Autophagy is the antiphage defense strategy (2)

By: James V. Kohl | Published on: January 17, 2018

(click to enlarge)

2/15/17 Energy as information and constrained endogenous RNA interference (video)
The 6.46 minute-long technical presentation (above) from the Precision Medicine Virtual Conference is difficult to understand.Thus, 10 months later, Nik Willmore asked:

12/24/17 What are your insights into CRISPR and mTOR, for a young audience? I’m not mocking you…yet, Humpty Dumpty. What is the basis of your unifying principle? Vibration? Bohmian morphogenetic fields? Modified Darwin? God? –Nik Willmore @nikwillmore

12/25/17 Replying to @nikwillmore @jhewitt123

God created the anti-entropic virucidal energy of sunlight and all energy-dependent biodiversity via the physiology of pheromone-controlled reproduction. I co-authored a book about that for a young audience in 1995/2002, and a 6-part series for https://RNA-mediated.com today.

1/1/18 Replying to @ChaplainWE @nikwillmore @jhewitt123

Do you understand any aspect of how to model biophysically constrained biologically-based energy-dependent top-town causation and bottom-up effects on cell type differentiation via the physiology of reproduction and autophagy? The “walking fish” walks straight from quantum physics to quantum souls (2)

1/9/18 Viral suppressors of RNAi employ a rapid screening mode to discriminate viral RNA from cellular small RNA

My paraphrased summary:

RNA interference (RNAi) is our indispensable antiphage defense mechanism. Viruses escape the defense system by the theft of quantized energy, which encodes RNAi suppressors that prevent elimination of viral RNAs. The suppressors ensure energy-dependent virus accumulation.

1/12/18 Human cytomegalovirus-encoded miR-UL112 contributes to HCMV-mediated vascular diseases by inducing vascular endothelial cell dysfunction

The significantly altered pathways mainly include the mitogen-activated protein kinase signaling pathway, cell adhesion molecules, chemokine signaling pathway, cytokine-cytokine receptor interaction, circadian rhythm-mammal, mineral absorption, protein processing in the endoplasmic reticulum, proximal tubule bicarbonate reclamation, vasopressin-regulated water reabsorption, and arachidonic acid metabolism. In conclusion, hcmv-miR-UL112 could serve as a potential biomarker, and the miRNA-mediated regulation of signaling pathways might play significant roles in the physiological effects of hcmv-associated diseases.

1/12/18 H5N1 influenza virus-specific miRNA-like small RNA increases cytokine production and mouse mortality via targeting poly(rC)-binding protein 2

We conclude that miR-HA-3p is the first identified influenza virus-encoded microRNA-like functional RNA fragment and a novel virulence factor contributing to H5N1-induced ‘cytokine storm’ and mortality.

Virus-encoded microRNA-like functional RNA fragments are not novel virulence factors. They link the virus-driven degradation of messenger RNA to all pathology in all living genera via the theft of quanitzed energy, which typically links the fixation of RNA-mediated amino acid substitutions to healthy longevity.
See: Viral MicroRNAs, Host MicroRNAs Regulating Viruses, and Bacterial MicroRNA-Like RNAs
All serious scientists know what goes wrong in the context of host microRNA-mediated regulation of viruses. They also know how it goes wrong. See Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution

The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.

The serious scientists do not claim that viruses evolve. Scientists who make claims about evolution typically do not know how to link the creation of sunlight from ecological variation to food energy-dependent pheromone-controlled ecological adaptation via the physiology of biophysically constrained reproduction and biophysically constrained viral latency. Indeed, most pseudoscientists do not know the difference between a mutation and an RNA-mediated amino acid substitution.
See for comparison: Mechanisms of Recombination conference Start: Sunday, May 20, 9.00am Finish: Tuesday, May 22, 6.45pm

Description

Genetic recombination provides an important mechanism for the repair of chromosome breaks caused by DNA damage or replication fork demise. Defects in the recombination process have been linked to cancer predisposition, in particular breast cancers caused by mutations in BRCA1, BRCA2 and PALB2, and also acute leukemias associated with the rare genetic disease Fanconi anemia. Understanding precisely how recombination occurs is of interest to workers in the fields of meiosis, DNA repair, replication, chromosome architecture and interactions, and chromatin biology.

Download provisional conference program
Excerpts:

Douglas Bishop (University of Chicago, US)
A primary function of the ATPase activity of E. coli RecA is to prevent accumulation of a toxic form of the protein bound to undamaged chromosomal sites

Maria Jasin (Memorial Sloan Kettering Cancer Center, US)
Protecting the genome by homologous recombination

The energy-dependent microRNA-mediated creation of enyzmes protects all organized genomes from the virus-driven degradation of messenger RNA that links the theft of quantized energy from mutations to all pathology. Pseudoscientists who do not start with the creation of energy, have bastardized Darwin’s claims. His claims were based on placing “conditions of life” before natural selection. Conditions of life are energy-dependent and biophysically constrained by the mechanisms of pheromone-controlled recombination, which have been linked to autophagy by all serious scientists since 1925.
See also my RNA-mediated Facebook page and/or my RNA-mediated Facebook group and other tweets @jvkohl
The number of my tweet impressions since December 21, 2017 has climbed to more than 68,000 as the number of published works that mention “microRNA” has climbed to nearly 69,000. See for comparison: The tipping point (revisited): 68,000 publications, which was published to my other blog site on December 21, 2017.
See also: What Darwinists Fail to Consider (discussion attempt)
See also, this discussion attempt about the “spark of life.”
See also: Noncoding RNA Helps Cells Recover from DNA Damage

“The most logical, simple explanation is that the [noncoding RNA] counteracts the protein encoding form…”

My comment to the Scientist:

There is clear evidence that femtosecond blasts of UV light repair DNA in the context of energy-dependent changes in the microRNA/messenger RNA balance and autophagy, which protects all organized genomes from virus-driven energy theft and the degradation of messenger RNA.

The failure to integrate the Nobel Prize winning works of Ben Feringa (Chemisty 2016) and Yoshinori Ohsumi (Physiology or Medicine 2016) prevents theorists from linking what organisms eat to their pheromone-controlled physiology of reproduction in the context of Schrodinger’s claims in “What is Life?”(1944) and this claim by Roger Penrose in the reprint edition:

“How often do we still hear that quantum effects can have little relevance in the study of biology, or even that we eat food in order to gain energy?” (Roger Penrose 8 August 1991)

See also: From Fertilization to Adult Sexual Behavior In our section on molecular epigenetics, we wrote:

Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans…

The food energy that is linked from alternative splicing techniques of pre-mRNA to the chemistry of protein folding and the pheromone-controlled physiology of reproduction in all living genera seems to be largely ignored by those who are not Nobel Laureates.