Energy dependent RNA-mediated immunity (4)

By: James V. Kohl | Published on: March 6, 2016

The Mitochondrial Basis of Aging

Excerpt: 

…the mutation at amino acid position 257 results in an enzyme that retains normal polymerase function but has impaired proofreading activity. Mice containing one or two copies of this proofreading-deficient POLG accumulate a significant level of mitochondrial mutations, and homozygous knockin mice exhibit an accelerated aging phenotype (Kujoth et al., 2005; Trifunovic et al., 2004). Nonetheless, while this model clearly links mitochondrial mutations to aging, it should be noted that the type and magnitude of mitochondrial mutations do not appear to faithfully replicate what is seen during normal aging (Williams et al., 2010). Thus, while the levels of mitochondrial mutations increase with age, it remains unclear whether this increase plays a fundamental role in the aging process.

My comment: The nutrient-dependent innate immune system protects all organized genome from virus-driven energy theft. The energy theft links the mutation at amino acid position 257 to the pathology. For comparison there is nothing that neo-Darwinian theories cannot do to link an accumulation of beneficial mutations to the evolution of a new species. Their theories do not need to address the experimental evidence that shows mutations are never beneficial.
Reported as: The Mitochondrial Basis of Aging

Excerpt:
Signaling pathways regulating the mitochondrial unfolded protein response and mitophagy are also reviewed, with particular emphasis placed on how these pathways might, in turn, regulate longevity.
Taken together, these observations suggest that mitochondria influence or regulate a number of key aspects of aging and suggest that strategies directed at improving mitochondrial quality and function might have far-reaching beneficial effects.

My comment: The observations of far-reaching beneficial effects link conserved biophysically constrained signaling pathways from chemotaxis and phototaxis in microbes to the physiology of reproduction in plants and animals. MicroRNA flanking sequences and energy-dependent hydrogen-atom transfer in DNA base pairs in solution are linked from changes in base pairs  to the physiology and reproduction of soil bacteria, which links the grasses that cows eat to the bull sperm microRNAome via microRNAs in milk.
The microRNAs in milk classically condition species-specific behaviors in mammals that link the behaviors to supercoiled DNA, which protects all organized genomes against virus-driven genomic entropy in the context of the physiology of human reproduction. The failure of the innate immune system to protect us against the transgenerational epigenetic inheritance of virus-driven entropy in nerve cells of the brain is manifested in the craniofacial morphology and brain damage caused by viruses like the Zika virus.
The damage done to the human brain during its development links microRNA flanking sequences and hydrogen-atom transfer in DNA base pairs from the sun’s biological energy to RNA-mediated cell type differentiation in all living genera via conserved molecular mechanisms of nutrient-dependent pheromone-controlled biodiversity in the nematodes, C. elegans and P. pacificus — a predatory nematode with teeth.
See also: A Biophysical Model of CRISPR/Cas9 Activity for Rational Design of Genome Editing and Gene Regulation
Excerpt 1)

The RNA-mediated Cas9 adaptive immunity system (CRISPR type II) has revolutionized genome engineering by enabling the precision cutting of DNA that can be customized to target any sequence [1,2,3,4,5,6], while being functional in a broad range of prokaryotes and eukaryotes, including bacteria, yeast, flies, fish, plants, worms, monkeys, mice, rats, rabbits, frogs, and human cell lines [3,7,8,9,10,11,12,13,14,15,16,17,18]. By forcing the host to repair these precision DNA cuts, the CRISPR/Cas9 system allows recombinant DNA to be inserted at desired genome locations, and therefore can be used for performing high-throughput gene knockouts, loss-of-function screening, artificial immunization, removal of latent genome-encoded viruses, and site-specific gene therapy applications [19,20,21,22].

Excerpt 2)

We combine statistical thermodynamics and kinetics to model Cas9:crRNA complex formation, diffusion, site selection, reversible R-loop formation, and cleavage, using large amounts of structural, biochemical, expression, and next-generation sequencing data to determine kinetic parameters and develop free energy models.

