Energy-dependent RNA methylation (6)
After I published Nutrient-dependent/pheromone-controlled adaptive evolution: a model, Lynnette Ferguson and Justin O’Sullivan invited me to submit this review of nutritional epigenetics for inclusion in a special issue of the journal “Nutrients.”
Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems (April 10, 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. 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.
My comment: My invited review was promptly returned without review. That’s why I published my review to the figshare.com site. I realized that the guest editors had “baited” me so that I would supply the latest information to them. Here are some examples of how the information was used by Lynnette Ferguson.
The Interaction between Epigenetics, Nutrition and the Development of Cancer (2015) Received 28 July 2014. This article belongs to the Special Issue Nutritional Epigenetics
The epigenetic modifications investigated include DNA methylation, histone modifications and the influence of microRNAs.
…it is imperative to understand the implications of diet on epigenetic modifications, and the effect of those modifications on the development of cancer today and in future generations. Such an understanding and an appropriate resultant response would help decrease the level of risk in future generations.
My comment: Claiming that interactions occur does nothing to explain cause and effect. Ferguson co-authored an article that took my explanations out of their context and put them back into the context of theories about interactions that have no explanatory power.
For comparison, see: Role of olfaction in Octopus vulgaris reproduction (18 October 2014)
Future work on O. vulgaris olfaction must also consider how animals acquire the odours detected by the olfactory organ and what kind of odour the olfactory organ perceives. The OL acting as control centre may be target organ for metabolic hormones such as leptin like and insulin like peptides, and olfactory organ could exert regulatory action on the OL via epigenetic effects of nutrients and pheromones on gene expression (Kohl, 2013; Elekonich and Robinson, 2000).
My comment: The authors linked the claims from my 2013 review to their experimental evidence of biologically-based cause and effect. It took only one citation to my published 2013 review by ethical researchers (Polese, Bertapelle & Di Cosmo) to defeat the attempts of people who attempted to steal the information and use it without attribution — as if it supported their ridiculous theories.
However, in this case, Eleckonich and Robinson (2000) had also cited our 1996 Hormones and Behavior review of RNA-mediated cell type differentiation: From Fertilization to Adult Sexual Behavior. We included a section on molecular epigenetics that linked microRNAs, which at the time were called pre-mRNAs, to the physiology of reproduction in yeasts, all invertebrates, and all vertebrates. When they cited my 2013 review and Elekonich and Robinson (2000), Polese, Bertapelle & Di Cosmo (2015) established a context-based history of advances in understanding molecular epigenetics.
For contrast, Lynnette Ferguson has repeatedly attempted to sneak though the back door of serious scientists with this article: Genomic instability in human cancer: Molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition and this comment from Are We Eating Our Way to Prostate Cancer—A Hypothesis Based on the Evolution, Bioaccumulation, and Interspecific Transfer of miR-150
The discovery of miRNA in sperm effectively overshadowed the previous experimental findings that worms and plants used miRNA in a transgenerational inheritance pattern , as it indicated that mammalian miRNAs evolved from other mammals, mimicking their divergent inheritance pattern. There is another seemingly neglected mechanism of miRNA inheritance—which is of paramount importance in the context of miR-150 and oncogenesis—can plant miRNA be recognized and allowed to play epigenetic roles by the mammalian immune system upon oral ingestion? . The discovery that miRNA evolution is linked to complex food web interactions is crucial to our current knowledge, as it involves miRNA in the nutrigenomics of oncogenesis (Figure 2).
See for comparison: The Bull Sperm MicroRNAome and the Effect of Fescue Toxicosis on Sperm MicroRNA Expression (Dec 2, 2014).
In the context of my 2013 review, the authors helped to establish facts about RNA-mediated cell type differentiation that we presented in our 1996 review. They linked Einstein’s claims from Schrodinger’s claims (1944) to Dobzhansky’s claims (1973) about amino acid substitutions.
The claims about energy-dependent RNA-mediated amino acid substitutions are still being ignored by most theorists. After it became clear that biologically uninformed pseudoscientists would continue stealing information from me and begin linking the information on microRNAs to amino acids and cancer, I decided to forgo further attempts to publish in journals.
In February 2015, I founded this domain: RNA-mediated.com and the FB discussion group: RNAmediated. I’ve continued to disseminate facts about energy-dependent cell type differentiation that you are not likely to see represented anywhere else, until after I have detailed them.
I also prepared and presented several poster sessions with recorded narratives that are available from Labroots conferences with the following themes.
Neuroscience: From hydrogen atom transfer in DNA base pairs to ecosystems (March 2, 2016)
This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on DNA base pairs in solution and RNA-mediated amino acid substitutions to chromosomal rearrangements via pheromone-controlled changes in the microRNA / messenger RNA balance.
