The tipping point (revisited): SETD2

“Darwin had a huge data set and no mechanism—where would he publish today? This is a problem!” — Arturo Casadevall

Yesterday, it became obvious that Darwin could publish in Nature Genetics.  No problem. These researchers made simplistic unsupported claim and their nonsense passed peer review.

See: SETD2 regulates the maternal epigenome, genomic imprinting and embryonic development (4/29/19)

…chromatin defects, including aberrant imprinting, persist in these embryos, leading to embryonic lethality after implantation. Thus, these data identify SETD2 as a crucial player in establishing the maternal epigenome that in turn controls embryonic development.

They start with the ridiculous claim that the maternal epigenome controls embryonic development. How could it? Their data appear to link the sun’s anti-entropic virucidal energy from the creation of an H3K36me3 methyltransferase to the maternal epigenome.

Their failure to link the creation of sunlight to the energy that links the creation of ATP to the creation of RNA establishes the reason for their failure to understand that top-down causation is energy-dependent.

For comparison, Darwin clearly started with “conditions of life,” which all serious scientists know are energy-dependent and biophysically constrained by the physiology of reproduction.

Evidently, touting nonsense for 160 years is not enough time to get theorists to reconsider their ridiculous claims about the maternal epigenome.

See also: Defining the core essential genome of Pseudomonas aeruginosa (4/29/19)

Abstract excerpt:

…analysis of four strains was typically sufficient in P. aeruginosa to converge on a set of core essential genes likely to be essential across the species across a wide range of conditions relevant to in vivo infection, and thus to represent attractive targets for novel drug discovery.


Importantly, defining the core essential genome for different species will enable comparative genomics studies to understand differing evolutionary or adaptive programs adopted by the different species, and to distinguish targets that may be ideal for species-specific versus broad-spectrum targeting. For important pathogens such as P. aeruginosa, our hope is that defining a core essential genome by selecting diverse strains across its phylogenetic tree will enable more effective discovery and development of much needed antibacterial therapeutics.

For comparison, the core essential genome of Pseudomonas fluorescens exemplifies how the anti-entropic virucidal energy of ultraviolet light, biophysically constrains viral latency via the physiology of pheromone-controlled reproduction.

Moving forward: Virus-Specific Target Capture Coupled with NGS for Rapid and Sensitive Respiratory Virus Detection

The technology allows examination of seasonal respiratory virus genomic variation in the context of ecological variation and adaptations they place back into the context of evolution and the distribution of several respiratory viruses.

“This includes evaluating the match of vaccine to circulating influenza virus strains and the correlation between virus strains and clinical severity of infections. The recently developed Human Pan Viral sequencing methods by Illumina and Twist Bioscience will enable similar studies not only for respiratory viruses, but for all types of human viral pathogens across all sample types of interest.”

This will force all pseudoscientists and other biologically uninformed theorists to place their findings into the context of this fact:

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

See: Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution (2013)

Koel et al. (p. 976) show that major antigenic change can be caused by single amino acid substitutions.

The claim that the change caused by single amino acid substitutions is linked to influenza virus evolution exemplifies human idiocy.  Food odors and pheromones link feedback loops to biophysically constrained viral latency in all living genera. The virus-driven degradation of messenger RNA is  linked to the hecatombic evolution of all diseases. That does not mean the viruses evolve. It means that species sometimes fail to ecologically adapt.

See: Virus-mediated archaeal hecatomb in the deep seafloor and Eukaryotic plankton diversity in the sunlit ocean



Author: James Kohl

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