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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Epigenetically-effected metabolic shifts and ecological adaptations

Epigenetics of Trained Innate Immunity:

Documenting the epigenetic landscape of human innate immune cells reveals pathways essential for training macrophages.

By Ruth Williams | September 25, 2014 [open access]

Excerpt: “...they then analyzed genome-wide distributions of four epigenetic indicators of gene activity: DNAse hypersensitivity and three different histone modifications—trimethylation of histone H3 at lysine 4, monomethylation of histone H3 at lysine 4, and acetylation of histone H3 at lysine 27. They also analyzed genome-wide transcription and transcription factor binding.
Together the analyses pointed to specific genes and pathways that defined the four cell types, as well as the genes’ surrounding regulatory regions. Of particular interest was the discovery that genes associated with signaling via cyclic adenosine monophasphate (cAMP)—a molecule regulating cell metabolism, among other processes—and glycolysis—a pathway that produces energy from glucose—were specifically activated in the trained macrophages.
The team went on to show that these two pathways were necessary for developing the trained phenotype.”
My comment: Three large teams collectively linked nutrient-dependent RNA-directed DNA methlylation from biophysically constrained ecological adaptations to the development of morphological phenotypes and the concurrent development of behavioral phenotypes.
1) The thermodynamics of protein biosynthesis and degradation and organism-level thermoregulation links ecological variation from nutrient-dependent gycolysis to experience-dependent RNA-mediated de novo Creation of odor receptor genes.
2) Food odors induce the de novo Creation of odor receptor genes. Odors can then classically-condition receptor-mediated behaviors that are directly linked to choices associated with nutrient uptake.
3) Receptor-mediated behaviors link nutrient uptake to the metabolic shift (see below), which links the metabolism of nutrients to species-specific pheromones.
4) Pheromones control the physiology of reproduction.
5) Nutrient-dependent pheromone-controlled reproduction enables fixation of RNA-mediated amino acid substitutions that stabilize methylated DNA in the organized genomes of species from microbes to man.
6) Pheromones classically condition differences in nutrient-dependent behaviors that lead to successful nutrient-dependent reproduction via amino acid substitutions that stabilize organism-level thermoregulation.
7) The nutrient-dependent pheromone-controlled stability of organism-level thermoregulation is perturbed by nutrient stress and social stress.
8) Organisms with the greatest DNA stability are ecologically adapted.
9) Nutrient-dependent pheromone-controlled organized genomes are morphologically and behavioral adapted to the ecological variations they are most likely to encounter.
From Science Magazine:

Metabolic shift may train immune cells [subscription required]

Received: Thu, 25 Sep 2014 22:56:29 -0400
My comment: Kondrashov (2012) linked nutrient-dependent gene duplication from ecological variation to ecological adaptations in yeast via the yeast hexose transporter and the rate of glucose transport into the cell. “One of the main duplicated gene families are the olfactory receptor proteins [18,117–119] so perhaps their duplication may lead to an increase in sensitivity to a particular odour may be adaptive under certain conditions.” http://rspb.royalsocietypublishing.org/content/early/2012/09/05/rspb.2012.1108.abstract
We linked the metabolism of nutrients to species-specific pheromones and sex difference in cell types via RNA-mediated events. http://www.ncbi.nlm.nih.gov/pubmed/9047261
Others have since linked nutrient-dependent pheromone-controlled differences in cell types to hormone-organized and hormone-activated behaviors. http://www.ncbi.nlm.nih.gov/pubmed/10980296
Thus, the ability of yeasts to recognize RNA-mediated sex differences in cell types appears to extend across species to recognition of nutrient-dependent glycolysis-induced learning and memory in the context of immune system recognition of cell type differences and gene duplication associated with pheromones that control the physiology of reproduction in species from microbes to man.
That link from the epigenetic landscape to the physical landscape of DNA in organized genomes is exemplified in the honeybee model organism.
“The honeybee already serves as a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, the development of the brain and behavior, mental health, longevity, and diseases of the X chromosome (Honeybee Genome Sequencing Consortium, 2006). Included among these different aspects of eusocial species survival are learning and memory, as well as conditioned responses to sensory stimuli (Maleszka, 2008; Menzel, 1983).” http://www.socioaffectiveneuroscipsychol.net/index.php/snp/article/view/17338
This report seem to clarify several aspects of how glycolysis is linked from nutrient uptake to cell type differentiation and ecological speciation. Biodiversity is associated with RNA-mediated amino acid substitutions and recognition of cell type differences by conspecifics and heterospecifics due to differences in their diet, glycolysis, and the pheromones they produce.
My comments on the most recent attempt to keep the focus on evolution via definitions with no experimental evidence of biologically-based cause and effect is here:
 

