Energy-dependent RNA methylation (4)
Virus-driven energy theft causes the mutations that are linked to all pathology. That fact is critical to understanding everything currently known to all serious scientists about energy-dependent RNA methylation and healthy longevity.
Unfortunately, here’s another attempt to put everything known about the de novo creation of genes back into the context of evolution, albeit without the typical focus on mutations and/or natural selection.
It takes an extreme amount of energy to counteract many attacks from layers of immune responses, including special attack peptides (see post on antimicrobial peptides or AMPs), and multiple enzymes.
See for comparison: Vitamin B3 may help prevent certain skin cancers and Vitamin/cancer evidence
See also: Are We Eating Our Way to Prostate Cancer—A Hypothesis Based on the Evolution, Bioaccumulation, and Interspecific Transfer of miR-150
I mentioned in a blog post yesterday that Lynnette Ferguson is the senior author and that she was one of the two people who asked me to submit an invited review of nutritional epigenetics to the journal “Nutrients.” My invited review Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems was returned without review.
Now, these authors claim: “This is a hypothesis-driven manuscript, so we have had our limitations in terms of finding desired published literature.” That claim shows how far some people may be willing to go to present the claims made by others about nutritional epigenetics and microRNAs as if they were based on original thoughts. Ferguson and others blocked publication of my review:
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.
My comment: Rarely do I find someone whose works have also been prevented from being distributed by those who want to use the information for their own personal gain at the cost of the suffering and death of anyone waiting for a cure for cancer, or for more effective treatment options with less severe side effects. But, I’m sure there must be others like me, who are waiting to see people like Lynnette Ferguson exposed for who they really are.
See also: Heterozygous colon cancer-associated mutations of SAMHD1 have functional significance
The three major determinants of DNA replication fidelity that control the spontaneous mutation rate are nucleotide selectivity by DNA polymerases, proofreading by replicative DNA polymerases, and the mismatch repair (MMR) system (6). Failures in the two latter determinants have now been firmly associated with the development of cancer (7), but they cannot account for the increased spontaneous mutation rates in most cancers (5).
The first determinant, nucleotide selectivity by DNA polymerases, can be affected by changes in the absolute and relative concentrations of the four deoxyribonucleoside triphosphates (dNTPs).
Reported as: Misregulation of DNA building blocks associated with the development of colon cancer
…studies in mice, yeast, and cultures of human cells showed that these cancer-specific mutations eliminated the SAMHD1 function and that this led to an elevation and imbalance in dNTP levels and hence an increased mutation rate.
“What’s so remarkable about our observation is that even if only one of the two SAMHD1 gene copies is lost, it affects dNTP levels with an increased mutation rate as a result. Together with a deficiency in the protein MLH1, which is involved in the correction of mutations and is often mutated in colon cancers, we can see a huge increase in the number of emerging mutations,” explains Professor Andrei Chabes.
The journal article cites: Grantham R (1974) Amino acid difference formula to help explain protein evolution. Science 185(4154):862–864. According to Scholar.google.com, Grantham (1974) has been cited in 1566 other articles, and many of the other articles have been cited thousands of time.
For comparison, in 1973, Dobzhansky claimed that “…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).”
My comment: Energy-dependent DNA replication fidelity links biophysically constrained cell type differentiation from the innate immune system to supercoiled DNA in all living genera via the physiology of nutrient-dependent reproduction. Supercoiled DNA protects all organized genome from virus-driven entropy. For example, nutrient-dependent microRNAs have been linked to the stability of organized genomes by RNA-mediated amino acid substitutions that link RNA-mediated DNA repair from adhesion proteins to cancer prevention.
See also: WEBINAR: Epigenetics in human health and disease
Epigenetics defines the set of distinct and heritable molecular mechanisms able to influence gene expression without altering the primary genetic sequence. Common epigenetic factors include DNA modifications (methylation or hydroxymethylation), chromatin modifications (histone methylation or acetylation), and non-coding RNA expression (micro RNA or long non-coding RNA transcripts). The past decade has seen a marked increase in the number of scientific publications focusing on epigenetics research. As a result, the basic understanding as to how epigenetic pathways interact with diverse and consistently changing cellular environments to help regulate gene expression has grown as well. When normal epigenetic pathway function is disrupted, disease may result.
This webinar highlights two specific areas of biomedical research in which the dysregulation of epigenetic mechanisms play prominent roles in disease etiology. The first presenter, Dr. Peter Jones, will discuss the complex role that epigenetics dysfunction plays in cancer progression and how recent findings suggest novel avenues to exploit for therapeutic development. The second presenter, Dr. Than, explains how the developing placenta can be influenced by the surrounding maternal environment and identifies altered DNA methylation patterns at specific gene loci associated with prenatal health indications. The potential role for disease diagnostics will also be discussed.
Dr. Peter Jones co-authored: MicroRNAs: critical mediators of differentiation, development and disease
miRNAs are a fundamental part of coordinated gene regulation in eukaryotic cells and the recent explosion of reports on miRNA involvement in various biological processes continues unabated. It now seems that miRNA involvement in a cellular pathway or function is the rule rather than the exception, although the specific and intricate roles of each miRNA will take some time to determine. Several human diseases, from neurological disease to heart disease to cancer, are caused or propagated by miRNA misexpression, which has generated great interest in therapies, diagnoses and prognoses based on disease-specific miRNAs. Recent work in this regard has shown tremendous promise and the successful translation of miRNA research from novel bench work to medical practice and patients may open up a new avenue to treat disease in humans.
See also: The Epigenetic Inheritance of Metabolic Disease
The oocytes and sperm from the diabetic mice passed epigenetic information, affecting males and female offspring differently.
My comment: The article includes a link to this ridiculous video representation from 2012.
See also: April 4, 2016
For comparison, see:
This is the review article that led Lynnette Ferguson and Justin O’Sullivan to ask me for the invited review of nutritional epigenetics.
Nutrient-dependent/pheromone-controlled adaptive evolution: a model
The “Criticisms…” of an undergraduate whose thesis was about abiogenesis may have led Lynnette Ferguson and Justin O’Sullivan to realize that I was not supporting the pseudoscientific nonsense of neo-Darwinian theories. See: Criticisms of the nutrient-dependent pheromone-controlled evolutionary model. Or, I may have made that fact perfectly clear in the invited review that was returned without review.
“…calcitriol is the active form of vitamin D. Its effects on the microRNA(miRNA)/messenger RNA (mRNA) balance appear to protect against perturbed protein folding, which is associated with colorectal cancer. MiRNA-627 targets the mRNA that encodes an enzyme linked to histone demethylation and amino acid substitutions that increase stability of hydrogen bonds in DNA, which are important to protein folding (Padi, Zhang, Rustum, Morrison, & Guo, 2013).”
My comment: The energy-dependent cause and effect relationship has now been bastardized and portrayed as if “oncohistones” cause cancer.
See: Histone H3K36 mutations promote sarcomagenesis through altered histone methylation landscape
The authors link virus-driven energy theft to loss of function histone mutations via these amino acid substitutions.
1) lysine 27–to–methionine (K27M)
2) glycine 34–to–arginine/valine (G34R/V)
3) glycine 34–to–tryptophan/leucine (G34W/L)
4) lysine 36–to–methionine (K36M)