Cytosis can be used to teach everything from base editing to RNA editing to everyone over age 10. They will learn how to link the creation of energy to biophysically constrained viral latency via the physiology of pheromone-controlled reproduction.

Ecological adaptation: a new definition of heredity (4)

Experimentally Induced Metamorphosis in Axolotl (Ambystoma mexicanum) Under Constant Diet Restructures Microbiota Accompanied by Reduced Limb Regenerative Capacity (2018)

Our results show that distinct bacterial communities inhabit individual organs of Axolotl and undergo substantial restructuring through metamorphosis.

The restructuring during metamorphosis is biophysically constrained by feedback loops that link olfaction from food odors and pheromones to the creation of enzymes in bacteria and the secretion of the vertebrate decapeptide hormone GnRH (gonadotropin releasing hormone).
See: Gonadotropin-releasing hormone agonist binding in tiger salamander nasal cavity (1993)
The authors presciently linked food odors and pheromones from epigenetic effects on feedback loops to gonadotropin-releasing hormone (GnRH) and microRNA-mediated morphological and behavioral diversity, and also to differences in the behavior of monogamous and polygamous prairie voles.
See: The prairie vole vomeronasal organ is a target for gonadotropin-releasing hormone (2001)
For comparison, Larry Young claimed that the evolution of viruses caused the differences in prairie vole behavior. He linked the virus-driven differences from three other hormones to the evolution of heterosexual love. See: Virus Evolution Amazing Documentary Full HD National Geographic Documentary 2015
Others, who are like Larry Young, have failed to link anything known to serious scientists from sensory input to energy-dependent changes in the creation of enzymes, receptors and hormones. The anti-entropic energy-dependent creation of enzymes by bacteria links the creation of receptors and hormones in vertebrates to protection of organized genomes from the virus-driven degradation of messenger RNA, which links mutations to all pathology.
See for comparison: 2013 Isaac Asimov Memorial Debate: The Existence of Nothing

Isaac Asimov, “…perhaps, the last polymath of our civilization.”

Originally a zoology major, Asimov switched to chemistry and earned a Doctor of Philosophy degree in biochemistry in 1948. In 1977, he contracted HIV from a blood transfusion. He was president of the American Humanist Association, which suggests that his atheism led to his death via his ignorance.
For example, in 1964, Dobzhansky wrote:

“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.”

If Isaac Asimov was the last polymath of our civilization, we are doomed. Clearly his ridiculous beliefs have led to the teaching of pseudoscientific nonsense about evolution despite the claims of Schrödinger (1944) and those who will link the anti-entopic virucidal energy of sunlight from the physiology of reproduction to biophysically constrained viral latency and all biodiversity during Schrödinger at 75 – The Future of Biology – September 2018
See for comparison: How One Child’s Sickle Cell Mutation Helped Protect the World From Malaria
Once again, so-called science journalist Carl Zimmer shows that he does not know the difference between a mutation and an RNA-mediated amino acid substitution.
See: Updates of the HbVar database of human hemoglobin variants and thalassemia mutations

Single nucleotide substitutions or indels can lead to several hemoglobin variants owing to amino acid replacements, while molecular defects in either regulatory or coding regions of the human HBA2, HBA1, HBB or HBD genes can minimally or drastically reduce their expression, leading to α-, β- or δ-thalassemia, respectively.

Hemoglobin variants alter the oxygen carrying capacity of red blood cells. They are clear indicators of how ecological variation must be linked to ecological adaptation via food energy-dependent changes in the microRNA/messenger RNA balance and the pheromone-controlled physiology of reproduction.
There are more than 1700 human variants. Anyone who claims that the variants are mutations should be required to link them from the transgenerational epigenetic inheritance of morphological and behavioral phenotypes in all living genera to ecologically adapted human populations.
The alternative is sexist and racist. Much more is needed than a new definition of heredity. All intelligent people must dismiss the neo-Darwinian pseudoscientific nonsense about mutation-driven evolution. Then, we can start over with accurate representations of top-down causation and biophysically constrained viral latency.
But first see: EPA’s Scott Pruitt Doesn’t Buy Evolution

Andrew Rosenberg, director of the Center for Science and Democracy at the Union of Concerned Scientists, counters that Pruitt should not act as “the nation’s pastor.”

Andrew Rosenberg should become familiar with the extant literature or play the cell biology game “Cytosis” for ages 10+. There is no excuse for his level of ignorance.
Cytosis is a board game that details what takes place inside a human cell! Players compete to build enzymes, hormones and receptors and fend off attacking Viruses! In the context of everything known to serious scientists about biophysically constrained energy-dependent RNA-mediated cell type differentiation, a new tool is now available to help theorists link cause and effect via a mathematical model.
See: VarQ: a tool for the structural analysis of Human Protein Variants. The mathematical model has replaced neo-Darwinian theories with facts about how the energy-dependent structure of functional supercoiled DNA biophysically constrains viral latency.
See also: Inhibition of the Host Translation Shutoff Response by Herpes Simplex Virus 1 Triggers Nuclear Envelope-Derived Autophagy (2013)
and Role of bacterial efflux pumps in biofilm formation
Only a few people I know would link antibiotic resistance from Escherichia coli to Acinetobacter baumannii via the weekend resurrection of the bacterial flagellum in Pseudomonas fluorescens. Until they are willing to do it in a public forum, see: Evolutionary resurrection of flagellar motility via rewiring of the nitrogen regulation system.
Pseudoscientists and most other theorists are still focused on mutation-driven evolution. Isaac Asimov’s “humanist” influence has prevailed across more than one generation of students who learned how to link nothing to everything from people like Neil deGrasse Tyson, Lawrence Krauss, and Carl Zimmer.

