Light and life at base pair resolution (5)

By: James V. Kohl | Published on: January 1, 2019

Summary: Bayesian models exist only outside the context of food energy-dependent pheromone-controlled biophysically constrained viral latency and sympatric speciation. The Bayesian models will continue to be eliminated by facts about how energy must be linked to ecological adaptations and how the virus-driven degradation of messenger RNA has been linked to all pathology.
Follow-ups to the December 4, 2018 publication of:  A comparison of gene expression and DNA methylation patterns across tissues and species
I asked: Who decided to obfuscate the claims about natural selection for food energy-dependent codon optimality and put fixation of amino acid substitutions back into the context of evolutionary processes that automagically led to biophysically constrained adaptations in humans?
I asked before I found the collaborated efforts to obfuscate the role of ecological adaptation via the overlap of authors on: Reorganization of 3D Genome Structure May Contribute to Gene Regulatory Evolution in Primates (11/20/18)

…an understanding of 3D genome reorganization is key to explaining regulatory evolution.

Genome organization is energy-dependent and pheromones biophysically constrain ecological adaptations in species from microbes to humans. There is no such thing as regulatory evolution outside the context of regulation that prevents the virus-driven degradation of messenger RNA.
See: Nutrient-dependent Pheromone-Controlled Ecological Adaptations: From Angstroms to Ecosystems 4/18/18
For comparison, Yoav Gilad’s group is very motivated to attempt to change past claims about evolution to new claims about ecological adaptation. Ecological adaptations can be viewed in the context of another instance of overlap among authors.
Ssee: Natural Selection on the Olfactory Receptor Gene Family in Humans and Chimpanzees (2003)
Further studies of specific OR gene clusters in humans may identify the selected changes and shed light on what olfactory stimuli have exercised selective pressures on the human OR gene repertoire.
See also: Loss of Olfactory Receptor Genes Coincides with the Acquisition of Full Trichromatic Vision in Primates (2004)
Linking the loss or receptors to trichromatic vision is another way to link the virus-driven degradation of messenger RNA that causes the loss of genes to evolution via the fossil record.
See: Genomics: ENCODE explained (2012, subscription required) Yoav Gilad joined forces with Jonathan K. Pritchard and Joseph Ecker.
This was reported in Science Magazine as: ENCODE Project Writes Eulogy for Junk DNA
All of my past comments to Science and many other publications have been removed along with the comments of others. Their support for neo-Darwinian pseudoscientific nonsense trumps facts. That’s why Penissi reported the eulogy was for junk DNA, in the context of ridiculous claims about promoters and more distal elements, such as enhancers, which automagically communicate their regulatory information to each other outside the context of  the biophysically constrained linear organization of genes and transcripts on chromosomes that links energy-dependent networks of  chromosome loops and twists to all biodiversity in species from microbes to humans via light-activated microRNA biogenesis in plants.
For example, I wrote (what can no longer be found)

Isn’t the concept that is extended the one that involves the epigenetic “tweaking” of immense gene networks in ‘superorganisms’ that ‘solve problems through the exchange and the selective cancellation and modification of signals? For example, we’ve known that nutrient chemicals epigenetically effect intracellular signaling and stochastic gene expression and that pheromones do this also. Nutrient chemicals are required for individual survival and their metabolism to pheromones controls reproduction. If their epigenetic effects on stochastic gene expression was not responsible for de novo gene expression (e.g., for new odor receptors), we would have nothing but a theory of random mutations to explain species diversity that is obviously dependent on nutrition and species-specific pheromones for ecological, social, neurogenic, and socio-cognitive niche construction via adaptive evolution in species from microbes to man. Indeed, until now we have had only a theory to compare to the biological facts of evolved gene, cell, tissue, organ, organ system reciprocity, which is obviously due to the epigenetic “tweaking” of immense gene networks by nutrient chemicals and pheromones.

In 2016, Pritchard and Gilad teamed up again. See: RNA splicing is a primary link between genetic variation and disease (paywalled)

These splicing QTLs are major contributors to complex traits, roughly on a par with variants that affect gene expression levels. Our study provides a comprehensive view of the mechanisms linking genetic variation to variation in human gene regulation.

They twisted everything known about food energy-dependent alternative splicings of pre-mRNA and the expression of RNA-mediated amino acid substitutions into a horrid misrepresentation of how splicing QTLs contribute to complex traits. Indeed, they found no food energy-dependent enrichment of predicted splicing variants among signals identified in GWASs.
But now, every other serious scientist knows why they did not find what they were not looking for in the context of no hypothesis and no model.
See: False positives in trans-eQTL and co-expression analyses arising from RNA-sequencing alignment errors [version 1; referees: awaiting peer review] Alexis Batttle

Sequence similarity among distinct genomic regions can lead to errors in alignment of short reads from next-generation sequencing. While this is well known, the downstream consequences of misalignment have not been fully characterized.

The downstream consequences were predictable. The authors limit the use of mathematical models and suggest that only biologically uninformed theorists have used mathematical models in the past.
See also: Impact of regulatory variation from RNA to protein (2015) Alexis Batttle is the first author Yoav Gilad is the senior author. Jonathan K. Pritchard is a co-author.
They linked nutrient-uptake from seemingly futile thermodynamic cycles of protein biosynthesis and degradation via changes in the microRNA/messenger RNA balance and alternative splicings of pre-mRNAs, which are also known as microRNAs. But they will not use the term microRNA.  If they did, it would clarify the fact that nutrient uptake is anti-entropic and virucidal in the context of the creation of olfactory receptor genes that lead to increasing organismal complexity.
See also: Allele-specific expression reveals interactions between genetic variation and environment (2017) Alexis Batttle is the senior author

We have developed EAGLE, a hierarchical Bayesian model for identifying GxE interactions based on associations between environmental variables and allele-specific expression.

Bayesian models exist only outside the context of food energy-dependent pheromone-controlled biophysically constrained viral latency and sympatric speciation. The Bayesian models will continue to be eliminated by facts about how energy must be linked to ecological adaptations and how the virus-driven degradation of messenger RNA has been linked to all pathology.

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