I found this claim in an unpublished blog post from 4/14/15 while attempting to update other posts. Most of more than 1600 are missing the focus keyphrase “microRNA”
…the control of cellular and organism-wide homeostasis by the epigenetic effects that inhibit viral replication (e.g., proper nutrition and social stress inhibition), might be the best approach to prevent our evolution to another species, or our diet-driven and social stress-driven extinction.
In November 2012 I learned everything that happens to organized genomes in all species is microRNA-mediated. That fact eliminated all the gene-centric theories touted by neo-Darwinian theorists. I confirmed the fact with two others who attended the same presentation during the Society for Neuroscience Annual Meeting in New Orleans (2012) – after a speaker answered my question on his presentation.
I asked: Does everything in the genome occur downstream from effects on microRNAs?
I’ve updated the unpublished 2015 post because indexing on 1/2/22 of Analysis of circulating microRNA during early gestation in Japanese black cattle 12/5/21 led me to reexamine the claims in the context of The Bull Sperm MicroRNAome and the Effect of Fescue Toxicosis on Sperm MicroRNA Expression 12/2/14.
Since 1996, I’ve linked our section on molecular epigenetics in From Fertilization to Adult Sexual Behavior to what some people may claim has been unknown about endogenous microRNAs in organized genomes. Indeed, many people do not know how microRNAs biophysically constrained viral latency.
For example see: Howard Berg’s Random Walk through Biology
…flagellar rotation is driven by a proton motive force (14).
Anything driven by a proton motive force is not random. It is driven by God’s Creation of sunlight and humidity, which link pH-dependent supercoiled DNA to naturally attenuated viral endemicity via light-activated microRNA biogenesis in species from cyanobacteria to humans.
In 1996, microRNAs were called pre-mRNAs, which may be a source of confusion for those who have not followed the extant literature. It now includes nearly 133,000 indexed published articles that mention microRNA on PubMed.
Confused researchers have failed to link light-activated microRNA biogenesis from peptide synthesis at the origin of life and visualizing a protonated RNA state that modulates microRNA-21 maturation to Footprints of a Singular 22-Nucleotide RNA Ring at the Origin of Life 4/2/20.
But, I digress. I planned to tell you what I learned about biophysically constraints on viruses in 2012.
See for review: An Intrinsically Disordered Peptide from Ebola Virus VP35 Controls Viral RNA Synthesis by Modulating Nucleoprotein-RNA Interactions 4/9/15
In 2012, I learned that an energy-dependent angstroms to ecosystems approach links a loss of function mutation from highly conserved Tyr21 and His22 to alanine. Still, in 2015 there was no mention of how ecological variation and nutrient-dependent amino acid substitutions are linked to ecological adaptation and virulence manifested in the transmission of the Ebola viruses across species from bats to humans.
Their view of viral RNA templates seems to lack the perspective of how the balance of viral microRNAs and nutrient-dependent microRNAs leads to differentiation of types of viruses in the cell types of their hosts. Two questions arose:
1) Can thermodynamic cycles of protein biosynthesis and degradation continue to be ignored in discussions of viral RNA synthesis and cell type differentiation?
2) Does anyone know how mutations differentiate viruses and their virulence across species?
Long-term potentiation (LTP) is a form of synaptic plasticity that results in enhanced synaptic strength. It is associated with the formation and enlargement of dendritic spines—tiny protrusions accommodating excitatory synapses. Both LTP and spine remodelling are crucial for brain development, cognition and the pathophysiology of neurological disorders. The role of microRNAs (miRNAs) in the maintenance of LTP, however, is not well understood.
Authors in Nature Communications demonstrated that miR-26a and miR-384-5p specifically affect the maintenance, but not induction, of LTP and different stages of spine enlargement by regulating the expression of RSK3. They also examined the global effects of miRNA transcriptome changes during LTP on gene expression and cellular activities.
Their study revealed a novel miRNA-mediated mechanism for gene-specific regulation of translation in LTP. They identified two miRNAs required for long-lasting synaptic and spine plasticity and presents a catalogue of candidate ‘LTP miRNAs’
The link from the anti-entropic energy of the sun to nutrient-dependent microRNA biogenesis and repair of DNA damage by viral microRNAs also link entropic elasticity to the RNA-mediated protein biosynthesis and degradation required for epigenesis and epistasis may be the most important consideration given the obvious links from energy-dependent changes from angstroms to ecosystems via fixation of amino acid substitutions in organized genomes and cell type differentiation.
For instance, see Basis established for nitric oxide joining oxygen and carbon dioxide in respiratory cycle 4/10/15
…examined the respiratory cycle in mice lacking the one amino acid site that carries nitric oxide in their red blood cells. Low and behold, blood flow autoregulation was eliminated entirely – the animals could not oxygenate tissues.