Alternative splicing of pre-mRNA

From base editing to RNA editing (4)

Summary: To claim evolution, Koonin must link food energy from the pheromone-controlled physiology of reproduction to fixation of a beneficial mutation in the organized genome of one species that evolved into another species.
Search Results for “base editing” = 82 blog posts starting with Cell-type differentiation on February 7, 2014
Search Results for “RNA editing” = 95 blog posts starting with In theory, or supported by experimental evidence? October 22, 2014
See for comparison PubMed: “base editing” (33 citations) and “RNA editing” (4222 citations)
The failure to link energy-dependent base editing to RNA editing and RNA-mediated cell type differentiation in all publications about healthy longevity compared to pathology can be attributed to the pseudoscientific nonsense touted by theorists. In their ridiculous mathematical models, they claimed the emergence of energy could be linked to the evolution of all biodiversity. Their lack of experimental evidence, which is required to link biologically-based cause and effect to biodiversity, was placed into the context of “human idiocy” by Richard P. Feynman.

See Richard P. Feynman’s lecture on: Food energy. See for comparison see: Energy as information and constrained endogenous RNA interference.

Feedback loops link quantized energy as information to biophysically constrained RNA-mediated protein folding chemistry. Light induced energy-dependent changes link angstroms to ecosystems from classical physics to chemistry/chirality and to molecular epigenetics/autophagy.

The National Microbiome Initiative links microbial quorum sensing to the physiology of reproduction via endogenous RNA interference and chromosomal rearrangements. The rearrangements link energy-dependent fixed amino acid substitutions to the Precision Medicine Initiative via genome wide inferences of natural selection.

This detailed representation of energy-dependent natural selection for codon optimality links biologically- based cause and effect from G protein-coupled receptors to RNA-mediated amino acid substitutions and the functional structure of supercoiled DNA. Energy-dependent polycombic ecological adaptations are manifested in supercoiled DNA. Chromosomal inheritance links the adaptations from morphological phenotypes to healthy longevity via behavioral phenotypes. For contrast, virus-driven energy theft is the link from messenger RNA degradation to negative supercoiling, constraint breaking mutations, and hecatombic evolution. The viral hecatomb links transgenerational epigenetic inheritance from archaea to Zika virus-damaged DNA, which typically is repaired by endogenous RNA interference and fixation of RNA-mediated amino acid substitutions in organized genomes.

The failure to link energy-dependent base editing and energy-dependent RNA editing to healthy longevity predicted the failure to link the virus-driven degradation of messenger RNA to all pathology. See for instance: The Science of Personalized Nutrition

A single nucleotide polymorphism (SNP) or change occurs in nearly 1 in 1,000 base pairs and accounts for much of an individual’s uniqueness. Research on SNPs and other genetic variations like deletions, inversions, duplications and copy number variations (CNV), which represent up to 9.5 percent of the human genome, have changed the face of human nutrition and validated the concept that nutrition could and should be personalized. (Mullally, 2007)

A single nucleotide polymorphism (SNP) is a single base-pair difference in the DNA sequence of individual members of a species. SNPs in genes may lead to variations in the amino acid sequence, but SNPs can also occur in noncoding regions of DNA. Base editing of A•T to G•C in genomic DNA was linked from RNA editing to the physiology of pheromone-controlled reproduction and fixation of amino acid substitutions in organized genomes. The amino acid substitutions differentiate all cell types in all individuals of all living genera.
See: Programmable base editing of A•T to G•C in genomic DNA without DNA cleavage
Reported as: Base Editing Now Able to Convert Adenine-Thymine to Guanine-Cytosine

Bioengineer Feng Zhang of MIT’S Broad Institute notes in an email that the team employed “a comprehensive and creative approach” to achieve such precision. “As a field, we have been looking for ways to precisely rewrite parts of the genetic code,” writes Feng, whose own, CRISPR-based method to edit single bases in RNA was published today in Science. “Base editors move us closer to this goal.”

The CRISPR-based editing of single base pairs in RNA links the energy-dependent function of the innate immune system to all biophysically constrained biodiversity via the pheromone-controlled physiology of reproduction, which biophysically constrains viral latency. Natural selection for energy-dependent codon optimality, links the editing of single base pairs in RNA to every aspect of healthy longevity via RNA editing.
See: RNA editing with CRISPR-Cas13
Reported as: RNA Editing Possible with CRISPR-Cas13

“This work is an impressive study from a highly productive research group that suggests the possibility of editing RNA transcripts to alter their coding potential in a programmable manner,” David Liu…[who] has a report out today in Nature describing specific nucleotide editing of DNA by a similar method.