terrarium-eco-system

RNA-directed DNA methylation and RNA-mediated events

Many colleagues and most of my antagonists seem to be unwilling to accept the fact that RNA-directed DNA methylation links the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man. Lack of acceptance appears to be due to the fact that they think mutations and natural selection link evolutionary events to biodiversity. There is no model for that, but they refuse to accept the fact that RNA-mediated events link ecological variation to ecological adaptations.There is a model for that!
The RNA-mediated events are nutrient-dependent because nutrients provide the methly groups required for DNA methylation. In my model, experience dependent odor exposure induces the de novo Creation of receptors that allow nutrients to enter the cell. For example, the Creation of olfactory receptor genes enables nutrient-uptake, which enables DNA methylation. The RNA-mediated events link DNA methylation from nutrient uptake to thermodynamic cycles of protein biosynthesis and degradation. Degradation of proteins links the byproducts of nutrient-dependent RNA-mediated events from DNA methylation and the metabolism of nutrients to the production of species-specific pheromones. Pheromones control the nutrient-dependent physiology of reproduction in species from microbes to man via the conserved molecular mechanisms I just detailed.
The links from physics and chemistry to the thermodynamics of RNA-directed DNA-methylation via RNA-mediated events that link the epigenetic landscape to protein folding that enables increasing organismal complexity via nutrient-dependent pheromone-controlled de novo gene Creation may be impossible to describe to those who are not familiar with physics, chemistry, and the molecular biology of biologically-based cause and effect. However, that is no excuse for anyone to continue to proceed with mathematical models of evolution that do not first address Darwin’s ‘conditions of life.’ Conditions of life are nutrient-dependent, no matter who first suggested they be considered before natural selection of anything else occurred for anything except food. Organisms without enough food due not mature or cannot attract a mate by producing nutrient-dependent pheromones. Thus, the pheromones that control reproduction fit into the context of conditions of life that lead to biodiversity. The fact that RNA-mediated events link nutrient-dependent amino acid substitutions to cell type differentiation in species from microbes to man and that fixation of the amino acid substitutions occurs only in the context of successful nutrient-dependent reproduction seems to be ignored by evolutionary theorists as if that fact — along with physics, chemistry, and molecular biology — could continue to be ignored.
Who is ignoring the facts?
Karl Grammer co-authored our award-winning 2001 review: Human pheromones: integrating neuroendocrinology and ethology He recently mentioned that he would publish a mathematical model of how pheromones influence behavior. This would be a counter-measure that might limit the successful defense of my model. He thinks my attempts to eliminate the theories of evolutionists and human ethologists from consideration are a waste of time. I think it is past time to provide serious scientists with experimental evidence of biologically-based cause and effect and require them to defend their ridiculous theories based on their mathematical models.
However, others have offered a relatively simply mathematical model of RNA-mediated events that links epigenetic effects of pheromones on hormones (neuroendocrinology) to the affects of hormones on behavior (ethology) via feedback loops. See: Mathematical model: microRNA and epigenetic regulation.
Now see: Maternal Methyl Supplemented Diets and Effects on Offspring Health “Lastly, methyl components may lead to tissue/cell-specific effects. Such differences would suggest that these diets might aide in disease prevention in select organs or tissues but also exacerbate disease risk in others.”
Now others can skip the physics, chemistry, and molecular biology. The link from the nutrient-dependent pheromone-controlled physiology of reproduction to tissue/cell-specific effects is clear in the context of what is known about Feedback loops link odor and pheromone signaling with reproduction and what is detailed in the mathematical model:  Interplay of microRNA and epigenetic regulation in the human regulatory network.
The maternal methyl supplementation report links epigenetic effects on cell type differentiation in tissues of organs in organ systems of organisms from ecological variation to the nutrient-dependent pheromone-controlled physiology of ecological adaptations via conserved molecular mechanisms of ecological, social, neurogenic, and socio-cognitive niche construction that I detailed in my model.
Ask Karl Grammer and other theorists who think they can mathematically model the complexities of biologically-based cause and effect that lead to tissue/cell-specific effects and affects on behavior in my model these two questions:
1) Why haven’t you told us what biologically-based evolutionary event links DNA methylation to the morphological and behavioral phenotypes you think somehow arose in the context of mutations, natural selection, and the evolution of biodiversity.
2) What makes you think you can mathematically model the interplay of microRNAs and epigenetic regulation of RNA-mediated biodiversity that clearly occurs in the context of amino acid substitutions that differentiate all cell types in all individuals of all species?
Other have claimed: “We cannot conceive of a global external factor that could cause, during this time, parallel evolution of amino acid compositions of proteins in 15 diverse taxa that represent all three domains of life and span a wide range of lifestyles and environments.” Jordan et al., (2005)
RNA-mediated events link nutrient-dependent pheromone-controlled cell type differentiation in every individual of every honeybee colony via conserved molecular mechanisms linked to cell type differentiation in all cells of all organisms of all species. See: Epigenomics and the concept of degeneracy in biological systems
“Feeding a complex diet known as royal jelly to a growing female larva inhibits global DNA methylation, increases levels of juvenile hormone and correlates with changes in gene expression, which result in the queen phenotype. In contrast, larvae fed less-nutritious worker jelly develop into functionally sterile short-lived worker bees. However, there are no specific ‘queen’ or ‘worker’ genes in the Apis genome. During the initial critical 96 h of larval growth, multiple sensory and secretory systems are involved in receiving, processing and conveying the nutritional information to multilevel, interlocked signaling pathways. The contrasting phenotypes result from threshold-based processes driven by metabolic fluxes, hormonal changes and differential methylation and expression of many genes [83]. All these components have the capacity to respond to environmental change, but their combined and coordinated action has evolved in honey bees as a powerful mechanism for reprograming the entire developmental trajectory with profound consequences for cellular and organismal phenotypes [82–85].”
The honeybee is the model organism that links conserved molecular mechanisms of biophysically-constrained biologically based cause and effect in species from microbes to man.
Does anyone seriously think they can mathematically model that, or anything else about RNA-mediated cell type differentiation. Do they think they can continue to make their mathematical models appear to be consistent with the pseudoscientific nonsense of evolutionary theory and human ethology? If so, perhaps Karl will have help in his efforts to continue to keep others from learning about how ecological variation leads to RNA-mediated ecological adaptations in species from microbes to man.
He’s been doing that since 2001, and it has become more difficult to continue doing so when all biological facts continue to attest to the pseudoscientific nonsense population geneticists used to invent and define neo-Darwinian evolutionary theory. But, I think there is little hope for him if he tries to continue to mathematically model anything that has not become established as a biological fact via experimental evidence of biologically-based cause and effect.

