Hecatombic evolution via oncocers and oncohistones

By: James V. Kohl | Published on: October 16, 2016

Mutation-driven evolution is being replaced by a theory of hecatombic evolution that links oncocers and oncohistones to increasing organismal complexity via autophosphorylation and autophagy or something else as yet to be invented in the context of the new ridiculous theory.
See for comparison: Polycomb enables primitive endoderm lineage priming in embryonic stem cells
Abstract excerpt:

We show that altered transcription is the driver of these coordinated changes, known as lineage priming, in a process that exploits novel polycomb activities.

What they showed is consistent with the representations of what polycomb enables in the context of claims made in our 1996 Hormones and Behavior review.
From Fertilization to Adult Sexual Behavior

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…

My comment: It is difficult to move forward with experimental evidence when neo-Darwinian theorists want to retard all progress or stop it and reverse it. Indeed, most of them seem willing to let you believe in anything except for facts about species-specific cell type differentiation, even when it must be biophysically constrained by the same molecular mechanisms in all living genera.
See also: Did evolution autophosphorylate your kinases? and Did evolution autophosphorylate your kinases? (2)
No experimental evidence of biologically-based cause and effect links neo-Darwinian theories to evolution via natural selection. Natural selection for energy-dependent codon optimality is the only validated way to link energy-dependent cell type differentiation from the biophysically constrained RNA-mediated protein folding chemistry, which links supercoiled DNA to protection from virus driven energy theft and all pathology caused by viruses in all living genera. That fact forces pseudoscientists to invent new terms like “hecatomb” and “oncocer” and “oncohistone” to confuse anyone who does not believe in their nonsense about the evolution of morphological and behavioral diversity from a common ancestor.
See for example:  Oncocers: ceRNA-mediated cross-talk by sponging miRNAs in oncogenic pathways

Oncocers are ceRNAs taking crucial roles in oncogenic pathways processed in many types of cancer, and this study analyzes oncocer-mediated cross-talk by sponging microRNAs (miRNAs) in these pathways.

My comment: This may come as a surprise to anyone who has already published one of more than the 54,000 journal articles that link energy-dependent changes from angstroms to ecosystems in all living genera via microRNA flanking sequences and messenger RNA degradation in the context of autophagy and chromosomal rearrangements.
See also:  Histone H3K36 mutations promote sarcomagenesis through altered histone methylation landscape

Missense mutations (that change one amino acid for another) in histone H3 can produce a so-called oncohistone…

My comment: Why not continue to call missense mutations the same thing they have always been called and call energy-dependent RNA-mediated amino acid substitutions what they have always been called in the context of the differentiation of all cell type in all individuals of all genera?
Mutations cannot differentiate cell types. They link virus-driven energy theft to all pathology. Is that why we others invent and/or define terms such as oncocers and so-called oncohistones? It is because of the complete failure by pseudoscientists to link mutations from energy-dependent changes in angstroms to ecosystems in the context of biologically-based cause and effect? Serious scientists have done that!
What caused pseudoscientists to fall so far behind that they are forced to invent new terms with definitions that defy logic in the context of what they previously portrayed as mutation-driven evolution?
See for example: Mutation-Driven Evolution

…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world. In this view of evolution there is no need of considering teleological elements.

My comment: Who is so ignorant that they think there is no need to consider teleological elements in the context of biologically-based cause and effect.
See for consideration: Scoring System for Analyzing Vessel Development in Embryoid Bodies


Tyrphastin 1296 inhibits the autophosphorilation of PDGFß receptor (PDGFRß) which results in an inhibition of the PDGF pathway [17]. Endothelial sprouting, branching and pruning during angiogenesis depend on PDGFB/PDGFRß signalling [18].

My comment: The inhibition of autophosphorilation makes it obvious something causes phophorilation. It should be equally obvious that autophosphorilation (sp?)/autophosphorylation cannot be attributed to the magic of neo-Darwinian pseudoscientific nonsense.
Even with the invention of new terms for microRNAs and new terms for amino acid substitutions, anyone still touting neo-Darwinian theory will continue to appear to know nothing about how biophysically constrained energy-dependent phosphorylation occurs in the context of links from autophagy to all biodiversity. They need only claim that something evolves to demonstrate their ignorance.