My comment: Any model that links free energy to cell type differentiation and healthy longevity will also link energy theft by viruses to pathology via what is known about hydrogen-atom transfer in DNA base pairs in solution. The transfers do not, as some people claim, simply make the base pairs disappear.
Neo-Darwinists have consistently linked virus-driven loss of function from the disappearance of base pairs to mutations and/or natural selection, which they link the evolution of new species. They seem to think that if they can edit the genes that typically prevent virus-driven entropy, they can protect their theories.
See for comparison: CRISPR/cas9, a novel genomic tool to knock down microRNA in vitro and in vivo
Excerpt:

…we investigated the potentials of CRISPR/cas9 as an innovative strategy serving miRNA loss-of-function studies, and our results support that CRISPR/cas9 is a more efficient, specific, economic, convenient, and stable technology for knocking down miRNA…

My comment: Their strategy forces the innate immune system to attempt to repair virus-driven DNA damage via replacement with nutrient-dependent RNA-mediated amino acid substitutions. The substitutions  link the sun’s biological / virucidal energy to the creation of nucleic acids and the energy links microRNAs to hydrogen-atom transfer in DNA base pairs via microRNA flanking sequences adhesion proteins and supercoiled DNA via the physiology of reproduction in all living genera. However, currently there is only experimental evidence that links the microRNA flanking sequences to biophysically constrained  RNA-mediated protein folding and all biodiversity found among all invertebrates and vertebrates. All the links from bacteria living in ocean sediments or soil bacteria that Schrodinger claims the sun’s anti-entropic energy from soil bacteria to the answer to his question “What is Life?” have not been fully detailed.
Excerpt:

Indeed, in the case of higher animals we know the kind of orderliness they feed upon well enough, viz. the extremely well-ordered state of matter in more or less complicated organic compounds, which serve them as foodstuffs. After utilizing it they return it in a very much degraded form -not entirely degraded, however, for plants can still make use of it. (These, of course, have their most power supply of ‘negative entropy’ the sunlight)

My comment: However, for comparison to neo-Darwinian theory, Roger Penrose wrote: 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?
Perhaps the most supportive experimental evidence for the role of a creator God is weekend evolution of the bacterial evolution, which is nutrient-dependent and pheromone-controlled. Even if the experimental evidence of the biophysically constrained nutrient-dependent physiology of reproduction cannot yet be extended across species via what is know to serious scientist, the experimental evidence proves that neo-Darwinists are biologically uninformed, or that they don’t want to mention the experimental evidence because it forces them to acknowledge the proof of creation as they continue to try and make all new claims that link metabolic networks to genetic networks in all living genera fit their ridiculous theories.
The ridiculous theories can be compared in the context of the varieties of apples that grow on the same tree to the variety of organisms that link the nutrient-dependent physiology of reproduction from hydrogen-atom energy transfer in DNA base pair in solution to what other organisms must find to eat so that they can reproduce despite the energy theft by viruses that leads to all pathology.

https://www.youtube.com/watch?v=3Ms04x6MvMY

See also: Degradation of Phage Transcripts by CRISPR-Associated RNases Enables Type III CRISPR-Cas Immunity

This article was reported as:

A newly discovered form of immunity helps explain how bacteria fight off viruses

Excerpt:

“Harmful viruses immediately begin replicating, but beneficial ones implant themselves into the bacterial genome,” says Luciano Marraffini, assistant professor and head of the Laboratory of Bacteriology. “By using a wait-and-see approach, and tolerating the initial phase of the infection, the bacteria are able to make an intelligent choice.”

My comment: Intelligent choice appears to be linked to intelligent design of the innate immune system via the sun’s biological energy and the creation of nucleic acids.

Paul Harrington (2006) claims that Roger Penrose in the 1960s attempted to incorporate ‘spin’ into a discrete model of space-time; positing that space-time is created, itself, from underling processes to include helicity. Spin being more ‘primal’ than space. Penrose developed the Twistor Space ‘model’, from a new mathematical entity, the ‘twistor’. Points in Twistor Space (PT) map to lines in conventional space-time. This implied a point is non-local in twistor space. Challenges arose, in adopting ‘primal spin’… that suggest a reading of “The Road to Reality: A Complete guide to the Laws of the Universe

See also:  Re-criticizing RNA-mediated cell evolution: a radical perspective

My comment: Have any other theoretical physicists linked the sun’s biological energy to the theories of neo-Darwinists in an attempt to link physics, chemistry, and conserved molecular mechanisms of biophysically constrained protein folding chemistry to Einstein’s ideas about molecular mechanics and Dobzhansky’s examples of how amino acid substitutions are linked to RNA-mediated cell type differentiation in all living genera? Or is this the only support for my model?


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