Feng Zhang (base editing) gives a pat on the back to David Liu (RNA editing), and Liu reciprocated, or vice versa. Taken together, they are making face-saving attempts that ignore everything known to serious scientists about biophysically constrained viral latency.

The tool itself could be further developed, adds computational biologist Eugene Koonin of the National Center for Biotechnology Information who also was not involved in the study. “This paper is not the end of the road,” he says. It’s possible that Cas13b could be fused to a variety of editing enzymes that would allow a range of different sequence changes. The possibilities are numerous, Koonin says, and “the best is still to come.”

Koonin is a biologically uninformed science idiot who has followed in the footsteps of others like him. Their computations link mutations to evolution across millions of years. The computational biologists are evolutionary biologists who have failed to link food energy from the creation of enzymes and the the RNA-mediated editing of the enzymes, which is required to link differences in sequence changes from fixation of RNA-mediated amino acid substitutions in organized genomes to the prevention of virus-driven messenger RNA degradation. All serious scientists have linked the virus-driven degradation of messenger RNA from mutations to all pathology. Koonin’s claim that “the best is still to come” is moronic.
Every link to energy-dependent RNA-mediated cell type differentiation via the pheromone-controlled fixation of amino acid substitutions has been detailed in the context of experimental evidence. But, Koonin (2016) made this ridiculous claim:

The proper question is: how has this sequence evolved? And the proper null hypothesis posits that it is a result of neutral evolution: that is, it survives by sheer chance provided that it is not deleterious enough to be efficiently purged by purifying selection. To claim adaptation, the neutral null has to be falsified.

To claim evolution, Koonin must link food energy from the pheromone-controlled physiology of reproduction to fixation of a beneficial mutation in the organized genome of one species that evolved into another species.
If Koonin and others like him cannot provide an example of how biologically-based evolution occurs, there is only the pseudoscientific nonsense of their mathematical models for comparison to facts about: How flu shot manufacturing forces influenza to mutate

“Now we can explain — at an atomic level — why egg-based vaccine production is causing problems,” said TSRI Research Associate Nicholas Wu, Ph.D., first author of the study, published recently in the journal PLOS Pathogens.

Clearly, an explanation — at the atomic level — of how viruses adapt to the cell types of one species during the production of an egg-based vaccine must be linked from atoms to ecosystems in all living genera via adaptations in the host.
See for example: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems (2014)

The genesis of variation is manifested in ecological variation, which confers the ability to adapt via nutrient-dependent epigenetically-effected pheromone-controlled ecological, social, neurogenic, and socio-cognitive niche construction. Niche construction is manifested in organismal complexity. Everything about ecological adaptation appears to make sense in the light of what is currently known about molecular biology. What is currently known about the conserved molecular mechanisms that link the epigenetic landscape to the physical landscape of DNA can now be compared to any forthcoming explanations that attempt to make sense of how mutation-driven evolution might occur.

A rendering of how changes in an electron's motion (bottom view) alter the scattering of light (top view), as measured in a new experiment that scattered more than 500 photons of light from a single electron. Previous experiments had managed to scatter no more than a few photons at a time. Credit: Extreme Light Laboratory|University of Nebraska-Lincoln

From base editing to RNA editing

Base Editing Now Able to Convert Adenine-Thymine to Guanine-Cytosine

“Nature conveniently provides us with cytosine deaminase enzymes that operate on DNA,” Liu tells The Scientist.

The creation of quantized energy in sunlight links energy as information from electrons to ecosystems via the physiology of reproduction in all living genera. The claim that “Nature” provides us with cytosine deaminase enzymes makes it seem that the enzymes emerged and automagically evolved to become purposeful and meaningful in the context of ridiculous theories about mutation-driven evolution.
See for comparison: All about that base (video parody)
See also: RNA Editing Possible with CRISPR-Cas13

Introducing specific sequence changes into RNA molecules could allow researchers to answer questions about alternative splicing mechanisms, translation, and even editing, he says. “There’s a lot of scope.”

The entirety of that scope was addressed in the context of energy-dependent RNA-mediated cell type differentiation in our section on molecular epigenetics from this 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.
All biophysically constrained RNA-mediated energy-dependent cell type differentiation has since been linked from the pheromone-controlled physiology of reproduction to supercoiled DNA via the fixation of amino acid substitutions and chromosomal rearrangements.
The facts about the amino acid substitutions in the context of transgenerational epigenetic inheritance link electrons to ecosystems via the cryo-EM technology that won the 2017 Nobel Prize in Chemistry.
See: Chemists know (video parody)
See also:

Feedback loops link quantized energy as information to biophysically constrained RNA-mediated protein folding chemistry. Light induced energy-dependent changes link angstroms to ecosystems from classical physics to chemistry/chirality and to molecular epigenetics/autophagy. The National Microbiome Initiative links microbial quorum sensing to the physiology of reproduction via endogenous RNA interference and chromosomal rearrangements. The rearrangements link energy-dependent fixed amino acid substitutions to the Precision Medicine Initiative via genome wide inferences of natural selection. This detailed representation of energy-dependent natural selection for codon optimality links biologically- based cause and effect from G protein-coupled receptors to RNA-mediated amino acid substitutions and the functional structure of supercoiled DNA. Energy-dependent polycombic ecological adaptations are manifested in supercoiled DNA. Chromosomal inheritance links the adaptations from morphological phenotypes to healthy longevity via behavioral phenotypes. For contrast, virus-driven energy theft is the link from messenger RNA degradation to negative supercoiling, constraint breaking mutations, and hecatombic evolution. The viral hecatomb links transgenerational epigenetic inheritance from archaea to Zika virus-damaged DNA, which typically is repaired by endogenous RNA interference and fixation of RNA-mediated amino acid substitutions in organized genomes

rp_levels-of-organization.jpg

Virus-driven mutation or amino acid substitution

A computer program just ranked the most influential brain scientists of the modern era

Excerpt:

“My first thought was, ‘Who could I tell without appearing immodest?’” he said. “I then realized the only people who would want to hear about this are my children!”

My comment: Oxytocin-related peptides are 9-13 amino acids long, but they can be recognized in genomic sequences. That allows them to be placed into the context of claims that link the nutrient energy-dependent de novo creation of G protein-coupled receptors to the development of brain-based behavior via the pheromone-controlled physiology of reproduction.

Fixation of RNA-mediated amino acid substitutions is the link from biophysically constrained RNA-mediated protein folding chemistry in yeasts to all cell type differentiation in all cells of all individuals of all living genera via the decapaptide, gonadotropin releasing hormone (GnRH), which is 10 amino acids long. A single amino acid substitution links achiral glycine in position 6 to all morphological and behaviorial diversity via what is known about energy-dependent ligand-receptor interactions. The interactions link quantized energy from the sun to the anti-entropic virucidal effects of ultraviolet light, which facilitates RNA-mediated DNA repair.
The obvious links from the energy-dependent creation of the innate immune system to supercoiled DNA, which protects all organized genomes from virus-driven energy theft, were placed into the context of the evolution of prairie vole monogamy and human heterosexual love by Larry Young in VIRUS EVOLUTION ( AMAZING DOCUMENTARY). Young is not on the list of the most influential brain scientists of the modern era, but perhaps he should be considered.
Watch him link virus-driven energy theft to bonding and love in the context of more pseudoscientific nonsense than you may ever see again. Then, examine what is known to serious scientists about energy-dependent autophagy. Wait to see who will be next to link energy-dependent autophagy from cell type differentiation to all biodiversity by what is known about the differences between C. elegans and P. pacificus, a predatory nematode with teeth.

For comparison, see: Polycombic ecological adaptation as a science, not a theory (2)

My comment: Polycombic ecological adaptation appears to link energy-dependent epigenetic effects on hormones (i.e., proteins) to chromatin structure in telomeric regions, which links the effect on transcription and silencing of various genes to hormone-organized and hormone-activated affects on behavior. The hormone-organized and hormone-activated behaviors link the epigenetic landscape of yeasts to the physical landscape of supercoiled DNA in species from bacteria to invertebrates and all vertebrates via the de novo creation of G protein-coupled receptors, which link chemotaxis and phototaxis to all biodiversity.

The most influential brain scientists appear to have missed what is known about the energy-dependent links from chemotaxis and phototaxis to all biodiversity. That fact was put into the context of this claim by Jaak Panksepp:

My feeling is that the social brain has many levels. If you don’t understand the foundational level, then you can do brain imaging until you’re blue in the face, but you still will not understand the process at a deep causal level.

See also: Oxytocin mediated behavior in invertebrates: an evolutionary perspective

Excerpt:

While the presence of the peptide’s gene in the genome does not necessarily mean that a cyclized, mature peptide with functional receptors is made by the organism, peptide sequence homology serves as the best available proxy for determining which lineages have the oxytocin neuromodulatory system, defined as a functional, mature peptide with one or more functional receptors.

See for comparison: Evolution of gonadotropin-releasing hormone (GnRH) structure and its receptor

Excerpt:

The discovery of the fact that one decapeptide molecule, among the GnRHs, was constructed perfectly at the beginning of 400 million years evolution and that it is not possible to improve its physiological potency using the any natural amino acid is, in my opinion, important, fascinating and beautiful.

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: The failure of the most influential brain scientists of the modern era to link nutrient energy-dependent RNA-mediated amino acid substitutions to sex differences in cell types and all other differences in the cell types of all individuals of all species exemplifies the disastrous failure of the neo-Darwinian “Modern Synthesis.” It was invented before anyone knew about the role that nutritional epigenetics must play in healthy longevity and before anyone knew the role that virus-driven energy theft plays in all pathology.