See for example:  Evolution of protein phosphorylation across 18 fungal species


Living organisms have evolved protein phosphorylation, a rapid and versatile mechanism that drives signaling and regulates protein function.

My comment: If living organisms evolved protein phosphorlation, did the evolution of protein phosphorylation occur in the context of autophosphorilation? If so, anyone who is familiar with the how the term autophagy has been used in the context of energy-dependent cell type differentiation can try to place the energy-dependent de novo creation of G protein-coupled receptors into the context of the claim that living organisms have evolved protein phosphorylation via autophosphorylation, which is an energy-dependent link from cell type signaling to cell type differentiation in all living genera. How could an energy-dependent link evolve outside the context of getting energy into a cell?

Simple put, autophosphorylation and the evolution of protein phosphorylation cannot be placed into the context of what is known to serious scientists about energy-dependent RNA-mediated amino acid substitutions in all living genera. Viruses steal the energy that is required and use it for fixation of amino acids that increase the virulence of the virus.

See also: Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution

The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.

My comment: Three years ago I forced the authors of this article to admit to that scientific truth. Now I’m convinced that if it’s not the Zika virus that leads to the viral apocalypse, it will be another virus that has ecologically adapted faster than the infected human populations can adapt. For example, the influenza virus adapts every year, which is why most people get a yearly vaccine. Did you get your vaccine this year? Why? Why not? Did you make your decision based on any scientific facts?

See: Scientific method: Defend the integrity of physics

…the issue boils down to clarifying one question: what potential observational or experimental evidence is there that would persuade you that the theory is wrong and lead you to abandoning it? If there is none, it is not a scientific theory.

The imprimatur of science should be awarded only to a theory that is testable. Only then can we defend science from attack.

See also: The Darwin Code by Greg Bear


Collecting facts from many sources, I tried to assemble the outline of a modern appendix to Darwin, using ideas derived from disciplines not available in Darwin’s time: theories of networks, software design, information transfer and knowledge, and social communication–lots of communication.
My primary inspiration and model was variation in bacteria. Bacteria initiate mutations in individuals and even in populations through gene transfer, the swapping of DNA by plasmids and viruses.

My comment: Greg Bear and I share a similar approach. I collected facts from work in different departments of  medical laborartories to help determine what was going to kill the next person who would die. It was always the same, a problem with the transfer of energy as information. Cell types stopped communicating effectively and failed energy-dependent communication signals the death of all living organisms. What prevented effective communication? Blood gas analyses always suggested the problem was a change in pH, which is an assessment of hydrogen-atom transfer in DNA base pairs in solution. How did subatomic particles get into the hydrogen atom, and when did they do that so that the transfer of energy could lead to phosphorylation, or autophosphorylation (without the energy)?

What is causing my trouble communicating facts about energy-dependent cell type differentiation to others? Are they neo-Darwinian theorists who believe in the magic of autophosphorylation? Are they young earth creationists who also are physicists, chemists, or molecular biologists? No matter who they are, except for family members, atheists, and pseudoscientists, I have no trouble communicating with others who are not scientists.
For example, Greg Bear appears to be an inspired Deist who is much more informed than Dobzhansky was when Dobzhansky (1973) claimed this in Nothing in Biology Makes Any Sense Except in the Light of Evolution:

…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.

How can we compare Greg Bear’s claims to the claims of others, whether or not they are scientists? Why was I one of the people he invited to fact-check his representations before he sent the manuscript for Darwin’s Children to the publisher? How can anyone else tell the difference between a Deist, an atheist, a secular humanist, or an old earth creationist?
Do secular humanists, atheists, and old earth creationists think that what physicians refer to as a natural death is not caused by virus-driven energy theft? Where does the energy of life go when someone you love is “gone.” Did an oncocer steal it? Did an oncohistone cause them to die of “natural causes?” Have neo-Darwinian theorists cause the death of millions? Does it matter?
I can compare some differences between life and death to what I know about young earth creationists who have linked everything known about nutritional epigenetics to healthy longevity and everything known about virus-driven energy theft to all pathology. Is there an easier way to explain what I think is the lack of any differentiating characteristics between secular humanists, atheists, and old earth creationists?
If they do not believe the facts about energy-dependent autophagy that serious scientists believe in, what do they believe about creation and how biodiversity arose? Do they believe in the emergence of energy and autophosphorylation?
Phosphorylation links autophagy to energy-dependent RNA-mediated protein folding and healthy longevity, or from virus-driven energy theft to all pathology. Have you ever wondered where the energy comes from that enables autophosphorylation, which is a type of post-translational modification of proteins. Autophosphorylation is generally defined as the phosphorylation of the kinase by itself.

