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).

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New technique used in report of atomic-level ecological adaptations

Archaerhodopsin variants with enhanced voltage-sensitive fluorescence in mammalian and Caenorhabditis elegans neurons

Directed evolution of a far-red fluorescent rhodopsin

reported as:

New technique uses a genetic tool and light to view and map neuronal circuits

Excerpt 1): “This [directed evolution] experiment demonstrates how rapidly these remarkable bacterial proteins can evolve in response to new demands. But even more exciting is what they can do in neurons, as Viviana discovered,” says Arnold.
Excerpt 2): After incorporating Archer1 into neurons that were a part of the worm’s olfactory system—a [THE] primary source of sensory information for C. elegans —[and every other species on this planet] the researchers exposed the worm to an odorant. When the odorant was present, a baseline fluorescent signal was seen, and when the odorant was removed, the researchers could see the circuit of neurons light up, meaning that these particular neurons are repressed in the presence of the stimulus and active in the absence of the stimulus. The experiment was the first time that an Arch variant had been used to observe an active circuit in a living organism.
Excerpt 3): “As neuroscientists we often encounter experimental barriers, which open the potential for new methods. We then collaborate to generate tools through chemistry or instrumentation, then we validate them and suggest optimizations, and it just keeps going,” she says. “There are a few things that we’d like to be better, and through these many iterations and hard work it can happen.”
My comment: The experimental barriers are insignificant compared to the barriers of ignorance represented in this news article. The collaboration appears not to include efforts made by biophysicists to convince theorists that the chemistry of protein folding required for increasing organismal complexity is biophysically constrained by the second LAW of thermodynamics, which is linked from chemistry to perturbed protein folding via nutrient stress and social stress manifested in “heat shock” that alters protein folding. Neurons “…repressed in the presence of the stimulus and active in the absence of the stimulus…” respond to the presence or absence of chemical cues associated with food odors an social odors called pheromones. If enough food is present and not too many pheromone-producing conspecifics, no response is required. But when ecological variation leads to an absence of food or too many conspecifics, an ecological adaptation is required, which is why circuits of neurons light up. If the neuronal circuitry did not light up, there could be no link from ecological variation to any potential ecological adaptation. The population of organisms would die of starvation; they would not evolve.
The researchers link light-induced amino acid substitutions across species that they may think have evolved via conserved molecular mechanisms. But the report on light-induced cell type differentiation and ecological adaptations manifested in the behavior of cells in the nematodes organisms suggests the proteins somehow evolved. Proteins do not ‘evolve.’ Behaviors do not ‘evolve.’
Proteins are produced in the context of of nutrient-dependent thermodynamic cycles of biosynthesis and degradation. Amino acid substitutions that stabilize DNA in the organized genomes of species from microbes to man must lead to cell type differentiation accompanied by changes in behavior or the amino acid substitutions will not be fixed in the DNA at any stage of morphological or behavioral development.
The behavioral changes in C. elegans are clearly nutrient-dependent and pheromone-controlled. They arise during nutrient-dependent ecological niche construction and pheromone-controlled social niche construction, which lead to the construction of neurogenic niches in nematodes.
For example, the nematode P. pacificus has teeth and exhibits predatory behavior because its diet varies from that of the nematode C. elegans. A nutrient-dependent amino acid substitution links the differences in these species protein production to their pheromone-controlled physiology of reproduction, which is how the epigenetic landscape is linked to the physical landscape of DNA in the organized genomes of species from microbes to man. Proteins don’t evolve; behaviors don’t evolve and species don’t evolve. See: System-wide Rewiring Underlies Behavioral Differences in Predatory and Bacterial-Feeding Nematodes and Signaling Crosstalk: Integrating Nutrient Availability and Sex and Feedback loops link odor and pheromone signaling with reproduction.
This news report included too much of the magic of evolutionary theory in what could otherwise have been a report used to link ecological variation to ecological adaptation via conserved molecular mechanisms in species from microbes to man. It is either a report on cause and effect for dummies who believe in evolutionary theories, or a report from dummies who thinks that proteins evolve. For example, if bacterial proteins evolve, bacteria can evolve to become nematodes and nematodes can evolve to become mammals.
What these reports actually show is how rapidly light-induced amino acid substitutions lead from nutrient-dependent amino acid substitutions to ecological adaptations in bacterial proteins that link their nutrient-dependent pheromone-controlled physiology of reproduction to ecological adaptations manifested in the morphological and behavioral phenotypes of species from microbes to man via conserved molecular mechanisms in an atoms to ecosystems model of biophysically-constrained cause and effect. Simply put, they start with quantum physics and end with evolution without an evolutionary event that links nutrient-dependent RNA-mediated events from ecological variation to ecological adaptations via conserved molecular mechanisms of species from microbes to man.
 