Pseudoscientists invented a theory based on de Vries definition of mutation, and more theories were added in the absence of experimental evidence that could link top-down causation to cell type differentiation in all genera. Instead of energy-dependent cell type differentiation, we got this:

For comparison, see: Mutation-Driven Evolution

Excerpt:

Mutation… includes nucleotide substitution, insertion/deletion, segmental gene duplication, genomic duplication, changes in gene regulatory systems, transposition of genes, horizontal gene transfer, etc.

My comment: The definition above links mutations to any change in any genome.

See for comparison: Updates of the HbVar database of human hemoglobin variants and thalassemia mutations

Excerpt:

Single nucleotide substitutions or indels [insertions/deletions] can lead to several hemoglobin variants owing to amino acid replacements, while molecular defects [mutations] in either regulatory or coding regions of the human HBA2, HBA1, HBB or HBD genes can minimally or drastically reduce their expression, leading to α-, β- or δ-thalassemia, respectively.

My comment: The facts about nutrient energy-dependent amino acid substitutions link hemoglobin variants from ecological adaptation to healthy longevity and the facts also link molecular defects from mutations to the pathology of α-, β- or δ-thalassemia, respectively. It would be difficult to include facts about biophysically constrained energy dependent cell type differentiation in the context of any other model that links amino acid substitutions to healthy longevity and links mutations to all pathology in all living genera.

Unfortunately, some medical laboratory scientists are still not getting the message about the difference between a mutation and fixation of an amino acid substitution.

See: Towards a Cure for Sickle Cell Anemia Through CRISPR

Excerpt:

There is much more to be done before this type of work can used to treat people, including making sure that this type of genome editing isn’t introducing unintended effects. However, this is the next step toward an actual cure for the disease, which is very rare in medicine.

My comment: This reporter does much more than most who continue to misinform other medical professionals. She fails to recognize the fact that serious scientists have been complaining about the potential pitfalls of the CRISPR/Cas9 genome technique. It is being phased out of the potential treatment regimen because researchers have realized they first need to understand how RNA-mediated cell type differentiation is biophysically constrained before causes the constraints to potentially be broken by a virus that quickly adapts and causes the death of millions in the context of a “science fiction becomes fact” scenario / movie script.

Scientists edit genome to cure sickle cell anemia

HbVar: A Database of Human Hemoglobin Variants and Thalassemias
My comment: All variants are energy-dependent ecological adaptations that require fixation of amino acid substitutions in supercoiled DNA via the physiology of reproduction, which links the supercoiled DNA to protection from virus-driven energy theft and genomic entropy in all genera. Only biologically uninformed theorists fail to learn the difference between mutations and amino acid substitutions.

See also:  Journal of Neuroscience Research An Issue Whose Time Has Come: Sex/Gender Influences on Nervous System Function

Addressing Sex as a Biological Variable

See for comparison: From Fertilization to Adult Sexual Behavior (1996)

Excerpt:

The general sense of the word “environment” as something exterior to the person is retained, even if that something influences intraperson processes. In addition, we focus directly on molecular events themselves. Here the “environment” involved can be that within a DNA segment. We also expand the notion of “biologically based sex differences.”

Tweeted to John Hewitt: Our works intersect again https://www.ncbi.nlm.nih.gov/pubmed/27814653 and http://dx.doi.org/10.1002/jnr.23886 Life is good in the absence of theories!

Genetic and epigenetic factors underlying sex differences in the regulation of gene expression in the brain

Mitochondrial genome and epigenome: two sides of the same coin

Addendum: Energy-dependent biophysically constrained protein folding chemistry links RNA-mediated amino acid substitutions to supercoiled DNA via the physiology of pheromone-controlled reproduction in species from marine microbes to humans.

Alternative splicing of pre-mRNA

Polycombic ecological adaptation as a science, not a theory (2)

Evolutionary Constraints in the β-Globin Cluster: The Signature of Purifying Selection at the δ-Globin (HBD) Locus and Its Role in Developmental Gene Regulation

Conclusion:

… the results here presented indicate that purifying selection is driving not only HBD evolution but also its neighbor pseudogene, HBBP1. In the light of recent advances in the characterization of the β-globin cluster, we propose that the complex patterns of diversity observed in this genomic region arose from distinct functional constraints related with the intricate process of chromatin and protein interactions coordinating the differential expression of genes at the β-globin cluster during development.

My comment: No experimental evidence of biologically-based cause and effect suggests that any locus of genes or any pseudogene has ever evolved. Purifying selection cannot drive evolution. Only energy-dependent variations can can be linked to polycombic ecological adaptation, and only virus-driven energy theft has been linked to the creation of pseudogenes in the context of biophysical constraints on viral latency.

See for comparison: microRNA Function Is Limited to Cytokine Control in the Acute Response to Virus Infection

Excerpt:

miRNA function is generally limited to cytokine levels in response to RNA viruses

Reported as: Mount Sinai Researchers Use Cellular miRNA-Elimination Tool to Study Viral Infection Dynamics

Excerpt:

…while the loss of miRNAs had a negligible impact on the cell’s immediate reaction to a virus or the short-term biology of the cell, sustained depletion had dramatic results on gene expression that was coupled to a burst of cytokines. The researchers concluded in the paper that miRNA function is limited to modulating the biology of the cell over long periods of time.