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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.

poster-from-jesse

Insect homology and diversity attributed to mutations

Ancient homology underlies adaptive mimetic diversity across butterflies

Excerpt: “Surprisingly, our results suggest that modulation of this conserved developmental gene has occurred in tandem between these two deeply divergent butterfly lineages, implying an unexpected and remarkable level of predictability in the evolutionary process.”
Reported as: A single evolutionary road may lead to Rome
Excerpt: “Copying errors and genomic viruses directly lead to the wing patterns of these beautiful butterflies,” Gallant said. “It’s these accidents that allow the evolutionary process to move forward. When I look over a field of butterflies, it makes me wonder what types of ‘mistakes’ are happening right now that may lead to important evolutionary changes years from now? What evolutionary processes will we someday be able to predict?”
My comment: Dobzhansky (1964) predicted that bird-watchers and butterfly-collectors would never become serious scientists, and his predictions are still coming true in reports like this one.
Two more generations of researchers have since been taught to believe in a ridiculous theory about mutations, natural selection. and the evolution of biodiversity, which is clearly nutrient-dependent and pheromone-controlled by RNA-mediated events in species from microbes to man. Instead, this group finds that the nutrient-dependent ecological adaptations manifested in the wing morphology of butterflies is caused by mutations that somehow predictably lead to evolution.
Would that be by natural selection — instead of by the nutrient-dependent pheromone-controlled physiology of reproduction? It could be if perturbed protein-folding linked nutrient uptake to increasing organismal complexity. But in all other species from microbes to man the epigenetic landscape is linked to the biophysically-constrained physical landscape of DNA in organized genomes via the pheromone-controlled physiology of reproduction.
Take Darwin’s pigeons, for example, because 1) the EphB2 gene is a strong candidate for the derived head crest phenotype  2) that trait evolved just once and 3) it spread throughout the species. 4) The crest also originates early in development by 5) localized molecular mechanisms and the reversal of feather bud polarity.” See: Genomic Diversity and Evolution of the Head Crest in the Rock Pigeon
Link the EphB2 gene and nutrient-dependent amino acid substitutions and chromosomal rearrangements in white-throated sparrows to their pheromone-controlled physiology of reproduction and you have the established link to morphology and behavior of the butterflies, birds, bees, and all other species on this planet via conserved molecular mechanisms.
Try to link mutations and natural selection for anything but food to biodiversity and you must invent theories about how random changes lead to predictable outcomes via changes in one gene in vertebrates and invertebrates.
Go ahead, make my day! Watch the butterflies and make predictions about evolutionary processes. Keep touting your ridiculous theories as serious scientists recognize why Dobzhansky (1973) mentioned 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.”
He seems to have predicted serious scientists would learn about nutrient-dependent amino acid substitutions that differentiate all cell types in all individuals of all species, but that evolutionary theorists would not. Did he believe the theorists would never be more than butterfly collectors and bird-watchers who didn’t learn anything about molecular biology? Did he believe that theorists could never grasp the facts about how ecological variation leads to ecological adaptations via conserved molecular mechanisms in species from microbes to man?

