Caption: Contemporary analyses of cell metabolism have called out three metabolites: ATP, NADH, and acetyl-CoA, as sentinel molecules whose accumulation represent much of the purpose of the catabolic arms of metabolism and then drive many anabolic pathways. Such analyses largely leave out how and why ATP, NADH, and acetyl-CoA (Figure 1) at the molecular level play such central roles. Yet, without those insights into why cells accumulate them and how the enabling properties of these key metabolites power much of cell metabolism, the underlying molecular logic remains mysterious. Four other metabolites, S-adenosylmethionine, carbamoyl phosphate, UDP-glucose, and Δ2-isopentenyl-PP play similar roles in using group transfer chemistry to drive otherwise unfavorable biosynthetic equilibria. This review provides the underlying chemical logic to remind how these seven key molecules function as mobile packets of cellular currencies for phosphoryl transfers (ATP), acyl transfers (acetyl-CoA, carbamoyl-P), methyl transfers (SAM), prenyl transfers (IPP), glucosyl transfers (UDP-glucose), and electron and ADP-ribosyl transfers (NAD(P)H/NAD(P)+) to drive metabolic transformations in and across most primary pathways. The eighth key metabolite is molecular oxygen (O2), thermodynamically activated for reduction by one electron path, leaving it kinetically stable to the vast majority of organic cellular metabolites

Ecological Adaptations vs the Randomness of Evolution (2)

Summary: See for comparison: Make ‘Em Resistant to Viruses

In the new proposal — which Science says was released in advance of a meeting today — GP-write leaders say “ultrasafe” cells could be developed by making some 400,000 changes to the human genome.

A Fast OneStep Digestion of DNA or RNA for Global Detection and Characterization of Nucleotide Modifications (link opens pdf)
Product information:

The Nucleoside Digestion Mix is an optimized mixture of enzymes that provides a convenient one-step method to generate single nucleosides from DNA or RNA for quantitative analysis by liquid chromatography-mass spectrometry (LC-MS), eliminating the need for sequential multi-step, time-consuming digestion protocols.

Digests both DNA and RNA to single nucleosides

A source of anti-entropic energy is required to create nucleosides and nucleotides. The quantized energy as information was available to modify nucleotides after the creation of sunlight.
See also: Nucleoside vs. Nucleotide

A nucleoside consists of a nitrogenous base covalently attached to a sugar (ribose or deoxyribose) but without the phosphate group. A nucleotide consists of a nitrogenous base, a sugar (ribose or deoxyribose) and one to three phosphate groups.

Nucleoside = Sugar + Base
Nucleotide = Sugar + Base + Phosphate

The link from the”optimized mixture of enzymes” to Digestion of DNA or RNA links the quantification of epigenetic modifications and the activity of nucleic acid modifying enzymes from energy-dependent microRNA biogenesis to the functional structure of cellular RNA, which has been linked to viral latency and ecological adaptations in all living genera.
The facts about the energy-dependent creation of microRNAs and ecological adaptations have been placed into the context of High-Resolution Epigenomic Atlas of Human Embryonic Craniofacial Development.

These data are provided in easily accessible formats for both craniofacial researchers and clinicians to aid future experimental design and interpretation of noncoding variation in those affected by craniofacial abnormalities.

The facts were reported in Blueprint for the skull: A search for cleft palate’s cause reveals a map of the facial genome

He studies the human genome, but not the genes that tell the body what proteins to make. Instead, he focuses on regulators, parts of the DNA that tell genes when and where to act. These regulators, also known as enhancers, tend to be linked to specific parts of the body.

microRNA cleft palate
1 of 33: A functional polymorphism in the pre-miR-146a gene is associated with the risk of nonsyndromic orofacial cleft.
enhancer cleft palate
1 of 35 Genome-Wide DNA Methylation Analysis During Palatal Fusion Reveals the Potential Mechanism of Enhancer Methylation Regulating Epithelial Mesenchyme Transformation.
The link from the energy-dependent creation of microRNAs to food energy-dependent genome-wide RNA-directed DNA methylation is perfectly clear until the term enhancer is used in the context of a potential mechanism regulating epithelial mesenchyme transformation.
The conserved molecular mechanisms of energy-dependent epigenetically-effected cell type differentiation are missing and the substitution of a potential mechanism of methylation can be used to support neo-Darwinian nonsense about mutation-driven evolution.
Even after pseudoscientists admit that their theories of craniofacial development are ridiculous, since development is energy-dependent and epigenetically effected, they try to place their findings back into the context of gene-centric theories.
Alternatively, they must know that the virus-driven theft of quantized energy links Zika virus-damaged DNA to craniofacial development with the most severe effects on the size of the brain and skull.
See also: Incomplete host immunity favors the evolution of virulence in an emergent pathogen

Partially protective vaccination can sometimes select for increasingly virulent pathogens.