Neuroscience: RNA mediated molecular epigenetics and virus driven entropy (March 2, 2016)
Energy-dependent molecular epigenetics support Einstein’s complete molecular mechanical theory via established links from microRNA flanking sequences to DNA base pair substitutions and amino acid substitutions in adhesion proteins.
Molecular Diagnostics What is life when it is not protected from virus driven entropy (March 30, 2016)
The anti-entropic force of virucidal ultraviolet light links guanine–cytosine (G⋅C) Watson–Crick base pairing from hydrogen-atom transfer in DNA base pairs in solution to supercoiled DNA, which protects the organized genomes of all living genera from virus-driven entropy.
Genetics and Genomics RNA-mediated physics, chemistry, and molecular epigenetics (May 3, 2016)
Olfaction and the innate immune system link energy as information from the epigenetic landscape to the physical landscape of supercoiled DNA.
See also: Endogenous retroviruses function as species-specific enhancer elements in the placenta (February 10, 2013)
We speculate that ERV variation, exposed by the permissive epigenetic state within the placenta, allows the fetus increased evolvability against maternal defenses. Specifically, by relaxing epigenetic repression of ERV activity, the placenta gains access to a highly polymorphic source of enhancer elements that may dramatically influence its developmental phenotype (Fig. S5). As the placenta is a transient organ, the long-term advantage conferred by increased developmental evolvability would outweigh the potentially mutagenic effects of ERV activity. We propose this model as a plausible explanation for the persistence of placenta-specific ERV activity, which has been observed in all major mammalian taxa31.
My comment: Developmental phenotypes are energy-dependent in all living genera. After I was alerted to more recent claims about virus-driven pathology, my focus changed from energy-dependent RNA-mediated cell type differentiation to nutrient energy-dependent protection of complex functional structures like the bacterial flagellum and teeth. When I realized that virus-driven energy theft was the cause of all pathology, I paid more attention to reports that attested to the claims I had already included in my published works and publications on RNA-mediated cause and effect.
For example see: Water-Mediated Collagen and Mineral Nanoparticle Interactions Guide Functional Deformation of Human Tooth Dentin
The authors link what is known to physicists and chemists to the conserved molecular mechanisms of energy-dependent RNA-mediated cell type differentiation via differences in the diet of C. elegans and P. pacificus, a predatory nematode with teeth. Unfortunately, the “…optimization of tooth dentin to reliably resist…” that requires experience-dependent exposure to loads was placed into the context of “evolutionary optimization.”
Attempts have failed to explain to others why “evolutionary optimization” is not possible in the context of what is known to serious scientists about biophysically constrained RNA-methylation and energy-dependent protein folding chemistry, which must be linked to species-specific behavior via the physiology of reproduction.
No matter how much more information or raw insight is added to what is already known, theorists will not look at the experimental evidence, or perhaps they will simply continue to ignore it. People like Lynnette Ferguson, will continue to do what they have always done. They will steal the energy that serious scientists use in attempts to accurately portray what is currently known about biophysically constrained energy-dependent biologically-based cause and effect.
See for instance: Philosopher earns 14th retraction for plagiarism
My comment: As the experimental evidence continues to become an overwhelming threat to the pseudoscientific nonsense touted by theorists, we will see more claims like this:
This review is far from comprehensive or complete and yet hopefully shows the enormous complexity of viral latency and its regulation at the genetic and epigenetic levels. This information provides great opportunity for the development of innovative and highly selective therapeutic intervention. As viral latency is responsible for life-long pathogenesis and mortality risk, the tasks ahead are in sight, but challenges remain. — Epigenetics and Genetics of Viral Latency (May 11, 2016)
My comment: My reviews were conclusive and I established the fact that virus-driven energy theft must be biophysically constrained by the availability of nutrients and lack of social stress that predicts the changes in pH that lead to viral replication. The need to model cause and effect in the context of energy-dependent changes that link angstroms to ecosystems has become increasingly clear.
See also: Viral Reprogramming of the Daxx Histone H3.3 Chaperone during Early Epstein-Barr Virus Infection
These findings also demonstrate that host chromatin assembly is an important form of host cell intrinsic resistance to viral infection.
My comment: I have placed that claim into my model and repeatedly stated clearly that energy-dependent RNA-mediated amino acid substitutions are linked to supercoiled DNA, which protect the organized genomes of all living genera from virus-driven energy theft and genomic entropy. The virus-driven energy theft links mutations to all pathology. I reiterate:
“…viral latency is responsible for life-long pathogenesis and mortality risk…” – Lieberman (2016)
My comment: Energy-dependent RNA-mediated amino acid substitutions are responsible for life-long healthy longevity and decreased mortality risk.