My comment: In my model, energy-dependent changes in the microRNA/messenger RNA balance link nutrient energy-dependent changes to all healthy longevity and virus-driven energy theft is linked to all pathology. Over long periods of time, autophagy is the link to polycombic ecological adaptation or virus-driven hecatombic evolution of pathology via energy-dependent biophysically constrained RNA-mediated protein folding chemistry. For example, fixation of amino acid substitutions differentiates all cell types in all individuals of all living genera in the context of the physiology of reproduction. For comparison, virus-driven hecatombic pathology is linked from mutations to all pathology.

Simply put, in my model of polycombic ecological adaptation, differential gene expression is nutrient-dependent and controlled by the physiology of reproduction.

See: Nutrient-dependent/pheromone-controlled adaptive evolution: a model

Conclusion: 

…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: Claims about RNA-mediated polycombic ecological adaptation were first placed into the context epigenetic imprinting in our 1996 review.

See: From Fertilization to Adult Sexual Behavior

Excerpt:

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, 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: Polycombic ecological adaptation appears to link energy-dependent epigenetic effects on hormones (i.e., proteins) to chromatin structure in telomeric regions, which links the effect on transcription and silencing of various genes to hormone-organized and hormone-activated affects on behavior. The hormone-organized and hormone-activated behaviors link the epigenetic landscape of yeasts to the physical landscape of supercoiled DNA in species from bacteria to invertebrates and all vertebrates via the de novo creation of G protein-coupled receptors, which link chemotaxis and phototaxis to all biodiversity.

For comparison, see: Mutation-Driven Evolution

Excerpt:

Mutation… includes nucleotide substitution, insertion/deletion, segmental gene duplication, genomic duplication, changes in gene regulatory systems, transposition of genes, horizontal gene transfer, etc.

My comment: The definition above links mutations to any change in any genome.

See for comparison: Updates of the HbVar database of human hemoglobin variants and thalassemia mutations

Excerpt:

Single nucleotide substitutions or indels [insertions/deletions] can lead to several hemoglobin variants owing to amino acid replacements, while molecular defects [mutations] in either regulatory or coding regions of the human HBA2, HBA1, HBB or HBD genes can minimally or drastically reduce their expression, leading to α-, β- or δ-thalassemia, respectively.

My comment: The facts about nutrient energy-dependent amino acid substitutions link hemoglobin variants from ecological adaptation to healthy longevity and the facts also link molecular defects from mutations to the pathology of α-, β- or δ-thalassemia, respectively. It would be difficult to include facts about biophysically constrained energy dependent cell type differentiation in the context of any other model that links amino acid substitutions to healthy longevity and links mutations to all pathology in all living genera.

See for example:  Criticisms of the nutrient-dependent pheromone-controlled evolutionary model 

Excerpt:

…James Kohl presents an unsupported challenge to modern evolutionary theory and misrepresentations of established scientific terms and others’ research.

My comment: The claims of a biologically uninformed undergraduate student reviewer were placed into the context of modern evolutionary theory, which involves Masatoshi Nei’s simple-minded revision of neo-Darwinian pseudoscientific nonsense. Nei does not compare his theory of mutations to the facts about nutrient energy-dependent fixation of amino acid substitutions in supercoiled DNA. The problem appears to be the use of the term “mutation” in the textbook published on the same day as my 2013 review was published.

I linked the energy-dependent fixation of amino acid substitutions to all healthy longevity. Nei’s textbook misrepresentations did not link anything to healthy longevity, but linked mutations to what I claimed are nutrient-dependent pheromone-controlled polycombic ecological adaptations.

I failed to include what is known about energy-dependent codon optimality in the context of polycombic ecological adaptations because there was no experimental evidence of biologically-based cause and effect to support those claims at the time of our 1996 review or my 2013 review. For comparison, there has never been any experimental evidence of biologically-based cause and effect to support claims about mutation-driven evolution. Simply put, nothing known to serious scientists about cell type differentiation suggest that mutation-driven evolution can occur.

For comparison, see: New analysis of big data sheds light on cell functions
Excerpt:

With today’s technology, scientists are able to generate data about a cell’s or organism’s complete set of genes, proteins, RNA profiles, metabolites and much more—known as omic data. Using omic data, scientists can model complex biological interactions and gain a more holistic view of different cellular processes.

See also: Research Topic Multi-omic Data Integration

Excerpt:

Stable, predictive biomarkers and interpretable disease signatures are seen as a significant step towards personalized medicine. In this perspective, integration of multi-omic data coming from genomics, transcriptomics, glycomics, proteomics, metabolomics is a powerful strategy to reconstruct and analyse complex multi-dimensional interactions, enabling deeper mechanistic and medical insight.

My comment: Glycomics, transcriptomics, proteomics, metabolomics and genomics have established fact about the biological basis of complex multi-dimensional interactions that link the nutrient-dependent pheromone-controlled physiology of reproduction in bacteria from quorum sensing to the molecular mechanisms that enable deeper mechanistic and medical insight in the context of the National Microbiome Initiative and Precision Medicine Initiative.