Reported as: In nature, an imperfect immune system drives the evolution of deadly pathogens

As annual flu shot patrons know, immune systems are not perfect and must be constantly reinforced to protect against rapidly evolving pathogens.

Also:

…birds that eat at feeders are more likely to be infected with the disease, which causes red, swollen eyes and often blindness that results in death.

The link from what the birds and the bees eat to healthy longevity was detailed in my 2013 refutation of neo-Darwinian pseudoscientific nonsense.

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

Scientific creationists in the US have started to tout my model without attribution.
See: Are Evolution and Adaptation the Same? 

Mechanisms of adaptation are made up of complex integrated components, including environmental sensors, signaling pathways, feedback and feed-forward loops, and information control systems in the creature’s DNA.

See also: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems (2014)
See for comparison: Next-generation diagnostics with CRISPR

The sentinel discovery that prokaryotes (bacteria and archaea) have heritable adaptive immunity mediated through CRISPR and CRISPR-associated (Cas) proteins has led to transformative advances in molecular biology, most notably in gene editing (2).

The discovery of heritable adaptive immunity ended the pseudoscientific nonsense about mutation-driven evolution. It linked vaccinations and gene editing to unpredictable outcomes in species from microbes to humans by altering the perfection of our innate immune system. The alterations link the virus-driven degradation of our messenger RNA to all pathology.
But see: Cytosis for ages 10+

A board game taking place inside a human cell! Players compete to build enzymes, hormones and receptors and fend off attacking Viruses!

See for comparison: Make ‘Em Resistant to Viruses

In the new proposal — which Science says was released in advance of a meeting today — GP-write leaders say “ultrasafe” cells could be developed by making some 400,000 changes to the human genome.

"Evolution of Man. - Undoubtedly there once lived upon the earth races of men who were much lower in their mental organization than the present inhabitants.

Autophagy is the antiphage defense strategy (2)

2/15/17 Energy as information and constrained endogenous RNA interference (video)
The 6.46 minute-long technical presentation (above) from the Precision Medicine Virtual Conference is difficult to understand.Thus, 10 months later, Nik Willmore asked:

12/24/17 What are your insights into CRISPR and mTOR, for a young audience? I’m not mocking you…yet, Humpty Dumpty. What is the basis of your unifying principle? Vibration? Bohmian morphogenetic fields? Modified Darwin? God? –Nik Willmore 

12/25/17 Replying to

God created the anti-entropic virucidal energy of sunlight and all energy-dependent biodiversity via the physiology of pheromone-controlled reproduction. I co-authored a book about that for a young audience in 1995/2002, and a 6-part series for today.

1/1/18 Replying to

Do you understand any aspect of how to model biophysically constrained biologically-based energy-dependent top-town causation and bottom-up effects on cell type differentiation via the physiology of reproduction and autophagy? The “walking fish” walks straight from quantum physics to quantum souls (2)

1/9/18 Viral suppressors of RNAi employ a rapid screening mode to discriminate viral RNA from cellular small RNA

My paraphrased summary:

RNA interference (RNAi) is our indispensable antiphage defense mechanism. Viruses escape the defense system by the theft of quantized energy, which encodes RNAi suppressors that prevent elimination of viral RNAs. The suppressors ensure energy-dependent virus accumulation.

1/12/18 Human cytomegalovirus-encoded miR-UL112 contributes to HCMV-mediated vascular diseases by inducing vascular endothelial cell dysfunction

The significantly altered pathways mainly include the mitogen-activated protein kinase signaling pathway, cell adhesion molecules, chemokine signaling pathway, cytokine-cytokine receptor interaction, circadian rhythm-mammal, mineral absorption, protein processing in the endoplasmic reticulum, proximal tubule bicarbonate reclamation, vasopressin-regulated water reabsorption, and arachidonic acid metabolism. In conclusion, hcmv-miR-UL112 could serve as a potential biomarker, and the miRNA-mediated regulation of signaling pathways might play significant roles in the physiological effects of hcmv-associated diseases.