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Quantum physics meets Evolutionary Psychology News

Capturing the motion of a single molecule in real time as it oscillates from one quantum state to another

September 18, 2014


Excerpt: “It also moves researchers a step closer to viewing the molecular world in action — being able to see the making and breaking of bonds, which control biological processes such as enzymatic reactions and cellular dynamics.”

My comment: The making and breaking of bonds controls all biological processes. Luca Turin tried to do move researchers a step closer to viewing the molecular world in action and was hung out to dry by members of the Association for Chemoreception Sciences (AChemS). Chandler Burr wrote a book about Luca’s experiences. I sided with AChemS in a review of the book
The Emperor of Scent: A Story of Perfume, Obsession and the Last Mystery of the Senses. That was before they ignored details of RNA-mediated events and hung me out to dry as well.

Then I learned that Luca Turin was probably right about the “Molecular Vibration-Sensing Component in Human Olfaction”  I think that’s what Sinope Diogenes is trying to tell the Evolutionary Psychology News group and wonder why he is doing that.

Most evolutionary psychologists know nothing about molecular biology and they appear to believe that mutations and natural selection led to the evolution of biodiversity. Most have rejected all facts that show ecological variation leads to ecological adaptations via biophysically-constrained molecular mechanisms that ensure perturbed protein folding manifested in mutations does not lead to increasing organismal complexity. Simply put, the evolutionary psychologists I have encountered are less likely than serious scientists from AChemS to accept anything other than what they’ve been taught to believe in.
Most members of AChemS probably believe in the pseudoscientific nonsense of evolutionary theory, too. Few of their members could accept the fact that RNA-mediated events link insect to mammals via the epigenetic effects of olfactory/pheromonal input on hormone-organized and hormone-activated behaviors. In fact, no one publicly complained when Richard L. Doty, a sensory psychologist, proclaimed that mammalian pheromones don’t exist because of differences in the stereotypical behaviors of insects and mammals, which obviously are epigenetically-effected via conserved molecular mechanisms.
See: The Great Pheromone Myth ” In this provocative book, renowned olfaction expert Richard L. Doty rejects this idea and states bluntly that, in contrast to insects, mammals do not have pheromones.” But wait, see also: Humans Can Discriminate More than 1 Trillion Olfactory Stimuli. The disparity between the number of olfactory receptors and our detection abilities suggests two things.
1) Doty does not know that what humans and insects have in common, which links quantum physics via chemistry to the molecular biology of de novo Creation of odor receptors that detect food odor and pheromones in insects and in mammals.
2) Luca Turin’s ideas about links from biophysically-constrained ecological adaptations to nutrient-dependent pheromone-controlled hormone-organized and hormone-activated behaviors should be revisited whenever a generation of intelligent researchers learns enough about physics, chemistry, and conserved molecular mechanisms in species from microbes to man to look beyond the nose on their face, past the presentations at AChemS meetings, or up the nose of the sculpture in front of the Monell Chemical Senses Institute.

Physics

Some neuroscientists think a mutation led to human language development

Neuroscientists identify key role of language gene

Excerpt: “Neuroscientists have found that a gene mutation that arose more than half a million years ago may be key to humans’ unique ability to produce and understand speech.”
Excerpt: “…the gene that allowed us to speak may have something to do with a special kind of learning, The gene was first identified in a group of family members who had severe difficulties in speaking and understanding speech, and who were found to carry a mutated version of the Foxp2 gene.”
My comment:  See: RNA and dynamic nuclear organization. RNA-mediated events are biophysically constrained, which means they are a biologically plausible way to link the physics and chemistry of amino acid substitutions and protein folding to increasing organismal complexity via molecular biology.
RNA-mediated events associated with nutrient-dependent amino acid substitutions can also be compared to unknown evolutionary events that might automagically arise in the context of an alternative theory about constraint-breaking mutations and natural selection without RNA-mediated events.
What theory suggests a mutation led to amino acid substitutions and a disorder of language development in one small group of humans, but also links a mutation to the increased organismal complexity of the human brain via the conserved molecular mechanisms of RNA-mediated amino acid substitutions that differentiate cell types in species from microbes to man?
Who believes in the pseudoscientific nonsense of mutations, natural selection, and the evolution of biodiversity, which can be compared to the biological fact that ecological, social, neurogenic and socio-cognitive niche construction are RNA-mediated events — not undescribed evolutionary events?

