…an unexpected new biology that provides the code, the software for turning off cancer,” says the study’s senior investigator, Panos Anastasiadis, Ph.D., chair of the Department of Cancer Biology on Mayo Clinic’s Florida campus.
That code was unraveled by the discovery that adhesion proteins — the glue that keeps cells together — interact with the microprocessor, a key player in the production of molecules called microRNAs (miRNAs). The miRNAs orchestrate whole cellular programs by simultaneously regulating expression of a group of genes.
My comment: The nutrient-dependent microRNA/messenger RNA balance links viral microRNAs from perturbed protein folding to pathology. It also links nutritional epigenetics and pharmacognomics via what is currently known about the biophysically constrained chemistry of RNA-mediated gene duplication and thermodynamic cycles of RNA-mediated protein biosynthesis and degradation, which are perturbed by viruses and linked to all pathologies.
The Mayo Clinic appears to be making rapid advances based on what is known about links from viruses to pathology, which typically is biophysically constrained by nutrient-dependent microRNAs during thermodynamic cycles of RNA-mediated protein biosynthesis and degradation.
The cycles link the conserved molecular mechanisms of RNA-mediated gene duplication and amino acid substitutions to cell type differentiation in all cell types in all individuals of all living genera via the physiology of reproduction.
The physiology of reproduction links the epigenetic landscape to the physical landscape of DNA via metabolic networks and genetic networks that link nutritional epigenetics to pharmacogenomics via changes in the microRNA/messenger RNA balance that alter RNA-mediated protein folding.
In an invited review of nutritional epigenetics, I linked atoms to ecosystems via microRNAs.
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.
Bisphenol A (BPA) inhibits the methylation of imprinted genes during oogenesis [74,75] and affects the expression of microRNA targeting SOX family genes , while the endocrine disruptor and pesticide Methoxychlor leads to hypermethylation of Esr2 and induces Dnmt3b expression in the ovary .
My comment: Not surprisingly, both articles cite Zhang, L.; Hou, D.; Chen, X.; Li, D.; Zhu, L.; Zhang, Y.; Li, J.; Bian, Z.; Liang, X.; Cai, X.; et al. Exogenous plant MIR168a specifically targets mammalian LDLRAP1: Evidence of cross-kingdom regulation by microRNA. Cell Res. 2012, 22, 107–126.
In the invited review requested by the senior author of Insights from Space: Potential Role of Diet in the Spatial Organization of Chromosomes, I wrote:
… the finding that plant miRNAs are stable in the blood and other tissues of mice and humans (L. Zhang et al., 2012) establishes what appears to be an across-species causal link from the diversity of microbes such as bacteria and yeasts (Taylor et al., 2013) to nutrient-dependent epigenetically-effected changes in the miRNA/mRNA balance and the diversity of plants and animals (Coley & Kursar, 2014).
That places the findings from Mayo and the details from my invited review into the context of nutrient-dependent microRNAs and “Laws of Biology” that link the Laws of Physics to nutrient-dependent cell type differentiation via the RNA-mediated chemistry of protein folding, which is perturbed by the accumulation of viral microRNAs. The viral microRNAs are consistently linked to pathology in all genera. Focus on inhibition of methylation of imprinted genes by BPA during oogenesis in the context of affects on the expression of microRNA, fails to link nutrients to their anti-entropic effects on genomic stability. The focus on affects also might confuse serious scientists who know the difference between an epigenetic effect on gene expression and an affect on anything that occurs after the effect.
For example, the new discovery that cell type differentiation is linked to biologically-based cause and effect via signaling between microRNAs and cell adhesion molecules, was readily predicted by everything currently known about physics, chemistry, and the conserved molecular mechanisms of cell type differentiation in all genera.
See for example: Nutrient-dependent / Pheromone-controlled thermodynamics and thermoregulation: (a mammalian model of thermodynamics and organism-level thermoregulation) or this brief video representation from my presentation.
The role of viruses in pathology continues to be virtually ignored by researchers who don’t know the difference between effect and affect, and by those who do. For example, effects link atoms to ecosystems in the context of affects on the behavior of cell types and organisms.
See for examples:
…large-scale studies have revealed that many host miRNAs are modulated by the virus in order to accomplish its persistence, while other miRNAs are modulated by the host in order to achieve viral clearance.
…these mites act as incubators and potent vectors for honey bee viruses, hence, they have fostered the spread of virulent strains of the bees’ viruses6.
Helicobacter pylori is the principal cause of gastric cancer, the second leading cause of cancer mortality worldwide. However, H. pylori prevalence generally does not predict cancer incidence.
My comment: In my model, ecological adaptation to the viruses in the gut bacteria of invertebrates and vertebrates determines whether the nutrient-dependent anti-entropic effects of microRNAs has altered organism-level thermoregulation to enable protection from pathology that is caused by the accumulation of viruses and viral microRNAs.
The model also links the microbes that nematodes eat to differences in morphological and behavioral phenotypes via their pheromone-controlled physiology of reproduction, which is linked to all extant biodiversity via niche construction that includes ecological, social, neurogenic, and socia-cognitive niche construction.
THIS MODEL DETAILS HOW CHEMICAL ECOLOGY DRIVES ADAPTIVE EVOLUTION VIA: (1) ecological niche construction, (2) social niche construction, (3) neurogenic niche construction, and (4) socio-cognitive niche construction.
My comment: For a ridiculous misrepresentation of everything known about biophysically constrained cell type differentiation, see: The Shaping of Modern Human Immune Systems by Multiregional Admixture with Archaic Humans (2011)
…adaptive introgression of archaic alleles has significantly shaped modern human immune systems.
My comment: It is amazing that anyone could make such a ridiculous claim — even 4 years ago. The immune system adapts to ecological changes via nutrient-dependent gene duplication and fixation of amino acid substitutions in alleles that occurs in the context of RNA-mediated protein folding and the physiology of reproduction that links nutritional epigenetics and pharmacogenomics in this video representation, which is also from the Mayo Clinic.