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).

achiral-glycine

Seemingly futile cycles are not thermodynamically futile

Scientists discover an on/off switch for aging cells

The switch controls the growth of telomeres, the timekeepers of cells

Excerpt: Understanding how this “off” switch can be manipulated–thereby slowing down the telomere shortening process–could lead to treatments for diseases of aging (for example, regenerating vital organs later in life).”
My comment: Seemingly futile thermodynamic cycles of protein biosynthesis and  degradation appear to be confusing. I’m somewhat certain that the folks at Salk realize that cycles of biophysically-constrained nutrient-dependent RNA-mediated protein folding limit how the switches are epigenetically-effected by olfactory/pheromonal input. I’m unsure that what they know is being conveyed to others.
This news report says nothing about how the conserved molecular mechanisms of nutrient-dependent, RNA-mediated, pheromone-controlled cell type differentiation via amino acid substitutions differentiates cell types in species from microbes to man during their life-cycle transitions.See for example:

The journal article is behind a paywall. I have requested it from the corresponding author and may be able to link “Regulated assembly and disassembly of the yeast telomerase quaternary complex” to the thermodynamics of protein structure and function from what they say about “The balance between the assembly and disassembly pathways, which dictate the levels of the active holoenzyme in the cell…” and homeostasis. Obviously, homeostasis is manifested in organism-level thermoregulation.
Hopefully, I can match what is known about biophysical constraints on light-induced amino acid substitutions to nutrient-induced amino acid substitutions in plants and animals via Single-residue insertion switches the quaternary structure and exciton states of cryptophyte light-harvesting proteins. The rest of the story can then be compared to the ‘Just-So’ stories of evolutionary theorists who left physics and chemistry out of their ridiculous theories based on population genetics.
An open access article places the thermodynamic cycles of protein biosynthesis and degradation into the context of my model.  Thermodynamics with continuous information flow.
See: “FIG. 2. Bipartite examples” They use the terms from biology to link the sun’s biological energy to the de novo creation of light-induced amino acid substitutions and enzymes. They link nutrient-dependent RNA-directed DNA methylation from the enzymes to receptor-mediated cell type behavior.
Excerpt: “Measurement and feedback is performed through a nonautonomous process that simultaneously flips the bits, while switching the energy landscape. By biasing uphill potential flips with a nonequilibrium force (not shown), the particle can be driven preferentially uphill in order to extract work.”
My comment: The “nonequilibrium force (not shown)” is probably the anti-entropic “force” of the sun, which altered the equilibrium of cell from the time of their energy-dependent creation. The “flips”probably are base pair flips, which are linked from differences in hydrogen bond energies to cell type differentiation via amino acid substitutions in my model of nutrient-dependent  ecological adaptations.
Excerpt: “Researchers recently rediscovered a nutrient-dependent epigenetic variant that links vitamin C to what is probably a glucose and glucose dehydrogenase-dependent base pair change. The base pair change results in addition of a methyl group to a cytosine base, which takes on a hydroxyl group to form different 5-hydroxymethylcytosines (5hmCs). Different 5hmCs are associated with differences in cell types that have the same genetic backgrounds. Nutrient-dependent epigenetically-marked bases help to explain how hundreds of cell types in the human body and in the brain (Kriaucionis & Heintz, 2009) are differentiated and how they maintain their glucose-dependent and other nutrient-dependent receptor-mediated identities (Wu et al., 2014).”
Again See: “FIG. 2. Bipartite examples”
Excerpt: “…the enzyme, through a sequence of reactions (purple dotted), speeds up the removal of bound methyl groups M (purple). This feedback loop shifts the enzyme’s stability, so as to maintain it in the same adapted distribution…
My comment: The adapted distribution is nutrient energy-dependent RNA-directed via DNA methylation. Ecological adaptations occur via amino acid substitutions that stabilize RNA-mediated protein folding during thermodynamic cycles of protein biosynthesis and degradation that are RNA-mediated and perturbed by mutations.  These facts link physics from chemistry to the conserved molecular epigenetics of RNA-mediated cell type differentiation in all genera.
Obviously, more physicists should be taught to understand the accurate representations made of biologically-based cause and effect in “Life as physics and chemistry: A system view of biology.” However, most of them seem unwilling to abandon the pseudoscientific nonsense of their ridiculous theories and would rather prevent scientific progress than admit that they didn’t realize that the link to life from the sun’s biological energy was a more important consideration than mutations, natural selection, and evolutionary theory could ever become — even if serious scientists were not Combating Evolution to Fight Disease.
 

poster-from-jesse

Memory of repression and memory of behavior

H3K27me and PRC2 transmit a memory of repression across generations and during development

Reported as:

How epigenetic memory is passed through generations: Sperm and eggs transmit memory of gene repression to embryos

Date:

September 18, 2014

Excerpt: “There are dozens of potential epigenetic markers. In studies that document parent-to-child epigenetic inheritance, it’s not clear what’s being passed on, and understanding it molecularly is very complicated. We have a specific example of epigenetic memory that is passed on, and we can see it in the microscope. It’s one piece of the puzzle.”