poster-from-jesse

Biophysically constrained beginnings of RNA and DNA

Any anonymous participant in the discussion of: DNA may have had humble beginnings as nutrient carrier (Sep 01, 2014 by Adam Hadhazy) asks:
“when are you going to keep quiet?”
In a series of responses, I have explained the problem I have with honoring his request.
The following excerpts from Wikipedia and other sources are loosely strung together because there is no point to providing more extensive details of biologically-based cause and effect until others accept the fact that mutations and natural selection cannot lead to the evolution of biodiversity. Even without accepting the fact that nutrient-dependent amino acid substitutions differentiate the cell types of all individuals in all species, it should be clear that mutations do not. Until that fact becomes clear, nothing known about physics, chemistry, and molecular biology can be used to refute ridiculous theories. Here are examples of what cannot be used.
1) In mammals, phosphatidylserine is produced by base-exchange reactions with phosphatidylcholine and phosphatidylethanolamine. The products of this reaction are novel dinucleotides. Nicotinamide adenine dinucleotide (NAD) is a coenzyme found in all living cells. (The compound is a dinucleotide, since it consists of two nucleotides joined through their phosphate groups.)
The flipping of one base pair appears to result in Fragile X Syndrome, which is the most common form of mental retardation. It may represent what happens when an atomic-level change in nutrient-dependent energy perturbs protein folding.
For comparison, the nutrient-dependent flipping of a base pair associated with vitamin C uptake in mammals links frugivory in bats via morphological and behavioral phenotypes to their adaptive radiations. Their phenotypes link nutrient-dependent pheromone-controlled reproduction in all vertebrates and invertebrates to morphological and behavioral changes during the development of human preferences for food odors and pheromones.
2) Rather than be quieted by the pseudoscientific nonsense of evolutionary theorists who want others to believe that mutations and natural selection lead to the evolution of biodiversity, ecologists and other serious scientists continue to link biologically-based cause and effect from atoms to ecosystems via the conserved molecular mechanisms of amino acid substitutions that I detailed in my model.
Serious scientists know that models will lead to atomic level (nutrient-dependent) cures for diseases and disorders that evolutionary theorists claim are due to the same molecular mechanisms they think must link mutations to increasing organismal complexity manifested in morphological and behavioral phenotypes of species from microbes to man.
The difference between a serious scientist and a theorist (or any other idiot) is recognized by differences in their beliefs about biologically-based cause and effect. Theorists have no understanding of links between atoms and ecosystems; serious scientists attempt to understand the experimental evidence.
3) In metabolism, nicotinamide adenine dinucleotide is involved in redox reactions, carrying electrons from one reaction to another.
Most organisms synthesize NAD+ from simple components.[2] The specific set of reactions differs among organisms, but a common feature is the generation of quinolinic acid (QA) from an amino acid—either tryptophan (Trp) in animals and some bacteria, or aspartic acid in some bacteria and plants.[21][22] Besides assembling NAD+ de novo from simple amino acid precursors, cells also salvage preformed compounds containing nicotinamide. Despite the presence of the de novo pathway, the salvage reactions are essential in humans; a lack of niacin in the diet causes the vitamin deficiency disease pellagra.[28] This high requirement for NAD+ results from the constant consumption of the coenzyme in reactions such as posttranslational modifications, since the cycling of NAD+ between oxidized and reduced forms in redox reactions does not change the overall levels…
4) Rather than continue to examine facts that link the thermodynamic cycles of protein biosynthesis and degradation from atoms to ecosystems via organism-level thermoregulation, others may want to consider the alternative.
In “Mutation-Driven Evolution” for example, the claim is made that “…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world.”
That claim is not supported by any experimental evidence of biologically-based cause and effect, but many evolutionary theorists are convinced that the differences in morphology and behavior they can see are due to mutations that perturb protein folding at the level detailed in the Laws of Physics, which lead to everything known about chemistry and Kohl’s Laws of Biology, which are linked to the de novo Creation of olfactory receptor genes via the de novo Creation of RNA and DNA.
Addendum: Anyone willing to accept the fact that RNA and DNA somehow ‘evolved’ or that what’s known about the biophysical constraints that link ecological variation to ecological adaptations via conserved molecular mechanisms in species from microbes to man is not likely to lead to cures for diseases and disorders associated with mutations should participate in discussions on blog sites run by atheistic biology teachers like PZ Myers. For example see: One crank dies, another rises to take his place. Anyone willing to accept the fact that RNA and DNA were Created should examine the content of articles that represent what is known about the Laws of Physics; what is known about chemistry; and what is known about molecular biology. See for example: Darwin vs. Genetics: Surprises and Snags in the Science of Common Ancestry
In the context of biophysically-contrained ecological adaptations it may interest others to learn what is obviously missing from what’s being billed as the Theory of Everything. A theory of everything should have some explanatory power in the context of biologically-based cause and effect that does not link perturbed protein and nutrient-dependent ecological variation to pheromone-controlled ecological adaptations via the same molecular mechanisms. What if Hawkings’ disabled body could be linked from epigenetically-effected RNA and DNA to his highly functional mind? Would others be more interested in biological facts about the de novo Creation of proteins that can be compared to his theory of everything?
What if a nutrient-dependent flip in a single base pair led to amino acid substitutions that differentiate all the cell types of all individuals of all species via conserved molecular mechanisms? Could the link from Fragile X Syndrome and mental retardation be the same as the link to hemoglobin S and nutrient-dependent brain development in someone like you, or like Hawkings? If so, the link is likely to be nutrient-dependent amino acid substitutions that differentiate all cell types in all tissues of all organs in all organ systems of invertebrates and vertebrates via conserved molecular mechanisms of pheromone-controlled reproduction.
We can see the origins of that perspective on autophagy, which was the basis for my works in these two published works.
Effects of Carnitine on Fatty-Acid Oxidation by Muscle (1959)
DEPENDENCE OF RNA SYNTHESIS IN ISOLATED THYMUS NUCLEI ON GLYCOLYSIS, OXIDATIVE CARBOHYDRATE CATABOLISM AND A TYPE OF “OXIDATIVE PHOSPHORYLATION” (1964)
My comment: Both were co-authored by Bruce McEwen. He told me in 1991 that I would need to start with energy-dependent gene activation before my model of cell type differentiation could be completely validated. I did that in the following year with the help of Robert L. Moss and his co-authors in a series of published works that linked pheromones to gene activation in GnRH neurosecretory neurons of the mammalian hypothalamus.