1/12/18 H5N1 influenza virus-specific miRNA-like small RNA increases cytokine production and mouse mortality via targeting poly(rC)-binding protein 2

We conclude that miR-HA-3p is the first identified influenza virus-encoded microRNA-like functional RNA fragment and a novel virulence factor contributing to H5N1-induced ‘cytokine storm’ and mortality.

Virus-encoded microRNA-like functional RNA fragments are not novel virulence factors. They link the virus-driven degradation of messenger RNA to all pathology in all living genera via the theft of quanitzed energy, which typically links the fixation of RNA-mediated amino acid substitutions to healthy longevity.
See: Viral MicroRNAs, Host MicroRNAs Regulating Viruses, and Bacterial MicroRNA-Like RNAs
All serious scientists know what goes wrong in the context of host microRNA-mediated regulation of viruses. They also know how it goes wrong. See 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.

The serious scientists do not claim that viruses evolve. Scientists who make claims about evolution  typically do not know how to link the creation of sunlight from ecological variation to food energy-dependent pheromone-controlled ecological adaptation via the physiology of biophysically constrained reproduction and biophysically constrained viral latency. Indeed, most pseudoscientists do not know the difference between a mutation and an RNA-mediated amino acid substitution.
See for comparison: Mechanisms of Recombination conference Start: Sunday, May 20, 9.00am Finish: Tuesday, May 22, 6.45pm

Description

Genetic recombination provides an important mechanism for the repair of chromosome breaks caused by DNA damage or replication fork demise. Defects in the recombination process have been linked to cancer predisposition, in particular breast cancers caused by mutations in BRCA1, BRCA2 and PALB2, and also acute leukemias associated with the rare genetic disease Fanconi anemia. Understanding precisely how recombination occurs is of interest to workers in the fields of meiosis, DNA repair, replication, chromosome architecture and interactions, and chromatin biology.

Download provisional conference program
Excerpts:

Douglas Bishop (University of Chicago, US)
A primary function of the ATPase activity of E. coli RecA is to prevent accumulation of a toxic form of the protein bound to undamaged chromosomal sites

Maria Jasin (Memorial Sloan Kettering Cancer Center, US)
Protecting the genome by homologous recombination

The energy-dependent microRNA-mediated creation of enyzmes protects all organized genomes from the virus-driven degradation of messenger RNA that links the theft of quantized energy from mutations to all pathology.  Pseudoscientists who do not start with the creation of energy, have bastardized Darwin’s claims. His claims were based on placing “conditions of life” before natural selection. Conditions of life are energy-dependent and biophysically constrained by the mechanisms of pheromone-controlled recombination, which have been linked to autophagy by all serious scientists since 1925.
See also my RNA-mediated Facebook page and/or my RNA-mediated Facebook group and other tweets @jvkohl
The number of my tweet impressions since December 21, 2017 has climbed to more than 68,000 as the number of published works that mention “microRNA” has climbed to nearly 69,000. See for comparison: The tipping point (revisited): 68,000 publications, which was published to my other blog site on December 21, 2017.
See also: What Darwinists Fail to Consider (discussion attempt)
See also, this discussion attempt about the “spark of life.”
See also: Noncoding RNA Helps Cells Recover from DNA Damage

“The most logical, simple explanation is that the [noncoding RNA] counteracts the protein encoding form…”

My comment to the Scientist:

There is clear evidence that femtosecond blasts of UV light repair DNA in the context of energy-dependent changes in the microRNA/messenger RNA balance and autophagy, which protects all organized genomes from virus-driven energy theft and the degradation of messenger RNA.

The failure to integrate the Nobel Prize winning works of Ben Feringa (Chemisty 2016) and Yoshinori Ohsumi (Physiology or Medicine 2016) prevents theorists from linking what organisms eat to their pheromone-controlled physiology of reproduction in the context of Schrodinger’s claims in “What is Life?”(1944) and this claim by Roger Penrose in the reprint edition:

“How often do we still hear that quantum effects can have little relevance in the study of biology, or even that we eat food in order to gain energy?” (Roger Penrose 8 August 1991)

See also: From Fertilization to Adult Sexual Behavior  In our section on molecular epigenetics, we wrote:

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…

The food energy that is linked from alternative splicing techniques of pre-mRNA to the chemistry of protein folding and the pheromone-controlled physiology of reproduction in all living genera seems to be largely ignored by those who are not Nobel Laureates.

