Bee-birthed epigenetics and primate cell types

Summary: This is a fantastic video representation of how nutrient-dependent pheromone-controlled RNA-directed DNA methylation links ecological variation to RNA-mediated ecological adaptations via amino acid substitutions in all genera.

The Birth of a Bee


After the queen bee lays a single egg in a cell of the comb, the worker bees feed the egg for a few days until it hatches into a larva. The larva continues to eat and grow until Day 10. Then, the worker bees cap the cell, and 11 days later an adult honeybee emerges. Varma was captivated by “this crazy transformation, from one nasty-looking grub thing into this crazy-looking insect.”

My comment: Varma, albeit unknowingly, also captured on film what is currently known about the biophysically constrained nutrient-dependent pheromone-controlled chemistry of protein folding that links RNA-directed DNA methylation and RNA-mediated amino acid substitution to cell type differentiation and the morphological and behavioral phenotypes of all genera. Simply put,  fixation of the nutrient-dependent amino acid substitutions that differentiate cell types and species occurs via the physiology of nutrient-dependent reproduction in all genera.
See also Kohl (2013): Nutrient-dependent/pheromone-controlled adaptive evolution: a model

The honeybee already serves as a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, the development of the brain and behavior, mental health, longevity, diseases of the X chromosome, learning and memory, as well as conditioned responses to sensory stimuli (Kohl, 2012).


…the model represented here is consistent with what is known about the epigenetic effects of ecologically important nutrients and pheromones on the adaptively evolved behavior of species from microbes to man. Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.

Kohl (2012) concludes:

Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans (Keller et al., 2007; Kohl, 2007; Villarreal, 2009; Vosshall, Wong, & Axel, 2000).

Kohl (2013) concludes:

…the model represented here is consistent with what is known about the epigenetic effects of ecologically important nutrients and pheromones on the adaptively evolved behavior of species from microbes to man. Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.

My comment: Andrew Jones’  criticisms of my model appear to be primarily based on an a biology undergraduate’s conclusions from his mutagenesis experiments, which are included in his thesis: 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 itsdiscovery 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.

In Criticisms of the nutrient-dependent pheromone-controlled evolutionary model, this biology undergraduate concluded:

…James Kohl presents an unsupported challenge to modern evolutionary theory and misrepresentations of established scientific terms and others’ research. It was a mistake to let such a sloppy review through to be published.

The editor properly addressed the criticisms with his noteworthy claim:

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.

Others seem unable to grasp the difference between a model of biologically-based cause and effect and a theory of how abiogenesis and evolution enabled a system of heredity through natural selection. The difference is based on facts.
For example see: Hemaglobinopathies and Thalassemias: Essentials for Clinical Consultation and Interpretation
Excerpt (s):

Adult hemoglobin A consists of 2 alpha chains and 2 beta chains (α2β2). The α chain comprises 141 amino acids; the β chain 146.
Hemoglobinopathies typically have at least one amino acid substitution leading to synthesis of a variant globin chain.
Thalassemias, on the other hand, involve perturbation of the rate of globin chain synthesis (1).

My comment: Mutations perturb protein biosynthesis and degradation, which links mutations to thalassemias. Fixation of nutrient-dependent amino acid substitutions that differentiate the cell types of all genera links ecological variation to ecological adaptations.  Ecological adaptations are linked to hemoglobinopathies via neo-Darwinian evolutionary theory, which was invented by population geneticists. They used Hugo de Vries definition of “mutation” and linked it to their assumptions about how long it might take for one species to evolve into another species.
Andrew Jones “Criticisms” of my model exemplify the power of definitions and assumptions when they are taught to generations of biology undergraduates. Undergraduates, like Jones, may think that mutagenesis links abiogenesis and evolution to heredity via natural selection. Darwin’s representations of facts about the “conditions of life” that Darwin repeatedly insisted must precede consideration of natural selection in the context of his excellent theory, have been abandoned by people like Jones and whoever taught him to believe that mutations can somehow be linked to the evolution of biodiversity.
Note, Jones seems to have uncritically accepted the claim of Masatoshi Nei in a textbook that was published on the same day as my review (i.e., my model). Jones cites: Nei M. Mutation-driven evolution; 2013. Retrieved March 10, 2014 from books.google.com.
Nei’s textbook conclusion is that: “…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” (p. 199).
Many people, like Jones, have failed to realize there is no model for that. For comparison, Dobzhansky (1973) 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).  My model links Dobzhansky’s claim to what is currently known about the biophysically constrained chemistry of nutrient-dependent RNA-mediated amino acids and protein folding that links metabolic networks to genetic networks in all genera. My model has since been compared in the context of Dobzhansky (1973) in Combating Evolution to Fight Disease.

The evolutionary biologist Theodosius Dobzhansky famously noted that “nothing in biology makes sense except in the light of evolution,” but perhaps, too, “nothing in evolution makes sense except in the light of biology.” Although the latter might be an exaggeration, an important gap is being filled by molecular understanding of the genesis of variation that confers the ability to evolve.

My comment: The genesis of variation is nutrient-dependent. Mutations perturb the chemistry of protein folding that confers the ability to ecologically adapt to ecological variation. The pheromone-controlled physiology of reproduction ensures that ecological variation leads to ecological adaptation in species from microbes to man via RNA-directed DNA methylation and RNA-mediated amino acid substitutions. There’s a model for that! It’s my model. In the past two years no one has suggested that there is another model for comparison. Many have, like Andrew Jones, complained that they don’t like my model. This suggests that many evolutionary theorists are not going to help serious scientists who are Combating Evolution to Fight Disease. Hopefully, anyone who is considering the possibility of studying evolutionary biology in college, will not accept the teaching of evolutionary theorists who know nothing about what has been learned by serious scientists in the past two decades.
Following Dobzhansky’s lead from 1973 in Nothing in Biology Makes Any Sense Except in the Light of Evolution, to what is currently known, serious scientists have learned that RNA-directed DNA methylation and RNA-mediated amino acid substitutions link the light-induced de novo creation of amino acids to the creation of the membrane that enables photosynthesis, which enables all of nutrient-dependent cell type differentiation in all genera via the physiology of reproduction.  Simply put, the sun’s biological energy links cell type differentiation to all morphological and behavioral phenotypes via the conserved molecular mechanisms of epigenetically-effected cell type differentiation that leads to successful reproduction.
See also: A lighting requirement for life.

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