A two-faced protein enables RNA-mediated DNA repair (3)

By: James V. Kohl | Published on: December 9, 2015

See: A two-faced protein enables RNA-mediated DNA repair (2)
See: A two-faced protein enables RNA-mediated DNA repair
My comment: Attempts to place what is currently known about the links from atoms to ecosystems back into the context of neo-Darwinian pseudoscientific nonsense have been doomed to fail ever since Dobzhansky (1973) wrote: Nothing in Biology Makes Any Sense Except in the Light of Evolution.
He linked nutrient-dependent amino acid substitutions to cell type differentiation across species and also claimed

“…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).”

Others have since continued to reveal the reasons for the similarities and the differences in cell types that vary in the context of the fixation of these amino acid substitutions in organized genomes via the physiology of reproduction in all living genera. Indeed, it has become obvious that The pronoun ‘I’ is becoming obsolete.
The facts about symbiosis scare all evolutionary theorists because they know those facts cannot be placed into the context of their ridiculous theories. Still, they must try.
See:  Host Biology in Light of the Microbiome: Ten Principles of Holobionts and Hologenomes

…there is no fundamental rewriting of Darwin’s and Wallace’s theory of evolutionary biology involved in this concept. Like single nucleotide mutations, acquisition of new symbionts births raw genetic variation that evolution can operate on.

My comment: If you asked any theorist to explain how new symbionts are somehow acquired, or what level of importance they attribute to the automagical acquisition, they might claim that it fully supports the pseudoscientific nonsense of their ridiculous theories about increasing organismal complexity, which link beneficial mutations to evolution of new species. However, no experimental evidence of biologically-based cause and effect supports such ridiculous misrepresentations.
For comparison, see: Hidden Diversity in Honey Bee Gut Symbionts Detected by Single-Cell Genomics
and Experimental replacement of an obligate insect symbiont,
which was
Reported as: What’s mine is yours, and what’s yours is mine

Evidence of success came when not just the symbionts but also the recipient aphids developed a striking tolerance to high temperatures.

My comment: Three articles published on the same page of the same issue of DDNews address all current experimental evidence that is linked from protein biosynthesis and degradation to organism-level thermoregulation.
A shock to the system?

Small heat shock proteins are a type of protein that are constantly present, but are highly expressed when cells are exposed to stressful conditions and function as “catastrophe aid workers.”

The mediation of mTORC1

…David M. Sabatini, M.D., Ph.D., published groundbreaking research describing, for the first time, the identification and characterization of the cellular proteins responsible for sensing and mediating the metabolic effects of the amino acid leucine. The paper, published October 8 online in the journal Science, elucidates a key regulatory node related to leucine that was previously unknown within the multiple steps of the mTORC1 activation pathway. The anabolic amino acid, leucine, is critical in cellular protein and lipid synthesis and directly regulates mammalian physiology including skeletal muscle growth, insulin secretion and food intake.

Sifting through the genome

…we know that 90 percent of associated variants found in GWAS are outside of the protein-coding areas,” Pazin adds. “Eventually, we want to understand mechanistically how the variants function in regulating genes, and how differences in the way they function affect disease risk.”

My comment: Disease risk and predictable responses to treatments are RNA-mediated.
For more information about the difference between healthy longevity and pathology, listen to this podcast: Panel Discussion: How Can Life Extension Become as Popular as the War on Cancer?
My comment: The popularity of theories largely depends on funding.  For example, funding for the evolution industry has helped to support the “War on Cancer” because the ridiculous theories of pseudoscientists link beneficial mutations to evolution. Those ridiculous claims have led to millions of wasted dollars and wasted efforts by pseudoscientists who tried to find a difference between beneficial mutations and the mutations linked to pathology. All mutations eventually will be linked to pathology via the replication of viruses that causes all pathology.
Why do you think this researcher appears to be somewhat angry as he explains the link from metabolic networks to genetic networks in the context of healthy longevity via nutrient-dependent microRNAs linked from cell adhesion molecules to supercoiled DNA, which protects organized genomes from heat shock linked to pathology in the context of virus-driven entropy?