See also: Search Results for “autophagy”

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

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

Energy-dependent physical and biophysical constraints (3)

See first: Energy-dependent physical and biophysical constraints (2)
Emily Balskus Pins Down the Chemistry and Metabolism of Human Microbiomes
Summary: The chemistry and metabolism of all microbiomes is food energy-dependent and pheromone-controlled via the physiology of reproduction.
See: Feedback loops link odor and pheromone signaling with reproduction

My comment to The Scientist:

…trans-4-hydroxy-L-proline (Hyp) dehydratase, a newly discovered member of an abundant family of proteins, produced by gut bacteria, known as the glycyl radical enzymes, helps in metabolizing trans-Hyp, an amino acid that is rare in bacteria but is common in eukaryotes.

The de novo creation of energy-dependent RNA-mediated amino acid substitutions in supercoiled DNA protects the organized genomes of all living genera from the virus-driven degradation of messenger RNA, which has been linked from mutations to all pathology via the claims Schrodinger made in “What is Life?” (1944).

Indeed, in the case of higher animals we know the kind of orderliness they feed upon well enough, viz. the extremely well-ordered state of matter in more or less complicated organic compounds, which serve them as foodstuffs. After utilizing it they return it in a very much degraded form -not entirely degraded, however, for plants can still make use of it. (These, of course, have their most power supply of ‘negative entropy’ the sunlight.) (pp. 73 and 74)

See also: The Bull Sperm MicroRNAome and the Effect of Fescue Toxicosis on Sperm MicroRNA Expression

Natural selection for food energy-dependent codon optimality links the sense of smell in bacteria to the biophysically constrained viral latency that links ecological variation to ecological adaptations in species from microbes to humans via the conserved molecular mechanisms of RNA-mediated cell type differentiation.

Sunlight has since been placed into the context of quantized energy as information, which links our visual perception of mass and energy from the space-time continuum to the concept of the energy-dependent creation of quantum souls.
See also: Codon identity regulates mRNA stability and translation efficiency during the maternal-to-zygotic transition (2016) and From Fertilization to Adult Sexual Behavior (1996)
 

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.

rp_levels-of-organization.jpg

Energy-dependent creation and entropy

Theorists tend to use the term de novo when they don’t know.
If they don’t know how energy-dependent structures and functions are created, functional structures are created de novo.
See for example:  Lymphotoxin-Dependent B Cell-FRC Crosstalk Promotes De Novo Follicle Formation and Antibody Production following Intestinal Helminth Infection
If theorists don’t know what causes mutations, the mutations are de novo mutations.
See for example: Germline De Novo Mutations in GNB1 Cause Severe Neurodevelopmental Disability, Hypotonia, and Seizures
My comment: The energy-dependent de novo creation of functional structures readily extends what is known about viruses and energy theft to the creation of de novo mutations that cause all pathology. Serious scientists have linked the energy-dependent creation of nucleic acids from angstroms to ecosystems. They have linked virus-driven energy theft to all pathology via the creation of viral nucleic acids. Nucleic acids do not create themselves. Their creation is energy-dependent. Viruses steal the energy that links hydrogen-atom transfer in DNA base pairs in solution to pH and healthy longevity.
See, for instance: DNA and RNA structure: nucleic acids as genetic material
Excerpt:

Asking what holds two strands of DNA together presupposes there’s some other force trying to pull the strands apart. There is, and that force is none other than heat. Heat, after all, is just random motion of molecules, and the force of this vibrational motion depends on temperature.

Remember this:

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

See also: Viral forensic genomics reveals the relatedness of classic herpes simplex virus strains KOS, KOS63, and KOS79
Excerpt:

KOS63 and its variants have a mutation present in the TATA-box promoter region of the membrane protein US9, as well as a substitution at position 58 in the US9 gene. This substitution introduces an early stop codon, and truncates the last 32 residues of the US9 protein (Macdonald et al., 2012; Negatsch et al., 2011). This mutation removes the stop codon and elongates the neighboring open reading frame of US8A, a protein of undetermined function (Macdonald et al., 2012; Negatsch et al., 2011).