You can place that definition into the context of reports that must link autophosphorylation and autophagy to cell type differentiation in all cell types of all living genera. If you use the definition, you may understand why Vries 1902 definition of mutation led all pseudoscientists to believe that the automagical phosphorylation of kinase by itself led to endothelial sprouting, branching and pruning during angiogenesis.

If you substitute mutation-driven evolution for an explanation of everything known to serious scientists about PDGFB/PDGFRß signalling and all other signaling among all other cell types in all living genera, you will be accepted among those who claim that life emerged and  “living organisms have evolved” the ability to phosphorylate their kinases. You can tell others that evolution must be true because pseudoscientists claim it is.

But if you claim scientists say evolution is true, prepare yourself to submit your experimental evidence to support your ridiculous claim, or present the experimental evidence that you think led any serious scientist to claim that evolution is true.

Compare your evidence to the evidence cited in Nutrient-dependent/pheromone-controlled adaptive evolution: a model and we can compare models. Most pseudoscientists clearly have missed out on this fact:

See: Phosphorylation of basic amino acid residues in proteins: important but easily missed
See for comparison: Young phosphorylation is functionally silent

Evolutionary cell biology is still in its early days (1).

My comment: There is no such thing as evolutionary cell biology because cell types do not evolve. Cell types must adapt to viruses by biophysically constraining them in supercoiled DNA. That occurs only in the context of energy-dependent phosphorylation and autophagy.

See also: Intronic Non-CG DNA hydroxymethylation and alternative mRNA splicing in honey bees

Our identification of GO categories related to protein phosphorylation that were enriched for genes with methylated splice junctions is consistent with a similar finding in a recent study of species-specific alternative exons [45]. The authors present evidence that argues that alternative splicing is used to alter protein phosphorylation, which can alter protein stability, subcellular localization, activity, and other properties [45]. Further research is needed to determine the mechanism by which splice junction methylation and hydroxymethylation affect mRNA splicing.

My comment: Autophagy is the obvious mechanism that alters the speed of virus-driven mRNA degradation via energy-dependent DNA repair.

See also: Drivers of evolution hidden in plain sight

“This study is about understanding how evolution works, which tells you how species adapt to changing environments over many generations,” says Pedro Beltrao, a research group leader at EMBL-EBI. “For example, when you compare humans and chimps, they are obviously different, even though a good part of their genetic makeup is more or less the same. Our task is to figure out how diversity is generated, so that we can see in detail how life evolves. That helps us understand how plants and animals adapt and change, and how cancers or bacteria find their way around drugs.”

My comment: The difference in the cell types of chimpanzees and humans compared to gorillas is a single amino acid substitution, which was reported by Dobzansky in 1964 and 1973. This study links ecological variation to energy-dependent ecological adaptation via phosphorylation and RNA-mediated fixation of amino acid substitutions in the context of autophagy, which links supercoiled DNA and chromosomal rearrangements to protection of organized genomes from virus-driven entropy.
That protection is called biodiversity when it links ecological variation from the energy-dependent de novo creation of the innate immune system to ecological adaptation via the energy-dependent de novo creation of G protein-coupled receptors.
Calling it evolution or inventing evolutionary cell biology is something only biologically uninformed theorists will continue. Alternatively, if the invention of evolutionary cell biology is an attempt to support the evolution industry or big bang cosmology industry, pseudoscientists can keep referring to ecological adaptation as evolution for as long as they want.
All serious scientists already know how to link energy-dependent changes from angstroms to ecosystems in all living genera, and no species has ever evolved from another species.

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