Quorum Sensing Determines the Choice of Antiphage Defense Strategy in Vibrio anguillarum

The strategy links the innate immune system to energy-dependent healthy longevity or from virus-driven energy theft to all pathology.

See also: Counting viruses and bacteria in photosynthetic microbial mats.

The ratio has been linked from the sun’s quantized anti-entropic virucidal energy to RNA-mediated DNA repair via hydrogen-atom transfer in DNA base pairs in solution. The energy transfer links the innate immune system and microRNA flanking sequences from angstroms to ecosytems in the context of the physiology of reproduction and supercoiled DNA.

The facts are neo-Darwinian theory killers that have been ignored for more than 20 years. Whose lives did they think they were toying with — besides their own? The Precision Medicine Initative and National Microbiome Initiative have already linked the metabolic networks and genetic networks of all living genera with facts about RNA-mediated protein folding chemistry. It’s biophysically constrained! Surprise! Contraint-breaking mutations cannot be linked to Mutation-Driven Evolution outside the context of mathematical models, definitions and ridiculous assumptions (reported by you with exquisite consistency and clarity).

So now, they plan a meeting; try to quell discussion of virus-driven energy theft and disease and then want to discuss damage control with you.

Get ’em, Suzan!

See also: Histone H3K36 mutations promote sarcomagenesis through altered histone methylation landscape

Reported as:

Missense mutations (that change one amino acid for another) in histone H3 can produce a so-called oncohistone and are found in a number of pediatric cancers. For example, the lysine-36–to-methionine (K36M) mutation is seen in almost all chondroblastomas. Lu et al. show that K36M mutant histones are oncogenic, and they inhibit the normal methylation of this same residue in wild-type H3 histones. The mutant histones also interfere with the normal development of bone-related cells and the deposition of inhibitory chromatin marks.

My  comment: I cannot keep up with the amount of pseudoscientific nonsense that is being touted in the last few attempt to save the careers of those who have placed all virus-driven energy theft into the context of mutations and/or natural selection and evolution.

Today, I found this domain: Oncohistone.com  I suspect it was established to compete with information dissemination at RNA-mediated.com

But why? They are not linking energy-dependent changes in angstroms to ecosystems via RNA-mediated amino acid substitutions. They are not linking virus-driven energy theft to all pathology. They are linking a definition of missense mutations (that change one amino acid for another) to what they expect others to call oncohistones. That will help them continue to link mutations to pathology without linking virus-driven energy theft to the mutations.

I can’t remember if I already posted about that to this blog. But I wanted to ensure I placed it into the context of the domain they established and Suzan Mazur’s update on the Royal Society meeting.

The desperation is showing in every area of research where scientists have clung to definitions and assumptions for far too long.

See for comparison:  MicroRNA-based regulation of epithelial–hybrid–mesenchymal fate determination

Energy-dependent changes in hydrogen-atom transfer in DNA base pairs in solution link microRNA-based regulation of all cell type fate determination to healthy longevity or from virus-driven energy theft to pathology.

In Energy-dependent biodiversity (2) I mentioned this:

All the confusion about linking the mouse model to humans via energy-dependent hydrogen-atom transfer in DNA base pairs, which are linked to supercoiled DNA and protection of organized genomes from virus-driven energy theft and genomic entropy is missing.

My comment: The confusion must be viewed in the context of this article: Structure of the T4 baseplate and its function in triggering sheath contraction

Reported as: How viruses infect bacteria: A tale of a tail

The scientists were also able to identify a minimal set of molecular components in the baseplate that work together like miniature gears to control the activity of the virus’s tail. These components, and the underlying functional mechanism, are the same across many viruses and even bacteria that use similar tail-like structures to inject toxins into neighboring cells.

“These findings are important for our understanding of how these contractile tail-like systems work,” says Leiman. “But they also set a benchmark for the complexity of biological systems that can be described at the atomic level.” The human body contains almost as many bacteria as human cells (30-40 trillion), and the human gut microbiota will likely represent an important target for personalized medicine in the future. “It is clear that we need to understand the detailed mechanisms by which these bacteria interact with each other and how phages are involved in these interactions.”

See also: Evolutionary ‘probables’ a positive step


The new method samples evolutionary histories, called phylogenetic networks, and makes suggested connections between closely related species, or even multiple individuals within species.

“That’s one of the nice things about the Bayesian approach and why we went in that direction,” he said. “We don’t give biologists a single answer. We don’t say, ‘Here’s your optimal evolutionary history.’ We say, ‘Here’s a sample of evolutionary histories the method found while walking the space of possible evolutionary histories.'”

My comment: They don’t say anything about the fact that the history of any species is nutrient energy-dependent and controlled by the physiology of reproduction. If you asked them, they might claim that Mother Nature caused everything to happen automagically.

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