My comment: If you don’t know the difference between a mutation and an amino acid substitution, you know nothing about how energy-dependent RNA-mediated cell type differentiation is biophysically constrained in the context of thermodynamic cycles of protein biosynthesis and degradation.  But, you are among the majority.
See for comparison to what others do not know about energy-dependent cell type differentiation: Achieving diverse and monoallelic olfactory receptor selection through dual-objective optimization design
Excerpt:

Comparative Model Studies Reveal That Nature Chooses the Simplest and Robust Design of Feedback Regulation.

Conclusion:

 …enhancer elements may also help on recruiting histone modification enzymes, leading to coupling between the two layers of regulation. Future studies will reveal these possible fine-tuning elements and address its implications in other processes of gene regulations.

My comment: In other words, nature fine-tunes itself by choosing which genes must be regulated by feedback. Serious scientists joke about such ridiculous misrepresentations.
Structural diversity of supercoiled DNA (parody)
Chemists know (parody)
See also: New Insights into the Mysteries of Smell
Excerpt: 

In the new study, Dr. Xing and colleagues used these existing experimental data to create a computational model of how olfactory receptor expression can be both uniform across a single neuron, yet very diverse across the entire population of neurons. They then used this model to correctly predict several additional findings that have been demonstrated by other research groups, demonstrating that their model is valid.

My comment to the Neuroscince News site: Their model seems irrelevant compared to what is known about the biophysically constrained chemistry of energy-dependent protein folding.I plan to present this tomorrow at this free online conference.

http://www.labroots.com/virtual-event/genetics-genomics-2016

RNA-mediated physics, chemistry, and molecular epigenetics

Abstract: Olfaction and the innate immune system link energy as information from the epigenetic landscape to the physical landscape of supercoiled DNA. The sun’s biological energy is the source of the information that links angstroms to ecosystems via physics, chemistry, and molecular epigenetics.
RNA-mediated protein folding chemistry and amino acid substitutions link the anti-entropic quantized energy of sunlight from the virucidal effects of ultraviolet (UV) light to healthy longevity via biophysically-constrained energy-dependent hydrogen-atom transfer in DNA base pairs in solution and cell type differentiation.
Biomarkers link energy-dependent differences in base pairs and amino acid substitutions to biosignatures across the healthy life span. RNA-mediated amino acid substitutions also reveal the increasing complexity of interactions among cell types as pathology progresses. For comparison, successful reproduction links energy from supercoiled DNA to protection of all organized genomes from virus-driven energy theft and pathology.
This model links the sun’s biological energy from top-down causation in microbes to the most recent model of bottom-up gene activation and cell type differentiation in vertebrates. Citations to extant literature provide examples of what is currently known about how ecological variation leads to biophysically constrained cell type differentiation in the context of nutritional epigenetics and Precision Medicine, which clearly link metabolic networks and genetic networks to pharmacogenomics.
———————-
Summary: In the series of five blog posts “RNA-mediated physics, chemistry, and molecular epigenetics” (1-5), I included citations to experimental evidence of biologically-based cause and effect. The citations link energy-dependent changes from angstroms to ecosystems because that is what serious scientists do.

RNA-mediated physics, chemistry, and molecular epigenetics (5) 5/10/16

RNA-mediated physics, chemistry, and molecular epigenetics (4) 5/9/16

RNA-mediated physics, chemistry, and molecular epigenetics (3) 5/9/16

RNA-mediated physics, chemistry, and molecular epigenetics (2) 5/6/16

RNA-mediated physics, chemistry, and molecular epigenetics 5/4/16

Serious scientists do not link computer models of biologically-based cause and effect to cell type differentiation without an energy source. That’s what pseudoscientists do.
If the switch on a pseudoscientist’s computer is turned off, or their computer gets infected by a virus that steals its energy to replicate, pseudoscientists no longer have a model of anything. They have only their ridiculous theories, and the ridiculous theories of pseudoscientists do not link energy-dependent life to biodiversity via what is known to serious scientists.
See for comparison: Feedback loops link odor and pheromone signaling with reproduction and Combating Evolution to Fight Disease.