Physics

Darwinian theories vs Darwin's facts

Darwin’s Theories, submitted by Celia Secades of the Elesapiens website was the runner-up in the Third Annual NESCent Evolution Video Contest. (unfortunately, the video has been removed — perhaps for good reasons. For example:

My comment: No experimental evidence supports the representations of mutation-initiated natural selection in the video.
For comparison, tenOever on microRNA and Vaccines  addresses what is currently known about glucose-dependent RNA-mediated amino acid substitutions and self vs non-self identification in viruses to living species with varying degrees of nutrient-dependent pheromone-controlled ecologically-adapted organismal complexity.

Professor tenOever’s award-winning works cannot be placed into the context of Celia Secades “Darwinian facts” about evolution.
Darwin’s facts placed Darwin’s ‘conditions of life’ before natural selection. In the following four articles, we see that even in a virus (a non-living organism), glucose enables adaptations without mutation-initiated natural selection.
1) Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution (1) First, the amino acid substitutions are falsely attributed to mutations.
2) Stability-mediated epistasis constrains the evolution of an influenza protein 2) Next an article asked “How does epistasis arise from an evolutionary process that is conceived as proceeding through the incremental accumulation of mutations?’ Obviously, epistasis does not arise via mutations. The article places the evolutionary process into the context of biophysical constraints via an analogy to words. “WORD→WORE→GORE→GONE→GENE. Implicit in this analogy is the idea that there are biophysically constraints on evolution—for example, the original parent sequence does not tolerate three of the four eventual changes, as GORD, WERD and WOND are not words.” The fact that those words are nonsense words attests to the fact that mutation-driven evolution is a nonsensical theory.
3) Glycolytic control of vacuolar-type ATPase activity: A mechanism to regulate influenza viral infection 3) This article links glycolysis and influenza virus infection. The amino acid substitution in the human influenza virus that enables new antigenic properties is obviously nutrient-dependent, even when the nutrient (i.e., glucose) must come from an infected cell.
Aerobic Glycolysis in the Human Brain Is Associated with Development and Neotenous Gene Expression 4) Aerobic glycolysis in the human brain links amino acid substitutions from the epigenetic landscape of  the influenza virus to the physical landscape of DNA in the organized genomes of living cells in different organisms via the conserved molecular mechanisms that enable nutrient-dependent pheromone-controlled ecological, social, neurogenic and socio-cognitive niche construction during the ecological adaptations that are manifested in increased organismal complexity of species from microbes to man.
Evolutionary theorists may object to the idea of crossing species barriers via what is known by molecular biologists about conserved molecular mechanisms, but that’s because evolutionary theorists don’t know enough about biology to reject the theory of mutation-driven evolution. Even though no experimental evidence supports it, theorists cling to their ridiculous theory because it’s all they have. There is no “fall-back” position. Either ecological adaptations are responsible for species divergence or mutation-initiated natural selection somehow enables increasing organismal complexity.
The video about how natural selection somehow enables increasing organismal complexity is only appropriate for an audience of children who are not expected to ask any questions about how mutations could be fixed in the genome so that they could be naturally selected. It is horribly inappropriate for use as a teaching tool for students age 5 or older, who are more likely to ask: “Is there a model for that?”
Since it has been removed, others may want to see those that remain, and attempt to determine whether anything they claim makes sense in the context of what is known about physics, chemistry, and molecular biology.
Also see the links to viral microRNAs from this blog site.