See also: Retrotransposon derepression leads to activation of the unfolded protein response and apoptosis in pro-B cells
Reported on 6/7/16 (with my emphasis) as:
“I don’t see a lot of research on the role of #epigenetics in suppressing endogenous retroviruses, so I was intrigued by this one. The investigators in this article in Development turn off the gene Setdb1, a histone methylator, and let slip the dogs of MLV. I’m certain one of our regular visitors will find this interesting.
Working on mouse cells, the team of researchers from Germany’s Ludwig Maximilians University and elsewhere discovered that releasing Setdb1’s hold on endogenous retroviruses definitely allows murine leukemia virus (MLV) to ramp up protein production, ultimately killing the host cells. Of course.
Previously, it hadn’t quite been clear whether cells lacking Setdb1 died due to viral protein production or some other reason, and this work is a solid step toward the former explanation.
Check out the article here in Development.
-CW New England Biolabs”
My comment: I am a regular visitor at the New England Biolabs FB page and a regular contributor of comments on the information they disseminate. But, given the return without review of my invited review by the guest editors who requested it, I have become increasingly suspicious of what may be subtle attempts to “bait” me, again.
Fortunately, others are moving forward. See for example: The Quantum Nature of Drug-Receptor Interactions: Deuteration Changes Binding Affinities for Histamine Receptor Ligands (May 9, 2016) reported by John Hewitt on June 7, 2016 as: Using the ‘deuterium switch’ to understand how receptors work
…olfaction is probably the space where these deuterium switches and chiral switches most informatively converge to elucidate how receptors might operate. In fact, the authors explicitly highlight the fact that their histamine receptor model may have something to say about olfactory receptors. Importantly, both of these receptor classes belong to the so-called GPCR (G-protein coupled receptor) family that vertebrates use to detect odorants; half of our own 800 GPCRs are provisioned almost exclusively to olfaction.
The author’s main comments, here, center on the aromatic groups of molecules, features that are typically associated with delocalized electrons. For example, the imidazole ring of histidine (histamine’s the amino acid precursor) is aromatic at all pH values; four of its pi electrons form two double bonds and two from a nitrogen lone pair. The authors propose that a major fallout of deuteration is that the aromatic moiety shrinks the effective C–D distance relative to its C–H value. Aromatic C–H bonds act as proton donors and form weak hydrogen bonds with water molecules and proton acceptors at the receptor binding site.
My comment: Thanks for trying to help others to understand the overwhelming complexity, John Hewitt. I noticed that they cited “Molecular vibration-sensing component in Drosophila melanogaster olfaction,” which was co-authored by Luca Turin, but these authors failed to link cell type differentiation from all invertebrates to all vertebrates via what is known about nutritional epigenetics, microRNA flanking sequences, RNA methylation, the innate immune system, supercoiled DNA, behavior, and consciousness.
Others may want to see “Dose-Dependent Effects of the Clinical Anesthetic Isoflurane on Octopus vulgaris: A Contribution to Cephalopod Welfare” and other works by Anna Di Cosmo’s group. Michael Crawford’s group has also made progress by ignoring claims about “quantum Darwinism” and focusing on the energy-dependent de novo creation of GPCRs, like olfactory receptor genes. See for example: A quantum theory for the irreplaceable role of docosahexaenoic acid in neural cell signalling throughout evolution
For comparison, see: Periodic Scarred States in Open Quantum Dots as Evidence of Quantum Darwinism
It describes the transition from quantum to classical world as a “decoherence” process that involves a kind of evolutionary progression somewhat analogous to Charles Darwin’s concept of natural selection.
My comment: I’ve mentioned repeatedly that serious scientists have always had the choice to stop investigating claims that Feedback loops link odor and pheromone signaling with reproduction in species from microbes to humans.
SARCASM ALERT: Why should pseudoscientists be the only people who accept the claim that mutations and natural selection replaced the sun’s biological energy as the anti-entropic source that links ultraviolet light to prevention of virus-driven energy theft in all living genera via decoherence in the context of “…a kind of evolutionary progression”? The pseudoscientists need only continue to ignore that fact that Darwin insisted that they ensure “conditions of life” were considered before natural selection.
Darwin’s “conditions of life” are energy-dependent and controlled by the physiology of reproduction. There is no experimental evidence of biologically-based cause and effect that links the energy-dependent physiology of reproduction from mutations to the diversity of morphological phenotypes and all experimental evidence of biologically-based cause and effect links energy-dependent RNA methylation from the innate immune system to supercoiled DNA.