A theorist’s answer to any accurate representation of biologically-based cause and effect linked to healthy longevity or to pathology will always be something like this, which is posed as a question.
Was early animal evolution co-operative?

In their new ‘savannah’ hypothesis, they propose that concentration of nutrients both above and below the sediment-water interface were enhanced around the stationary Ediacarans, and the creation of these resource “hot spots” created a very diverse environment, ideal for both diversification and for investment of energy into movement. Rather than the Ediacarans and later animals being direct competitors then, the Ediacarans themselves created a permissive environment that was ideal for higher animals to evolve in. This idea fits well into a modern view of evolution, called “ecosytem engineering” whereby key species (such as beavers) influence the environment in order to create new evolutionary and diversity opportunities for other species. Perhaps then, the Ediacaran taxa weren’t impediments but the drivers of the evolution that was eventually to lead to all the rich animal diversity we see today.

My comment: What evolved? How? Ridiculous questions that start with assumptions about animal evolution in the context of the creation of “hot spots” that created diverse environments are not likely to be considered by serious scientists. Those who are creationists will claim that the theorists are starting with the de novo creation of energy-dependent differences and all serious scientists who understand what is known about cell type differentiation will link their creationist arguments from atoms to ecosystems via nutrient-dependent adaptations and the physiology of reproduction in all living genera.
Questions about what evolved and how have been asked and answered by all serious scientists since Dobzhansky (1964) complained that:

The notion has gained some currency that the only worthwhile biology is molecular biology. All else is “bird watching” or “butterfly collecting.” Bird watching and butterfly collecting are occupations manifestly unworthy of serious scientists! I have heard a man whose official title happens to be Professor of Zoology declare to an assembly of his colleagues that “a good man cannot teach zoology. A good man can teach, of course, only molecular biology.

My comment: For example, here’s the answer to the question about what evolved. NOTHING! And, here’s the answer to how anything evolves via beneficial mutations: IT CAN’T!

Here are more details that will help other serious scientists answer questions about energy-dependent cell type differentiation in the context of ridiculous theories.
The Hologenome Concept: Helpful or Hollow?

We argue that the wrong approach is to start with the assumption that associated organisms have evolved to function as a cooperative unit and that the task is simply to characterize mutually beneficial adaptations. This assumption is often incorrect, and embracing it uncritically will slow progress. A more parsimonious approach is to adopt the null hypothesis that interacting lineages have not evolved exceptional hologenome-selected traits, and to test specific hypotheses regarding such traits.

My comment: As a reminder of what all serious scientists have known about assumptions for at least two decades, see this claim from Lynn Margolis via Suzan Mazur.

[W]hat Haldane, Fisher, Sewell Wright, Hardy, Weinberg et al. did was invent…. Evolution was defined as “changes in gene frequencies in natural populations.” The accumulation of genetic mutations was touted to be enough to change one species to another…. Assumptions, made but not verified, were taught as fact.

See also:  Incorporating significant amino acid pairs and protein domains to predict RNA splicing-related proteins with functional roles

Abstract excerpt:

Alternative splicing, which is an important post-transcriptional regulation in eukaryotes, gives rise to multiple mature mRNA isoforms, which encodes proteins with functional diversities. However, the regulation of RNA splicing is not yet fully elucidated…

My comment: Precisely one year after I published my most recent review, which linked RNA-mediated events from amino acid substitutions to cell type differentiation with examples from different species, Jay R. Feierman eliminated me from participation on the International Society for Human Ethology’s human-ethology yahoo group.
Feierman wrote: 

I’m not going to post more from Kohl until he answers the very direct and simple question posed to him by anon, which is whether he (Kohl) believes that RNA splicing can change DNA.

