microRNAs, glycosylation, and genomes

By: James V. Kohl | Published on: May 29, 2015

Summary: Given what is currently known about RNA-mediated cell type differentiation in all genera, it may be impossible for theorists to link mutations to evolution via glycosylation.

miRNA proxy approach reveals hidden functions of glycosylation

Abstract excerpt: Glycosylation, the most abundant posttranslational modification, holds an unprecedented capacity for altering biological function.
Journal article excerpt:

…glycans play a role in every major disease (1), and there are clinical examples of drugs targeting glycosylation enzymes… suggesting that glycosylation enzymes may provide fallow ground for drug development. Multiple biological pathways governed by different miRNA often are involved in disease processes. Our approach enables these miRNA networks to be leveraged to yield the most critical enzymes to target in a disease state.

Reported as:  Micro RNA Decoy Reveals Hidden Function of Glycosylation

Posted by Science Mission on Thursday, May 28, 2015


This work indicates that miRNA can act as a relatively simple proxy to decrypt which glycogenes, including those encoding difficult-to analyze structures (e.g., proteoglycans, glycolipids), are functionally important in a biological pathway, setting the stage for the rapid identification of glycosylation enzymes driving disease states.

My comment: Misrepresentations of biologically-based cause and effect are common among theorists. MicroRNAs do not automagically emerge, which means that glycosylation enzymes cannot drive disease states. Serious scientists have provided details that link nutrient-dependent microRNAs to glycosylation. The detailed links between metabolic networks and genetic networks are responsible for cell type differentiation in all genera.
The light-induced de novo creation of amino acids is linked to the nutrient-dependent creation of microRNAs that alter RNA-directed DNA methylation and RNA-mediated amino acid substitutions. The substitutions link nutrient energy from the sun to its epigenetic effects on base pairs and to the differentiation of all cell types in all individuals of all genera via their physiology of reproduction.  Fixation of beneficial amino acid substitutions links the physiology of reproduction to all of extant biodiversity. Fixation is manifested in morphological and behavioral phenotypes as individual differences; population-wide differences; and species-specific differences.
Viral microRNAs appear to be “reminders” of the creation of nutrient-dependent microRNAs.  They link entropic elasticity to genomic entropy via perturbed protein folding and mutations when nutrient stress and/or social stress cause uncompensated changes in the thermodynamic cycles of protein biosynthesis and degradation that are typically controlled by nutrient-dependent microRNAs. The nutrient-dependent microRNAs enable DNA organization via organism-level thermoregulation.
Proper control of DNA organization by nutrient-dependent microRNAs is an essential aspect of life on this planet. Without the finely-tuned balance of nutrient-dependent microRNAs and viral microRNAs, nothing would prevent virus-driven genomic entropy. Instead, viruses and mutations would lead from ecological variation to to mass extinctions associated with failed adaptations of individuals, populations, and species.
Hugo de Vries definition of “mutation”  and assumptions about the time it might take for one species to evolve into another have not been placed into the context of glycosylation by population geneticists. Like other evolutionary theorists, they simply assumed mutations could somehow link perturbed protein folding in individuals to the biodiversity of species.
See for example: Mutation-Driven Evolution

Selective advantage of the mutation is determined by the type of DNA change, and therefore natural selection is an evolutionary process initiated by mutation. It does not have any creative power in contrast to the statements made by some authors” (p. 196).

The light-induced creation of amino acids is linked from RNA-mediated amino acid substitutions and the creation of new genes.

Nutrient-dependent/pheromone-controlled adaptive evolution: a model.


the epigenetic ‘tweaking’ of the immense gene networks that occurs via exposure to nutrient chemicals and pheromones can now be modeled in the context of the microRNA/messenger RNA balance, receptor-mediated intracellular signaling, and the stochastic gene expression required for nutrient-dependent pheromone-controlled adaptive evolution. The role of the microRNA/messenger RNA balance (Breen, Kemena, Vlasov, Notredame, & Kondrashov, 2012; Duvarci, Nader, & LeDoux, 2008; Griggs et al., 2013; Monahan & Lomvardas, 2012) in adaptive evolution will certainly be discussed in published works that will follow.

Serious scientists can now compare what is known about physics, chemistry, and molecular biology to the misrepresentations of theorists who have claimed that mutations link biologically-based cause and effect. Given what is currently known about RNA-mediated cell type differentiation in all genera, it may be impossible for theorists to link mutations to evolution via glycosylation.
It will be interesting to see them try, or to watch them continue to ignore what is already known.
See also:

Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems

This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent pheromone-controlled ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity in species from microbes to man. Species diversity is a biologically-based nutrient-dependent morphological fact and species-specific pheromones control the physiology of reproduction. The reciprocal relationships of species-typical nutrient-dependent morphological and behavioral diversity are enabled by pheromone-controlled reproduction. Ecological variations and biophysically constrained natural selection of nutrients cause the behaviors that enable ecological adaptations. Species diversity is ecologically validated proof-of-concept. Ideas from population genetics, which exclude ecological factors, are integrated with an experimental evidence-based approach that establishes what is currently known. This is known: Olfactory/pheromonal input links food odors and social odors from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man during their development.

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