See for example: ‘Oming in on RNA–protein interactions

Excerpt:

…the interactions between pre-mRNA and proteins fine-tune alternative splicing in a manner that can gradually create new protein functionalities without the need to create additional genes and without affecting existing proteins [4-6].

See for comparison: From Fertilization to Adult Sexual Behavior

Excerpt:

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…. 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: Detailed examples of how the interactions between pre-mRNA and alternative splicings create new genes in the fine-tuned energy-dependent functional structure of supercoiled DNA explain how all cell types of all individuals of all living genera are protected from virus-driven energy theft. Energy-dependent RNA-mediated amino acid substitutions are fixed in organized genomes via the physiology of reproduction, which helps to prevent the transgenerational epigenetic inheritance of nearly all pathology by linking innate immune system to supercoiled DNA.

For comparison, viruses steal the energy that is required for cell type differentiation, which is how mutations are linked to all pathology. All differences between healthy longevity and virus-driven human pathology can be explained in the context of how nutrient energy-dependent microRNAs. The nutrient energy-dependent microRNAs are carried by erythrocytes in species with circulating blood.

See: Pitfalls of analysis of circulating miRNA: role of hematocrit

MicroRNAs are are delivered to the cell types on an as needed basis. When too few nutrient energy-dependent microRNAs are available, viruses use the existing energy they steal from cells to replicate. Eventually, the replication of the viruses causes the mutations, which are linked to all pathology. That’s why it is important to revisit the facts presented in the context of this article, which was published on 10/26/16

See: Multi-omic data integration enables discovery of hidden biological regularities
I reported this here as: Polycombic ecological adaptation as a science, not a theory for comparison to Biological evolution as a philosophy, not a science.
Despite several attempts to discuss the difference between science and philosophy, no progress was made.
See for example: Evolutionary assumptions (revisited)
See also the impasse that was reached in this attempt to discuss the anti-entropic virucidal energy of the sun.
It is worth joining The Battlefield FB group to see that others would rather hold on to their theories and opinions despite the overwhelming amount of experimental evidence that I have used to support my claims. For me, it is time to move forward and focus on the rediscovery of hidden biological regularities.
Finally, others have discovered that small intranuclear proteins generate alternative splicing techniques of pre-mRNA, which is how microRNAs link hydrogen-atom transfer in DNA base pairs in solution to the conserved molecular mechanisms of energy-dependent cell type differentiation, and to all cell type differences in all individuals of all living genera.
For comparison, this is an example of how virus-driven energy theft is linked viral replication and to virulence:
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.

For an example of how nutrient energy-dependent RNA-mediated amino acid substitutions are linked to healthy longevity via the physiology of reproduction, see:

…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: The facts stated above have forced theorists to invent evolutionary cell biology.
See Evolutionary cell biology: Two origins, one objective
Reported as: Why some junk DNA is selfish, but selfish genes are junk
Excerpt:

“A commonly held but incorrect stance is that essentially all of evolution is a simple consequence of natural selection.” They point out, for example, that many pathways to greater complexity of both genomes and cells don’t confer any selective fitness.

My comment: Greater complexity requires a link from ecological variation to polycombic ecological adaptation, which links supercoiled DNA to protection from the virus-driven hecatombic evolution of all pathology.
My comment: New theories are worthless if they do not include information on the role of energy in cell type differentiation or the role of virus-driven energy theft in all pathology.
See for comparison the facts about: Detection of hemoglobinopathies and thalassemias using automated separation systems
See also: In vivo correction of anaemia in β-thalassemic mice by γPNA-mediated gene editing with nanoparticle delivery
Excerpt: 

The combination of nanoparticle delivery, next generation γPNAs and SCF treatment may offer a minimally invasive treatment for genetic disorders of the blood that can be achieved safely and simply by intravenous administration.

My comment: That fact suggests all suffering and death caused by hemoglobin variants is caused by neo-Darwinian theorists who do not know how the variants link ecological variation to polycombic ecological adaptation.

Reported as: Scientists edit gene mutations in inherited form of anemia
Excerpt:

The researchers found that the technique corrected the mutation to such a degree that the mice no longer had symptoms of thalassemia. After 140 days, they tested hemoglobin levels in the animals and found them to be normal.
“The fundamental result here is that with nanoparticles containing PNAs, along with template DNA, and simple IV infusion of molecules, we achieved enough gene editing to effectively cure the anemia in mice that had thalassemia,” Glazer said.

My comment: The ability to correct the mutation requires a link from energy-dependent changes in hydrogen-atom transfer in DNA base pairs in solutions such as blood. That’s how their IV therapy works. It changes the microRNA/messenger RNA balance and that forces the innate immune system to repair the damaged DNA.
See also:  Two novel loci, COBL and SLC10A2, for Alzheimer’s disease in African Americans
Excerpt:

Two SNPs at novel loci, rs112404845 (P = 3.8 × 10−8), upstream of COBL, and rs16961023 (P = 4.6 × 10−8), downstream of SLC10A2, obtained genome-wide significant evidence of association with the posterior liability.