.

human-evolution

Comparing divergent model organisms

Comparative analysis of the transcriptome across distant species

Excerpt: Overall, our results underscore the importance of comparing divergent model organisms to human to highlight conserved biological principles (and disentangle them from lineage-specific adaptations).
My comment: In the detailed comparisons of divergent model organisms portrayed in Nutrient-dependent/pheromone-controlled adaptive evolution: a model, I underscored what is known about cell type differentiation in species from microbes to man. By placing what is known into the context of nutrient-dependent amino acid substitutions and biodiversity controlled by the metabolism of nutrients to species-specific pheromones, I thought it would be clear that the best approach to understanding how biodiversity arose was to model it. Conclusion: “Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.”
The model arose from prior published works that clearly linked the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man. See for example: Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Conclusion: “Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans…”
Now “…comparing divergent model organisms to human…” continues  “…to highlight conserved biological principles…”
These conserved biological principles are obviously the conserved molecular mechanisms of nutrient-dependent pheromone-controlled cell type differentiation we detailed in our 1996 Hormones and Behavior review article in the context of sex differences in cell types. Did anyone who is not an evolutionary theorist think that cell type differentiation occurred differently in different cells of different individuals in different species?
See for review our section on: “Molecular epigenetics” in From Fertilization to Adult Sexual Behavior
“Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes (Saunders, Chue, Goebl, Craig, Clark, Powers, Eissenberg, Elgin, Rothfield, and Earnshaw, 1993; Singh, Miller, Pearce, Kothary, Burton, Paro, James, and Gaunt, 1991; Trofatter, Long, Murrell, Stotler, Gusella, and Buckler, 1995). Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, 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.”
See also: Alternative RNA Splicing in Evolution but try to think in terms of how ecological variation leads to ecological adaptations via nutrient-dependent alternative splicing of pre-mRNA. I tried to convey this message yesterday: There are no evolutionary events. There are only epigenetically-effected amino acid substitutions that differentiate cell types and pheromone-controlled cell type differentiation enables biodiversity. There is no model of how biodiversity arises via evolutionary events, because it doesn’t.