achiral-glycine

Ecological variation and niche construction: 1, 2, 3

Part 1

From its most basic expression in grazing and predatory nematodes with differences in morphological and behavioral phenotypes, neurogenic niche construction is nutrient-dependent and pheromone-controlled. One of these two worms has teeth. It also recognizes self vs other differences and eats other worms. “The patterns of synaptic connections perfectly mirror the fundamental differences in the feeding behaviours of P. pacificus and C. elegans”, Ralf Sommer concludes.
Evolutionary theorists concluded and continue to claim that “…without mutation, evolution would not be possible. This is because mutations provide the “raw material” upon which the mechanisms of natural selection can act.”  That suggests the differences in synaptic connectivity and differences in behavior in P. pacificus arose via mutations in C.elegans that led to natural selection and the evolution of predatory behavior associated with the evolution of teeth.
For contrast, Starvation-Induced Transgenerational Inheritance of Small RNAs in C. elegans and everything currently known about differences in the immune systems of animals suggests ecological variation led from nutrient-dependent RNA-directed DNA methylation to RNA-mediated events and amino acid substitutions that differentiate the cell types of the two nematodes. All other experimental evidence of biologically-based cause and effect attests to the fact that RNA-mediated events link ecological variation to ecological adaptations manifested in the morphological and behavioral phenotypes of species from microbes to man via conserved molecular mechanisms.
Suzanne Clancy, who stated that “…without mutation, evolution would not be possible”,  should try to explain how she arrived at that conclusion in the context of explaining that “… the alteration of a single nucleotide in the gene for the beta chain of the hemoglobin protein (the oxygen-carrying protein that makes blood red) is all it takes to turn a normal hemoglobin gene into a sickle-cell hemoglobin gene. This single nucleotide change alters only one amino acid in the protein chain, but the results are devastating.”
What happens when the result of altering one amino acid in the protein change are not devastating?
Clancy (2008) wrote that “Beta hemoglobin (beta globin) is a single chain of 147 amino acids.” Thirty-five years earlier, Dobzhansky (1973) wrote that “…the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla.
Summary:
1) One altered amino acid of the chain in beta hemoglobin causes an inherited disease in some populations of modern humans. (per Clancy)
2) One altered amino acid of the chain in alpha hemoglobin causes species-wide differences in all populations of 3 different primates. (per Dobzhansky)
Five questions arise:
1) If the 3 different primates were two different nematodes, would they starve to death or mutate into a new species with a change in their diet.
2) Who is teaching others, like Jay R. Feierman, to believe that “Random mutations are the substrates upon which directional natural selection acts.” (https://groups.yahoo.com/neo/groups/human-ethology/conversations/topics/48229)
3) Why does any intelligent person believe “…that if you showed this statement to any professor of biology or genetics in any accredited university anywhere in the world that 100% of them would say that “Random mutations are the substrate upon which directional natural selection acts” is a correct and true statement.”
4) Similarly, why does any intelligent person believe they can tell me that  “Variation is not nutrient availability and the something that is doing the selecting is not the individual organism. A feature of an educated person is to realize what they do not know. Sadly, you don’t know that you have an incorrect understanding Darwinian biological evolution.”
5) Does anyone else think other intelligent people are not going to ask how nutrients could not be the substrates that enable Darwinian biodiversity when someone claims that random mutations are the substrates on which directional natural selection acts?

Part 2

All 5 questions from Part 1 have been addressed in the context of three articles published in Science, which were reported yesterday in an “In Depth” perspective by Elizabeth Pennisi on a “metabolic shift” linked to the immune system, which is required for self vs other recognition. See my comment: Metabolic shift may train immune cells. All three articles attest to the requirement for a link from ecological variation to ecological, social, neurogenic, and socio-cognitive niche construction via the gene-cell-tissue-organ-organ system pathway. Clearly, increasing organismal complexity arises via this established pathway that links embryonic development to adult development of morphological and behavioral phenotypes in vertebrates.
I have detailed a link in conjunction with details about the pathway from the epigenetic landscape to the physical landscape of DNA in the organized genomes of different species from microbes to man in Nutrient-dependent/pheromone-controlled adaptive evolution: a model. I included the examples of the two nematodes and an example of a primate population (i.e., modern humans in central China). Here is information about neurogenic niche construction in another model organism:

Sensory-specific modulation of adult neurogenesis in sensory structures is associated with the type of stem cell present in the neurogenic niche of the zebrafish brain