Reported as: Study Identifies Two New Genes Responsible for Alzheimer’s in African Americans
Excerpt:

In 2013, a genome-wide association study of AD in more than 5,500 African Americans identified two genetic risk factors for AD. This study looked at genetic variants across subjects’ entire genome and compared their frequency in cases versus controls.
By doing so they were able to identify two new genes (COBL and SLC10A2) associated with risk of AD in African Americans.

My comment: The author’s study results link hydrogen-atom transfer in DNA base pairs in solution to energy-dependent changes in the microRNA/messenger RNA balance. The neuroscience news report claims they identified two new genes. The neuroscience news report then links the genes — instead of the energy-dependent changes — to the disease in a human population. Many African Americans are examples of how ecological variation has been linked to polycombic ecological adaptation via hemoglobin variants. The adaptations include amino acid substitutions linked to the stability of organized genomes in populations where malaria is endemic. Failed adaptations are included in examples of virus-driven energy theft linked to mutations and the pathology of Alzheimer’s disease.

My comment: The ability to edit out gene mutations clearly links RNA-mediated amino acid substitutions to supercoiled DNA and all biodiversity.
See also: Inventing neo-Darwinism
See also: Pioneering Geneticist Explains Ambitious Plan to “Write” the Human Genome

Excerpt:

…he notes that with an editing tool like CRISPR, one base out of many can be altered, but with a synthesis approach, a hundred edits could be made. This sort of change, he tells JAMA, could make a cell resistant to multiple viruses.

My comments: All the changes in base pairs may already have been linked from natural selection for codon optimality and energy-dependent changes in RNA-mediated cell type differentiation to supercoiled DNA, which links the physiology of reproduction from the innate immune system to fixation of the amino acid substitutions that differentiate the cell types of all living genera. If so, what might happen to an organized genome when a hundred edits are made?

Will anyone be able to stop the hecatombic evolution of pathology via the polycombic ecological adaptation, which links autophagy to healthy longevity via protection of organized genomes from virus-driven entropy?

See also: Yale scientists edit gene mutations in inherited form of anemia Genetics & Genomics

A new gene therapy is being tested for its ability to treat thalassemia, a form of anemia caused by genetic mutations. So far, scientists have successfully corrected gene mutations causing the disease in mice, and now researchers are interested in seeing if the same approach will work effectively in humans.
“The fundamental result here is that with nanoparticles containing PNAs, along with template DNA, and simple IV infusion of molecules, we achieved enough gene editing to effectively cure the anemia in mice that had thalassemia. We demonstrated we have extremely low off-target effects.”

See for comparison:

Product Development Pipeline

Excerpt:

Each microRNA mimic in our pipeline is designed to replicate the activity of a single tumor suppressor miRNA and regulate the expression of key oncogenes across multiple oncogenic pathways which can prevent proliferation and induce apoptosis in cancer cells.

See also: VACRC Projects

Excerpt: Future Projects

 The Influence of Carbon Dioxide Enhancement on Plant Growth
 Thermoregulation in Honey Bees
 Biochemistry and Taxonomy in Pine Trees
 The Formation of Multiple Tree Rings in Bristlecone Pine Trees

The VACRC suddenly seems willing to take everything I have claimed about RNA-mediated cell type differentiation during the past twenty years and begin to investigate the claims. This would have been a desirable outcome 20 years ago, but now it might prevent progress via use of my model. The model links energy-dependent changes from angstroms to ecosystems in all living genera, it and links virus-driven energy theft to all pathology.

The Pacific Yew Tree and production of taxol is an example of how the physi0logy of reproduction in soil bacteria can be linked from plant growth to the honeybee model organism of thermoregulation and behavior, which must be linked to the biochemistry and taxonomy of all species. That becomes meaningful via the explanatory power of a model that links RNA-mediated amino acid substitutions to all energy-dependent biodiversity via the conserved molecular mechanisms of polycombic ecological adaptation we detailed in our 1996 review.

However, when others wait too long to accept a model that may already have led to a paradigm shift, they may also realize it. That fact was addressed by Kaveli Kull in the context of next week’s meeting of the Royal Society.

See: Kalevi Kull: Censorship & Royal Society Evo Event

Excerpt:

Nobody wants to belong to the party of losers. One of the best strategies in such a case is evidently an interpretation of the change as a gradual accumulation of knowledge while their work has always been at the cutting edge.

My comment: Some work by young earth creationists has been at the cutting edge since 1996, as indicated here: Where do viruses come from?

Excerpt:

‘Viruses tend to keep nutrients away from the big stuff and keep them going around in the little stuff,’ says Fuhrman. If so, viruses have shaped the entire structure of the ecosystem.”9

My comment: 9 is Holmes, B. (1996) Who Rules the Waves? New Scientist 152(2054):8-9, supp I have not read it in its entirety but the claim fits into the context of everything else I have learned about physics, chemistry, and conserved molecular mechanisms of RNA-mediated cell type differentiation, which appears to be biophysically constrained in all living genera via their nutrient-dependent pheromone-controlled physiology of energy-dependent reproduction.