neuronal-plasticity

Order and disorder: Ecological adaptations not mutations

In the context of order and disorder that includes what is known about quantum physics and light-induced amino acid substitutions in plants and animals, as well as the control of the functional rearrangement of influenza hemagglutinin, I’m beginning to see even more confusion/obfuscation enter the picture of biophysically-constrained ecological adaptations.
The nutrient-dependent ecological adaptations are now being put into the context of mutation-initiated natural selection and the evolution of biodiversity (i.e., “Evolution for Dummies”).
ECOLOGICAL ADAPTATIONS (not mutations)
Nutrient-dependent changes in the microRNA/messenger RNA balance are readily linked from ecological variation to ecological adaptations via conserved molecular mechanisms that eliminate mutation-initiated natural selection and evolution from consideration. However, since no experimental evidence of biologically-based cause and effect has shown that mutations are ever fixed in the organized genomes of any population of any species, researchers now refer to the amino acid substitutions that are fixed in the genome as if they were epimutations (translation: epigenetically-effected mutations).
For example, in this article about epimutations, microRNAs also are referred to as small RNAs and labeled sRNAs with this mention of what a small RNA is. “Most of these sRNAs average 21–24 nucleotides in length…”
A microRNA (abbreviated miRNA) is a small non-coding RNA molecule (containing about 22 nucleotides). Thus, the quantum leap from biophysically constrainted light-induced amino acid substitutions to the nutrient-dependent microRNA/messenger RNA balance that controls genome stability via epigenetically-effected amino acid substitutions is replaced with the concept of epigenetically-effected mutations, which are called epimutuations.
By mixing the theory of mutation-initiated natural selection and the evolution of biodiversity with biological facts about how ecological variation leads to epigenetically-effected ecological adaptations manifested in biodiversity, the senior author of the “epimutations” article sets the stage for his claim to be “the first” to find something new and important.
It could be like the discovery of other molecular phenomena like introns or microRNAs, where it all began with just one example,” said Heitman. “We think this discovery may turn out to be generalized fairly quickly.
What discovery? They link nutrient-dependent microRNAs from ecological variation to ecological adaptations in the context of conserved molecular mechanisms in species from microbes to man.
The researchers think these epimutations could be employed in a variety of situations, enabling an organism to adapt to an unfavorable environment and then adapt again when conditions improve.
DISCOVER THIS!
Nutrient-dependent epigenetically-effected alternative splicings of pre-mRNA, which can be called microRNAs or sRNAs result in RNA-mediated amino acid substitutions and chromosomal rearrangements that enable organisms to adapt to ecological change. When the supply of nutrients is reduced, starvation causes experience-dependent creation of receptors that enable nutrient uptake from a novel source.
If a novel source cannot be used, the pheromone-controlled physiology of nutrient-dependent reproduction leads to death of individuals and may lead to the extinction of any species that could not ecologically adapt via experience dependent de novo creation of receptors that let nutrients into the cell. The species in which de novo creation of receptors does not occur quickly enough do not mutate into another species that was somehow naturally selected to “evolve.”
Ideas about epimutations that include what is known about sRNAs but ignore facts about the nutrient-dependent microRNA/messenger RNA balance, amino acid substitutions, and epigenetically-effected morphological and behavioral diversity will make it possible for evolutionary theorists to continue touting their nonsense about mutation-initiated natural selection until serious scientists say ENOUGH!
In the context of order and disorder, some researchers have already said this. I’m not the only one who has had ENOUGH of the pseudoscientific nonsense from population geneticists.
[W]hat Haldane, Fisher, Sewell Wright, Hardy, Weinberg et al. did was invent…. The anglophone tradition was taught. I was taught, and so were my contemporaries, and so were the younger scientists. Evolution was defined as “changes in gene frequencies in natural populations.” The accumulation of genetic mutations was touted to be enough to change one species to another…. No, it wasn’t dishonesty. I think it was wish fulfillment and social momentum. Assumptions, made but not verified, were taught as fact.
If you’ve had ENOUGH of this pseudoscientific nonsense, and want to learn more about biological facts, you may also want to learn more about why Israeli middle schools are now teaching the theory of evolution.  They appear to be using it as an example of pseudoscientific nonsense that can be compared to what is known about ecological variation and how the disorder or variation leads to well-ordered de novo creation of olfactory receptor genes via nutrient-dependent amino acid substitutions that stabilize DNA in the organized genomes of species from microbes to man.
When will other school systems begin teaching students about the differences between ridiculous theories and biological facts about biophysically-constrained ecological adaptations are manifested in biodiversity?
Earlier today I received the reprint of an article published by serious scientists in the prestigious journal Cell: Starvation-Induced Transgenerational Inheritance of Small RNAs in C. elegans. After I read more about the starvation-induced link to cell type differentiation in C. elegans, I was not surprised to see the stated goal of Oded Rechavi’s lab in Israel:

“Our principle aim in the lab is to attack scientific dogmas.”