My comment: Knowing that the regulation of RNA splicing was not yet fully elucidated, Feierman had previously commented:

“[MODERATOR NOTE: I don’t believe that Jim Kohl has addressed the very specific question asked of him by anon, which is whether he (Jim Kohl) believes that RNA splicing makes new genes. A simple agree or don’t agree is needed to make the interactions in this thread worth posting.”]

My comment: Feierman effectively reduced all of the levels of biological complexity involved in cell type differentiation in species from microbes to man to an “agree or don’t agree” comment based on what an anonymous participant had proclaimed I was implying.
That anonymous participant was Andrew Jones, who never mentioned that he had written a letter to the editor of Socioaffective Neuroscience & Psychology​. The editor published his criticisms of my model.
Anyone interested in the pseudoscientic nonsense touted by evolutionary theorists and human ethologists will enjoy reading the criticisms of my model by Andrew Jones (aka anonymous_9001).
See:  Criticisms of the nutrient-dependent pheromone-controlled evolutionary model
See the editor’s response:

The 2013 review article by James Vaughn Kohl published in Socioaffective Neuroscience & Psychology and criticized in the above Letter to the Editor was subjected to standard peer review and the revised version was accepted by me after it had been accepted by both reviewers.

My comment: The criticisms show how people like Andrew Jones and people like Jay R. Feierman have managed to continue to convince others that “Random mutations are the substrate upon which directional natural selection acts” is a correct and true statement.” See for example, Jones’ thesis on mutagenesis: Lipid Encapsulation of Self Replicating Ribozymes

Despite their challenges, ribozymes have made an interesting niche for themselves in the field of abiogenesis. The evolution of a successful RNA polymerase ribozyme is a lofty goal. While its discovery would not be the be-all and end-all of abiogenesis research, it would represent an important stepping stone between prebiotic chemistry and life. The encapsulation of such a ribozyme is also an important step, as it would enable a system of heredity and evolution through natural selection. Based on progress in current research, it is only a matter of time before that ribozyme is discovered.

My comment: That statement, and Feierman’s claim about random mutations are based on a ridiculous theory. The claims ignore the accumulation of biological facts that link nutrient-dependent RNA-mediated amino acid substitutions to the differentiation of all cell types in all individuals of all species from microbes to man via conserved molecular mechanisms that obviously involve alternative splicings of pre-mRNA. We placed the alternative splicings into the context of the pheromone-controlled sexual differentiation of cell types in our 1996 Hormones and Behavior review. From Fertilization to Adult Sexual Behavior

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.

My comment: More than 45,000 publications now link nutrient-dependent microRNAs from cell adhesion proteins to supercoiled DNA and the stability of organized genomes in all living genera via alternative splicings and RNA-mediated events that link the pre-mRNAs / microRNAs to nutrient energy-dependent cell type differentiation.
With three blog posts on the same topic of the two-faced protein that enables RNA-mediated DNA repair,  I continue to repeat myself each time new experimental evidence of biologically-based cause and effect support the claims in the book I co-authored in 1995 with an update in 2002.
For comparison, others need only explain away differences in cell types by claiming links between mutations and their transcriptional history.
See: Somatic mutation in single human neurons tracks developmental and transcriptional history
Excerpt: We also observed a signature of methylated cytosine (meC) to thymine (T) transitions (fig. S8), which can occur as a result of replication-independent deamination of meC, in single-neuron SNVs.
My comment: Having observed such an obvious link from RNA-directed DNA methylation to cell type differentiation, why was the lack of differentiation that links mutations to the transciptional history of undifferentiated cell types in the brain also reported in the context of neo-Darwinian nonsense? What about the missing heritability that links cell type differentiation in C. elegans and P. pacificus from their nutrient-dependent pheromone-controlled physiology of reproduction to differences in their morphological and behavioral phenotypes?
See: System-wide Rewiring Underlies Behavioral Differences in Predatory and Bacterial-Feeding Nematodes

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