Genomic surveillance ends our world of RNA-mediated ecological adaptations

By: James V. Kohl | Published on: October 1, 2014

Why is this woman smiling?

1) Identifying Recent Adaptations in Large-Scale Genomic Data

Senior author: Sabeti with co-author Rinn
Excerpt: “As natural selection can only act on mutations that drive phenotypic variation…”.

2) Genomic surveillance elucidates Ebola virus origin and transmission during the 2014 outbreak 

Senior author: Sabeti.
Excerpt: “Because many of the mutations alter protein sequences and other biologically meaningful targets, they should be monitored for impact on diagnostics, vaccines, and therapies critical to outbreak response.”

3) RNA and dynamic nuclear organization

First author Rinn.
Excerpt: “… it is becoming increasingly clear that lncRNAs are important at all levels of nuclear organization—exploiting, driving, and maintaining nuclear compartmentalization.”

4) ‘Oming in on RNA–protein interactions

First author Rinn.
Excerpt: “…the interactions between pre-mRNA and proteins fine-tune alternative splicing in a manner that can gradually create new protein functionalities without the need to create additional genes and without affecting existing proteins [4-6].”
My comment: Evolutionary theorists who think “…natural selection can only act on mutations that drive phenotypic variation…” may not realize that “…the interactions between pre-mRNA and proteins fine-tune alternative splicing in a manner that can gradually create new protein functionalities…” See our section on molecular epigenetics in From Fertilization to Adult Sexual Behavior “Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation…” (e.g., of cell types in species from yeasts to man).
Serious scientists may realize, too late, that nutrient-dependent RNA-directed DNA methylation — and pre-mRNA-mediated events that lead to mRNA-mediated amino acid substitutions — differentiate all cell types in all individuals of all living species. For example, without thinking, the non-living Ebola viruses may ecologically adapt with as little as a single amino acid substitution, like the one that differentiates all cell types of humans from chimpanzees and gorillas.
See: “…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.” Dobzhansky (1973).
What evolutionary theorists continue to think about natural selection acting on mutations that lead to the evolution of biodiversity will not matter if the Ebola viruses destroy humanity. People may ask as our species dies out: “What were the evolutionists thinking? Did they not know that Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution?
Did the theorists never ask: How does epistasis arise from an evolutionary process that is conceived as proceeding through the incremental accumulation of mutations?
Does any serious scientist still think that the accumulation of mutations leads to increasing organismal complexity? How could that happen?
Biophysically-constrained receptor-mediated nutrient-dependent pheromone-controlled ecological adaptations link the physiology of reproduction to behavioral phenotypes and morphological phenotypes in all living species based on the molecular mechanisms conserved in viruses.
Is there another model for that? Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems. See also: Origin of group identity: viruses, addiction and cooperation


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