Finally, serious scientists are no longer willing to wait for evolutionary theorists to start learning about biology. Like a few others, the Rechavi lab researchers are attacking the pseudoscientific nonsense of mutation-initiated natural selection and the evolution of biodiversity. Unfortunately, that claim went missing from the Oded Rechavi lab web page in September 2014. Perhaps it drew unwanted attention to the lab. No matter, the short perspective: RNA and dynamic nuclear organization helped to clarify the fact that “…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].” Clearly, the focus on RNA-mediated events and amino acid substitutions that stabilize DNA in organized genomes will lead to a future in which no serious scientist reports results in terms of mutations, natural selection, and the evolution of biodiversity.
How much clearer can it be that starving nematodes must adapt to ecological changes or their species becomes extinct. How much clearer can it be that ecological variation in the diet of nematodes is what causes nutrient-dependent amino acid substitutions that differentiate the pheromone-controlled cell types of different nematode species? In a news release published on January 13, 2013, Ralf Sommer said: “The patterns of synaptic connections perfectly mirror the fundamental differences in the feeding behaviours of P. pacificus and C. elegans.”
P. pacificus is a nematode species with teeth; C. elegans is a nematode species without teeth. The neuronal networks of the two species are wired differently and their nutrient-dependent pheromone-controlled reproduction is the most obvious cause of their differences in morphology and differences in their behavior.
No experimental evidence suggests that one species of nematode mutated into another. In fact, experimental evidence from C. elegans already has shown that mutations are not fixed in the DNA of the C. elegans organized genome. That finding “…set the stage for the development of more general theoretical models explaining the fate of new alleles…” but without fixed mutations in DNA, no model can explain the fate of new alleles in the context of natural selection that leads to the evolution of biodiversity. Mutations that are not fixed cannot be “naturally selected” and the result of the mutations cannot be evolutionary diversity.
Evolutionary theorists must invent new terms that can be used to describe how biodiversity arises, and some of them have decided to invent the term “epimutation” and attempt to explain how nutrient-dependent epigenetic changes in the organized DNA of species from microbes to man lead to the evolution of biodiversity. Shall serious scientists wish them luck with the invention of their new theories about epimutations and the evolution of biodiversity? Or will serious scientists mount an unending attack on the pseudoscientific nonsense of theorists and begin to make scientific progress that can more rapidly be made if people aren’t taught to believe in a ridiculous theory instead of biological facts about how ecological variation results in ecological adaptations? I hope that my published and unpublished works make it clear that I prefer the Rechavi lab’s attack strategy.

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

and

Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems

“This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent pheromone-controlled ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity in species from microbes to man. Species diversity is a biologically-based nutrient-dependent morphological fact and species-specific pheromones control the physiology of reproduction. The reciprocal relationships of species-typical nutrient-dependent morphological and behavioral diversity are enabled by pheromone-controlled reproduction. Ecological variations and biophysically constrained natural selection of nutrients cause the behaviors that enable ecological adaptations. Species diversity is ecologically validated proof-of-concept. Ideas from population genetics, which exclude ecological factors, are integrated with an experimental evidence-based approach that establishes what is currently known. This is known: Olfactory/pheromonal input links food odors and social odors from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man during their development.”

