Pathology constrains X-linked evolution

Long-range evolutionary constraints reveal cis-regulatory interactions on the human X chromosome

Excerpt: “Experimental methods are already able to indicate the interactions between enhancers and genes8, 13, 17, 18, 19 but they are strongly constrained by the tissue and time where and when the interaction takes place. In contrast, evolutionary linkage is independent of the tissue or time of expression of the gene, and is applicable to any sequenced vertebrate genome, as it was done here for human.”
My comment: Experimental evidence of nutrient-dependent RNA-mediated amino acid substitutions can now be compared to evolutionary linkages in the context of theories about mutations and natural selection. The ridiculous theories ignore the biophysically constrained chemistry of nutrient-dependent protein biosynthesis and degradation that links metabolic networks and genetic networks via gene expression to differentiation of cell types in different tissues.
Reported as:

DNA study could shed light on how genetic faults trigger disease

Excerpt: “A new technique that identifies how genes are controlled could help scientists spot errors in the genetic code which trigger disease, a study suggests.
The method focusses on those parts of DNA – known as enhancer regions – which regulate the activity of genes and direct the production of proteins that have key functions within the body.”
My comment:  See also: 1) Endogenous retroviruses function as species-specific enhancer elements in the placenta cited in 2) Viral Genome Junk Is Bunk 
1) “…species-specific ERVs contribute to the rapid divergence of the placental gene regulatory network. ERVs have affected diverse aspects of mammalian biology17,28,29, and have been influential in shaping placental evolution by contributing viral proteins that mediate placental growth, immunosuppression, and cell fusion30.”
2) “…RNA viruses got their genes from their hosts.”
Evolutionary constraints reportedly limit interactions that are reported in in the context of evolutionary linkages. There are no evolutionary linkages when the tissue in which genes are expressed and the time of their expression of the gene are applicable to sequenced vertebrate genomes. Instead, the sequenced genomes exemplify nutrient-dependent pheromone-controlled ecological adaptations in all vertebrates.
The link from  human endogenous retroviruses (HERVs) and viral proteins to nutrient-dependent RNA-directed DNA methylation and the anti-entropic effects of RNA-mediated amino acid substitutions is clear. It would be clearer if what is known about epigenetic effects on cell type differentiation via substitution of the amino acid glycine in the GnRH decapeptide of all vertebrates was not obscured by the use of terms in unusual contexts.
Genetic faults trigger disease, not evolution. Mutations do not link ecological variation to ecological adaptation in any individual of any species. In all vertebrates, substitution of achiral glycine in the GnRH decapetide appears to link other nutrient-dependent pheromone-controlled RNA-mediated amino acid substitutions to the biodiversity of morphological and behavioral phenotypes via metabolic networks linked to genetic networks.

Add a Comment

Your email address will not be published. Required fields are marked *