 modulates the transcriptional drive of a subset of nuclear receptors (e.g. the vitamin D and glucocorticoid receptors). Moreover, we demonstrate enrichment of psychiatric disorder risk in the target genes of nuclear receptors, sex-biased expression of several nuclear receptor genes in the adult brain of Brd1+/- mice, and that sex-biased genes in general are enriched with nuclear receptor genes particularly at the earliest developmental stage of the human brain. Overall, our data suggests that the spatio-temporal interaction between BRD1 and subsets of nuclear receptors in the brain is sex-biased and that hampered BRD1 mediated regulation of target genes governed by certain nuclear receptors may significantly contribute to sex differences in psychopathology.
For comparison, this was published on the same day: Evolutionary conserved neural signature of early life stress affects animal social competence
What do claims about evolutionary conserved neural signatures represent to serious scientists who understand the facts about energy-dependent top-down causation and biophysically constrained viral latency?