neuronal-plasticity

The quantum biology of consciousness

Everything known about quantum biology “…suggests conscious experience is intrinsically connected to the fine-scale structure of space–time geometry, and that consciousness could be deeply related to the operation of the laws of the universe.” See for review: Consciousness in the universe: A review of the ‘Orch OR’ theory.
These laws of the universe might lead others to think in terms of “laws of biology” (biological laws). Indeed, many informed scientists could expect that ecological, social, and neurogenic niche construction would result in socio-cognitive niche construction, which appears to be a manifestation of increasing complexity in ecologically adapted organisms. For constrast, nothing known about mutations and natural selection leads to any informative explanation of biologically based cause and effect that involves any laws of biology. Evolutionary theory is useless because only biological laws link sensory input from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man. Thus, the problem for evolutionary theorists is that cause and effect occur outside the context of the evolution of biodiversity.
In addition, we now know that cause and effect occur within the context of Darwin’s ‘conditions of life.’ See: Quantum biology: Algae evolved to switch quantum coherence on and off. The  news article reports that mutations perturb the function of  amino acid substitutions that link photosynthesis in algae to the laws of biology in other organisms via nutrient-dependent amino acid substitutions. In this report, light is the nutrient.
In other organisms, amino acid substitutions enable ecological adaptations that result from ecological variation, which includes variation in light linked to ecological adaptations manifested in eyes and in eye regression in blind cave fish. However,  these ecological adaptations are perturbed by mutations. Thus, attributing either the evolution of eyes or eye regression to mutations is a false attribution.
In the context of the quantum biology of consciousness, “They found that in two species a genetic mutation has led to the insertion of an extra amino acid that changes the structure of the protein complex, disrupting coherence.” This suggests that in all animals, the amino acid substitutions appear to link cell type differentiation via nutrient uptake and metabolism to species specific pheromones that control the physiology of reproduction.
Everything known about the photosynthetic, micronutrient, and macronutrient pathways that link ecological variation via base pair changes to ecological adaptations shows that mutations perturb the protein folding that is required for niche construction to result in increasing organismal complexity via amino acid substitutions. Mutations simply cannot result in the organismal complexity manifested in organisms with eyes.
For contrast, see: Evolution of the first genetic cells and the universal genetic code: A hypothesis based on macromolecular coevolution of RNA and proteins “The origin of homochiral amino acids and sugars is assessed. The integrated development of the Universal Genetic Code in shown in eight steps. Mutation rates limited the sizes of early nucleic acid genomes to about 200 bases.”
In the context of Kohl’s Laws of Biology, achiral glycine links the nutrient-dependent pheromone-controlled stabilized genomes of yeasts and mammals via the conserved molecular mechanisms of RNA-mediated amino acid substitutions. See:  Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems. Perhaps it will shed light on how the nutrient-dependent pheromone-controlled physiology of reproduction in algae is connected across species via amino acid substitutions in organisms from microbes to man. But, even if you are unable to see the light, there is still no experimental evidence that links it (e.g., the light) as a nutrient source to nutrient-dependent pheromone-controlled ecological adaptations.
As I said once before: “It’s time for biophysicists to tell theorists and pathologists how to differentiate between theories about the genesis of different cell types and the biological facts about the nutrient-dependent pheromone-controlled ecological adaptations that enable the genesis of different cell types in individuals of different species. Simply put, it’s time to stop trying to explain ecological adaptations in the context of mutations and evolution.”
See also: ‘Quantum smell’ idea gains ground” Let there be light as a nutrient source for life and cell type differentiation via amino acid substitutions — as noted by Dobzhansky (1973): Nothing in Biology Makes Any Sense Except in the Light of Evolution. As it turned out, nothing about evolution makes sense except in the light of what’s known about light as the first nutrient source for ecological variation and ecological adaptations. For comparison, mutation-driven evolution is pseudoscientific nonsense. Sunlight, for example, alters levels of the steroid hormone vitamin D, which stabilizes the genome of human populations in areas where malarial parasites forced the nutrient-dependent ecological adaptation of lactose persistence.

 

human-evolution

Nutrition, pheromones and cancer (2)

See: Nutrition, pheromones and cancer
Despite the inaccurate reporting of exeperimental evidence, the link from the nutrient-dependent pheromone-controlled microRNA / messenger RNA balance is becoming clearer. Unfortunately, due to the inaccurate reporting, others may need to take the free course: Epigenetic Control of Gene Expression, before they can begin to understand the scientific progress in cancer research, which is occurring because some researchers have dispensed with the pseudoscientific nonsense of evolutionary theory. See for example: Biogenesis of intronic miRNAs located in clusters by independent transcription and alternative splicing
Excerpt: “…alternative splicing might play a role in uncoupling the expression of clustered miRNAs from each other, which otherwise are generally believed to be co-transcribed and co-expressed.”
My comment: Nutrient uptake leads to miRNA biogenesis, alternative splicings, and RNA-mediated events that are responsible for the differentiation of cell types. Typically, cell type differentiation via amino acid substitutions leads to controlled growth of cells and to increasing organismal complexity. That fact makes it clear that something must go wrong when cell type differentiation is not controlled.
See for example: Intronic miR-3151 Within BAALC Drives Leukemogenesis by Deregulating the TP53 Pathway
Excerpt: “Whereas intergenic miRs are always regulated by their own promoters, intronic miRs can be either regulated with their host gene or regulated independently of their host gene (28, 29).”
Reported as: Gene within a gene contributes to aggressive leukemia
Excerpt: “…it is high expression of miR-3151 that really matters.”
The microRNA/messenger RNA balance is what really matters because it alters nutrient-dependent cell type differentiation via alternative splicings. When evolutionary theorists learn the cause of normal cell type differentiation, which leads to species diversity, they may stop telling people that mutations and natural selection cause evolution. If not, continuing to tout that nonsense will cause others who know that species diversity is nutrient-dependent and pheromone-controlled to claim that evolutionary theorists have prevented scientific progress towards a cure for cancer.

