MicroRNA are very mysterious. They are really relics of the RNA world—pieces of RNA that are highly reactive, very small and which pair and bind other RNA and facilitate catalytic reactions,” Mangone says. “We don’t know much about them—where they come from or how they regulate gene expression, but they are very misregulated in many diseases.
See also: Nutrient-dependent/pheromone-controlled adaptive evolution: a model Published 14 Jun 2013
…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.
My comment: Only if you lived among wolves or among theorists for the past 10 years would you not know that more than 55,000 indexed publications link energy-dependent changes in the microRNA/messenger RNA balance to healthy longevity. For comparison, all serious scientists also know that virus-driven energy theft links viral microRNAs from mutations to all pathology.
You need only search for “RNA mediated” to find information on how cellular and viral microRNAs are linked from energy-dependent changes to RNA-mediated amino acid substitutions and biophysically constrained protein folding chemistry. For example, this is all it takes to recognize the amount of pseudoscience that is packaged in claims that we don’t know much about microRNAs.
See also: Published to Figshare 10 April 2014
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.
The ubiquity of miRNA occurrence is reflected in the current literature, which reports a wide range of potential biomarker applications for this highly conserved molecule.
My comment: MicroRNAs are biomarkers that clearly link energy-dependent biophysically constrained changes in base pairs from RNA-mediated amino acid substitutions to cell type differentiation in all living genera. The energy-dependent links from the innate immune system to the physiology of reproduction also link all metabolic networks to all genetic networks in species from microbes to humans.
…we hypothesize that the novel, human-specific C-terminal sequence of modern ARHGAP11B has a key role in the mechanism by which this protein promotes BP amplification. In this regard, the present data show that this sequence is due to a single C→G base substitution, which creates a novel splice donor site that results in the replacement of the ancestral C-terminal sequence of the ARHGAP11B GAP domain. The present data also demonstrate that this single C→G base substitution underlies the ARHGAP11B-mediated BP amplification implicated in neocortex expansion.
A single base change in a human gene likely played an important role in evolutionary expansion of the human brain, researchers say.
My comment: They claim that a single cytosine to guanine substitution created a novel splice site. They failed to mention that base pair (BP) amplification is nutrient energy-dependent. They also failed to mention that the de novo creation of a novel splice donor site must be linked from the energy-dependent fixation of an RNA-mediated amino acid substitution to the physical landscape of supercoiled DNA via the physiology of reproduction.
Svante Paabo is one of the co-authors who reported this:
Hence, it is not the ARHGAP11 partial gene duplication event ~5 million years ago, as such, that impacted human neocortex evolution. Presumably, ARHGAP11A and ancestral ARHGAP11B coexisted as functionally similar proteins for some time after the gene duplication event. The ability of ARHGAP11B to amplify BPs likely arose more recently from a change that is tiny on a genomic scale but substantial in its functional and evolutionary consequences.
My comment: No experimental evidence of biologically-based cause and effect suggests that any partial gene duplication event ~5 million years ago could have linked a mutation and the altered de novo creation of genes that Svante Paabo (and co-authors) placed into the context of biophysically constrained biodiversity in:
My comment: Natural selection for energy-dependent codon optimality is the only way to link the de novo creation of genes from autophagy to RNA-mediated amino acid substitutions and nutrient-dependent polycombic ecological adaptation.
Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes (Saunders, Chue, Goebl, Craig, Clark, Powers, Eissenberg, Elgin, Rothfield, and Earnshaw, 1993; Singh, Miller, Pearce, Kothary, Burton, Paro, James, and Gaunt, 1991; Trofatter, Long, Murrell, Stotler, Gusella, and Buckler, 1995). 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.
…the two paralogs displayed similar RNA binding across the transcriptome, indicating that their differential targeting does not derive from their RNA interactions, but from possible different cofactor interactions.
My comment: The cofactors are nutrient energy-dependent microRNAs, which are linked to healthy longevity and all biodiversity and viral microRNAs, which are linked from mutations to all pathology.
…viral miRNAs may be particularly important for regulating the transition from latent to lytic replication and for attenuating potentially inhibitory host antiviral immune responses.
…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).”
…carbon either attenuated or potentiated light repression of ASN1 in light-grown plants. These studies indicate the interaction of carbon with blue, red, and far-red-light signaling and set the stage for further investigation into modeling this complex web of interacting pathways using systems biology approaches.
My comment: When did theorists decide to take the light as information and energy out of systems biology and ecological adaptations? Who decided to replace the anti-entropic virucidal energy of light with mutations and evolution?