Weaponized health communication (4)

Periodic links Subatomic to Cytosis for ages 10+

See: Weaponized health communication (3)

What a lot of people seem to forget on twitter is that people are watching. The point isn’t to argue with one person and get them to change their mind – you won’t. The point is about how the exchange appears to the far larger numbers who see it but don’t participate. 7/18/19

My blog posts are seen in the context of Tweets that make impressions on ~10K people each day as I continue to link light-activated global biogeochemical cycles of protein folding chemistry to every aspect of microRNA-mediated cell type differentiation form alternative splicings of messenger RNA to peptide-dependent health or from the virus-driven degradation of messenger RNA to all pathology.

See for instance: A human-specific switch of alternatively spliced AFMID isoforms contributes to TP53 mutations and tumor recurrence in hepatocellular carcinoma 3/1/18

Pre-mRNA splicing can contribute to the switch of cell identity that occurs in carcinogenesis.

For comparison, see the molecular epigenetics section of our 1996 Hormones and Behavior review of cell type differentiation. From Fertilization to Adult Sexual Behavior.

Our focus was on the sexual differentiation of cell types and we linked alternative splicings of pre-mRNAs to all biodiversity in species from yeasts to humans.

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 (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.

Human sex differences that obviously arise in the context of the food energy-dependent pheromone-controlled physiology of reproduction have been reported to have two different origins.

Light-activated phototropism and microRNA-mediated sex differences in mammals can be compared to claims about ecologically relevant magic traits in two published works, one from July 2019 and one from February 2019.

1) Conservation, acquisition, and functional impact of sex-biased gene expression in mammals 7/19/19

A survey of sex differences in gene expression using RNA sequencing data (left) leads to the discovery of both conserved (species-shared) and lineage- or species-specific sex biases in expression across the genome. Genes with conserved sex bias contribute to the sex difference in mean height in humans and other mammals, whereas lineage-specific changes can be partially explained by gains and losses of motifs for sex-biased TFs.

The authors linked food energy and the pheromone-controlled physiology of reproduction from our claims about RNA-mediated sexual differentiation in  Drosophila melanogaster and Caenorhabditis elegans to the gains and losses of motifs for sex-biased TFs.What’s a motif? What’s a TF.

Simply put the sex-biased TFs are biophysically constrained by what organisms eat and the fixation of RNA-mediated amino acid substitutions in the context of the transgenerational epigenetic inheritance of all morphological and behavioral phenotypes.

See for comparison:

2) Genetic dissection of assortative mating behavior 2/7/19

Ecologically relevant mating cues (sometimes known as “magic traits” [2,6]) are now predicted to be widespread in nature [6,7], and the last few years have seen considerable progress in our understanding of their genetic basis.

The authors claimed that sex differences automagically arose in the context of mating cues linked to the genetic basis of “magic traits.”

In our 1996 Hormones and Behavior review of RNA-mediated cell type differentiation, we included this claim:

Parenthetically it is interesting to note even the yeast Saccharomyces cerevisiae has a gene-based equivalent of sexual orientation (i.e., a-factor and alpha-factor physiologies). These differences arise from different epigenetic modifications of an otherwise identical MAT locus (Runge and Zakian, 1996; Wu and Haber, 1995).

The light-activated assembly of the microRNA-RNA-peptide nanocomplex has since been linked from claims about eukaryotic biodiversity in Eukaryotic plankton diversity in the sunlit ocean 5/22/15 and Virus-mediated archaeal hecatomb in the deep seafloor 10/12/16 to Spindle-shaped viruses infect marine ammonia-oxidizing thaumarchaea 7/18/19

The viral predation in thaumarchaea has forced all neo-Darwinian theorists to reinvent their claims in the context of facts about biophysically constrained viral latency.

See also:  A zoooviral human pathogen emerged through genomic recombination amongst human and nonhuman simian hosts 6/26/19

…recently isolated simian adenoviruses that contain cross-species genome recombination events from three hosts: human, chimpanzee, and bonobo. Zoonosis (nonhuman to human transmission) and anthroponosis (human to nonhuman transmission) may play significant roles in the emergence of human adenoviral pathogens.

More than 1800 human hemoglobin variants link the claims of Dobzhansky (1973) to biophysically constrained viral latency and sympatric speciation in all living genera via this fact from Nothing in Biology Makes Any Sense Except in the Light of Evolution

For example, the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla (p. 127).”

Isn’t it time for you to join others who are Combating Evolution to Fight Disease 3/7/14 by learning how to link what organisms eat and their physiology of pheromone-controlled reproduction to mate choice in human populations from all over the world via fixation of RNA-mediated amino acid substitutions. Isn’t it time you stopped calling amino acid substitutions “mutations?”

See: HbVar: A Database of Human Hemoglobin Variants and Thalassemias

Author: James Kohl

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