Light-induced-conformer-intercoversion-of-hydrogen-bond

A thought experiment

I may be confused about proximate and ultimate cause, especially if the role of transgenerational epigenetic inheritance is not central to the extended evolutionary synthesis. Isn’t transgenerational epigenetic inheritance the problem that led Dickins and Rahman to suggest a thought experiment; one where epigenetic mechanisms introduce shifts in learning bias for certain associations as would endocrine functioning? If so, my model (Kohl, 2012), which combines the epigenetic effects of nutrient chemicals and pheromones with biased endocrine functioning and adaptive evolution, may help move the modern synthesis forward.
I tried this before, but the evolutionary continuum from microbes to man (Kohl, 2007) seems too much to grasp in the context of biased endocrine functioning. However, the honeybee has since emerged as a model organism to exemplify nutrient chemical and pheromone-dependent epigenetic alterations in endocrine functioning. These epigenetic effects that bias endocrine functioning are required for the adaptive evolution of reproduction.
Reproduction is required for transgenerational epigenetic inheritance and species diversity, which is perhaps better represented in the threespine stickleback vertebrate model organism. However, in all invertebrate and vertebrate model organisms, nutrient chemicals establish the ecological niche of individuals, and the presence of conspecifics establishes their social niche (as also occurs with microbial species).
The honeybee best exemplifies how  ecological and social niches contribute to the hypothalamic gonadotropin releasing hormone (GnRH) neurogenic niche that is responsible for the adaptive evolution of the human brain. Simply put, what the queen eats determines her pheromone production and everything else about the social interactions in the colony, including the required epigenetic effects of pheromones on the neuroanatomy of the worker bee’s brains during the development of their diverse behaviors that change with exposure to different chemical input associated with a variety of other sensory input of lesser importance / salience.
Of course, that sounds too simple in the context of the extended evolutionary synthesis and human brain evolution. But the molecular biology is conserved across species, which is helpful for proof of concept. In placental mammals, for example, in utero nutrient chemical transfer is responsible for organization of the brain’s postnatal activation by nutrient chemicals and pheromones. The proper GnRH-driven behavioral response of the infant to activation by these chemicals ensures its survival, just as the proper response of the honeybee worker bee’s brain to nutrient chemicals and pheromones ensures its survival and helps to ensure the colony’s survival via changes in the neuroanatomy of its brain. (Parenthetically, spectral input may or may not be correlated with direct epigenetic effects on the brain, but it is not causal to brain development.)
Model organisms have their RNA-mediated molecular biology in common with all other organisms. No organism survives in the absence of sufficient nutrient chemicals. Ecological niches contract. And no species survives in the absence of reproduction controlled by pheromones. I think that’s why we are now seeing more reports on transgenerational epigenetic inheritance, with causal links to speciation via ecological and social niches in all species. We should soon see the addition of neurogenic niches in many others.
What I don’t see is anyone who is integrating the ecological, social, and neurogenic niches and considering the epigenetic effects of nutrient chemicals and pheromones in the context of endocrine disruption and transgenerational epigenetic inheritance. Nutrient chemicals and pheromones promote homeostasis and also allow adaptive evolution, including adaptive evolution of the human brain. Endocrine disruption causes atypical development of the brain and the body.
Isn’t that the apparent design we might all someday see in biology? Isn’t seeing the apparent design required to move forward from the Modern Synthesis to the Extended Evolutionary Synthesis?
Jim Kohl
www.pheromones.com
On 5/27/2012 3:26 AM, R.J.King@lse.ac.uk wrote:

jvkohl:
I fear that you may have confused proximate and ultimate. Easily done. Epigenetics, while fascinating, has no impact on the central doctine of genes as the sole information carriers. Epigenetics are just one more set of mechanisms by which genes achieve their ultimate aim of replication. I.e. they are part of the suite of adaptations. The University of Utah has an excellent site detailing this
http://learn.genetics.utah.edu/
May I particularly recommened this page which beautifully illustrates the way in which behaviours and epigenetics intereact in this way to calibrate personality to environment?
http://learn.genetics.utah.edu/content/epigenetics/rats/
My suspicion  is that the folk biology concept of "biology=fixed at birth" dies very very hard and keeps recurring in odd forms in even the best and brightest of us.