We will probably continue to see examples of how fixation of a single nutrient-dependent RNA-mediated amino acid substitution is epigenetically linked to the stability of organized genomes via the physiology of reproduction until only fools continue to tout the pseudoscientific nonsense about autoregulation, beneficial mutations, and evolution.
They should have stopped doing that in 1973, when Dobzhansky wrote: “…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).
Perhaps theorists didn’t believe Dobzhansky because in the same article he claimed to be a creationist. However, even other serious scientists took longer than most people think it should take before they started “Combating Evolution to Fight Disease” 3/7/14 by examining unsupported claims about billions to millions of years of mutation-driven evolution.
Excerpt from the description: “This new edition of the widely read Evolution in Four Dimensions has been revised to reflect the spate of new discoveries in biology since the book was first published in 2005, offering corrections, an updated bibliography, and a substantial new chapter.” Book excerpt: “What we have just said is very vague and speculative, and based on no evidence whatsoever. The reality is that biologists know so little about how the RNAi system works that it is premature to speculate at all about its origins. However, as with the chromatin-marking EISs, we are reluctant to accept the view that RNAi evolved primarily for genome defense, simply because we see no good reason why it should not have been selected as an epigenetic control system that contributed to cell heredity right from the beginning. “ (p. 327).
My comment: Evolutionary biologists still do not understand how physics and chemistry must be linked to RNA-mediated cell type differentiation via the conserved molecular mechanisms of light-activated top-down causation in all genera. This leads biologically uninformed science idiots to laugh at serious scientists who claim to be “Combating Evolution to Fight Disease” without consideration for what is known about the light-activated fixation of amino acids; the light-activated creation of the humidity-dependent potential of hydrogen (pH); and what is known about how RNA-directed DNA methylation links metabolic networks and genetic networks to fixation of amino acid substitutions in all cell types.
See for instance: Differentially Expressed miRNAs after GnRH Treatment and Their Potential Roles in FSH Regulation in Porcine Anterior Pituitary Cell 2/22/13
Hypothalamic-pituitary-gonadal axis (HPGA) governs almost all mammalian reproduction events, from fetal development, puberty to sexual maturity [1].
Increasing evidences point out Micro-RNAs (miRNAs) as a key regulatory layer that controls gene expression at the post-transcriptional level supporting crucial neurobiological events from the embryonic development to the adulthood but nothing is known about their putative role in the neuroendocrine control of reproduction.
See for comparison: Tuning fertility: miRNA regulation of GnRH genetic network Society for Neuroscience, San Diego, California 11/11/13
Their claim that “…nothing is known about their putative role in the neuroendocrine control of reproduction…” ignores every aspect of the model I have detailed during the past twenty six in a series of published works. A direct link to the abstract from the conference presentation with listed authors Messina, A., Giacobini, P. and Prevot, Vincent is no longer available, but see: A microRNA switch regulates the rise in hypothalamic GnRH production before puberty 5/2/16
Here we report that a multilayered microRNA-operated switch with built-in feedback governs increased GnRH expression during the infantile-to-juvenile transition…
Background: The prenatal migration of gonadotropin-releasing hormone (GnRH) neurosecretory neurons allows nutrients and human pheromones to alter GnRH pulsatility, which modulates the concurrent maturation of the neuroendocrine, reproductive, and central nervous systems, thus influencing the development of ingestive behavior, reproductive sexual behavior, and other behaviors.
Excerpt: “…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.
Skate and coelacanth are the only examples of animals with both type I and II GnRH receptors and all three peptide types, suggesting this was the ancestral condition in vertebrates.
My comment: That suggests a model of chemical ecology could link taxonomy from the coelacanth to the skate via differences and similarities in the amino acid substitutions found in molecules of GnRH and GnRH receptors. The link from the epigenetic landscape to the physical landscape of DNA could be differences in the amino acid substitutions that taxonomically link the organized genomes of species from microbes to man via an extant species, the coelacanth, that researchers thought was extinct. The question arises: If dinosaurs evolved into birds during the past 65 million years, why didn’t all species evolve into other species during the same time? Also, why didn’t bacteria that live in the sediment on the ocean floor evolve during the past 1.8 billion years? See:Sulfur-cycling fossil bacteria from the 1.8-Ga Duck Creek Formation provide promising evidence of evolution’s null hypothesis. 2/17/15
Although the apparent 2-billion-year-long stasis of such sulfur-cycling ecosystems is consistent with the null hypothesis required of Darwinian evolution—if there is no change in the physical-biological environment of a well-adapted ecosystem, its biotic components should similarly remain unchanged…
(click to enlarge)