Excerpt: “…modality-specific stimulation at distinct stages in the process of adult neurogenesis – chemosensory niches at the level of neuronal survival and visual niches in the size of the stem/progenitor population” are linked to the origins of niche construction in the embryo via conserved molecular mechanisms of transgenerational epigenetic inheritance in nematodes. Can anyone explain how niche construction evolved?
Obviously, there are many researchers who still think “…mutations provide the “raw material” upon which the mechanisms of natural selection can act.” Does anyone know how mutations and natural selection led to the evolution of niche construction and the nutrient-dependent pheromone-controlled biodiversity manifested in the morphological and behavioral phenotypes of species from microbes to man — and to sensory specific modulation of adult vertebrate brain development in vertebrates? If so, mutations and natural selection could lead from the evolution of pheromones to….

Part 3

Roles for learning in mammalian chemosensory responses

? EVOLUTION OF PHEROMONES ?
Excerpt 1) “When Karlson and Lüscher first proposed their definition of a pheromone they envisaged that their definition would be redefined and updated over time (Karlson and Lüscher, 1959).”
My comment: Their definition was clear. ”Pheromones are defined as substances which are secreted to the outside by an individual and received by a second individual of the same species, in which they release a specific reaction, for example, a definite behavior, or a developmental process.”
Excerpt 2) “… it still forms the core of most accepted definitions, such as the recent, slightly modified definition by Wyatt, “molecules that are evolved signals…” (Wyatt, 2014).
My comment: Portraying pheromones as if they are evolved signals, is not a slightly modified definition. Wyatt (2014) took pheromones from the context of ecological variation and nutrient-dependent ecological adaptations in insects and defined pheromones in the context of evolution. He bastardized the definition to make it fit what population geneticists invented and defined, which is now called neo-Darwinism. The population geneticists defined Darwin’s nutrient-dependent ‘conditions of life’ in terms of mutations, natural selection, and evolution. Wyatt and others must now have “molecules that are evolved signals…” to continue their pseudoscientific nonsense, which is based on statistics not biologically-based cause and effect. Population Genetics is, however, only a statistical association between something we had to infer and something we could observe.
Dobzhansky’s (1964) accurate portrayal of the observers follows: “…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!”
Dobzhansky’s portrayal serves as an introduction to claims by Wyatt and others who continue the bastardization of Darwin’s works as if food odors and pheromones evolved. The perturbed reality of the observers does not include ‘conditions of life’ that are nutrient-dependent. They ignore that fact that nutrients are metabolized to species-specific pheromones that control the physiology of reproduction in species from microbes to man.
Pheromones are nutrient-dependent. Ecological adaptations are nutrient-dependent and pheromone-controlled. Protein biosynthesis and degradation are biophysically contrained in the context of thermodynamic cycles that must lead to the stability of DNA in the organized genomes of organisms that require nutrient-dependent metabolic shifts to enable organism-level thermoregulation.
What evolved? How? Why hasn’t anyone described a biologically-based evolutionary event? Why is Wyatt trying to convince others that pheromones evolved when their production is obviously nutrient-dependent and clearly linked from RNA-directed DNA methylation to RNA-mediated amino acid substitutions that differentiate the cell types of all cells of all individuals of all species via the conserved molecular mechanisms that enable the nutrient-dependent pheromone-controlled physiology of reproduction in species from microbes to man?

Pheromones and Animal Behavior: Chemical Signals and Signatures

“A final chapter critically considers human pheromones and the importance of olfaction to human biology. Its breadth of coverage and readability make the book an unrivaled resource for students and researchers in a range of fields from chemistry, genetics, genomics, molecular biology and neuroscience to ecology, evolution and behavior.”
People like Wyatt continue to show others that if you don’t understand the Laws of Physics, you should not write books about “…a range of fields from chemistry, genetics, genomics, molecular biology and neuroscience to ecology, evolution and behavior.” Instead, you should write books that claim “…constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world.” Alternatively, you can keep claiming that pheromones in mammals do not exist or that human pheromones don’t exist because we are too highly evolved. After all, “WHAT are we going to do if it turns out that we have pheromones? What on earth would we be doing with such things? With the richness of speech, and all our new devices for communication, why would we want to release odors into the air to convey information about anything?” — Lewis Thomas (1971) “A Fear of Pheromones” as cited in the first book about human pheromones:

The Scent of Eros: Mysteries of Odor in Human Sexuality (1995/2002).