See: Maleszka et al (2013). They link oxidation of 5Mc to 5hmC from the main pathway that removes methyl tags from the genome to brain-increased levels of 5hmC in gene bodies that correlate with active transcription.
Excerpt: “Within the neuronal function-related genes, gain of 5hmC is accompanied by loss of H3K27me3…”
Taken together with what is known about nutrient-dependent pheromone-controlled cell type differentiation via amino acid substitutions in the honeybee and other model organisms, a model of RNA-mediated cause and effect suggests learning and memory of food odors and species-specific pheromones links transgenerational epigenetic inheritance via the molecular mechanisms that transmit a ‘memory of repression,’ which can be linked to behavior.
The link from conserved molecular mechanisms to transgenerational epigenetic inheritance of behavior appears to occur in the context of the systems complexity of nutrient-dependent changes in the microRNA/messenger RNA balance and the overwhelming influence of all epigenetic effects on cell type differentiation in all cells of all individuals of all organisms (i.e., of all genera). It is now clearer that control of cell type differentiation occurs via the combination of epigenetic effects on the development of morphological phenotypes and on the development of behavioral phenotypes during life history transitions via amino acid substitutions that stabilize DNA in organized genomes via nutrient-dependent pheromone-controlled ecological adaptations to nutrient availability. See also: Starvation-Induced Transgenerational Inheritance of Small RNAs in C. elegans

diseases-disorders

Exploding genomes and chromosomal rearrangements via RNA-mediated events

Gibbon genome and the fast karyotype evolution of small apes
This is an open access article reported as:

Gibbon genome sequence deepens understanding of primates rapid chromosomal rearrangements

Excerpt: The number of in the gibbons is remarkable, Rogers said. “It is like the genome just exploded and then was put back together,” he said. “Up until recently, it has been impossible to determine how one human chromosome could be aligned to any gibbon chromosome because there are so many rearrangements.”
My comment: Now that researchers have determined how so many chromosomal rearrangements can rapidly occur outside the context of mutations, they can link the genome of gibbons to the human genome via the following sequence of events:
1) nutrient-dependent changes in the
2) microRNA/messenger RNA balance,
3) alternative splicings of pre-mRNA, and
4) RNA-mediated events that link
5) amino acids substitutions to their fixation when they stabilize the DNA in organized genomes of species.
The nutrient-dependent chromosomal rearrangements can then be linked to the RNA-mediated stability of DNA in species from microbes to man via the conserved molecular mechanisms of reproduction isolation due to chromosomal rearrangement and species diversity due to the metabolism of nutrients to species-specific pheromones. which control the physiology of reproduction in species from microbes to man. Thus the conserved molecular mechanisms of RNA-mediated events have again eliminated any further consideration of mutations and natural selection in the evolution of biodiversity.
Until an evolutionary event is described, theorists may continue to invent and define their theories in terms that link mutated DNA to biodiversity and increasing organismal complexity that ‘just happens’ to somehow occur in explosions of chromosomal rearrangements like those that supposedly occurred during the Cambrian explosion. However, the fact that these explosions are nutrient-dependent and pheromone-controlled may mean that biodiversity arises in much less time that might otherwise be predicted in the context of pseudoscientific nonsense of population genetics and neo-Darwinism.
Note also, however, that Genome-wide DNA rearrangements are most exaggerated in ciliates, particularly in the model organism Oxytricha trifallax, which programs not only DNA deletion, but also total reorganization, through RNA-mediated events (Fang et al., 2012; Nowacki et al., 2008).
See the report here on that fact about the conserved molecular mechanisms of RNA-mediated events for comparison to unknown evolutionary events: In one of nature’s innovations, a single cell smashes and rebuilds its own genome

Physics

Baby talk: More misrepresentations of ecological adaptations

Evolution’s Baby Steps

Excerpt 1) “When organisms find themselves in a new environment, they develop in a way that helps them cope with their new surroundings. Their descendants may acquire mutations that encode that anatomy in their genes. Eventually evolution takes them beyond where plasticity alone could take them.”
My comment: It’s time for science journalists to stop touting this nonsense (above).
Ecological variation leads from nutrient uptake in new environments to RNA-mediated amino acid substitutions. If the nutrient-dependent amino acid substitutions stabilize the DNA in organized genomes, the metabolism of nutrients leads to the controlled physiology of reproduction by species-specific pheromones.
Nutrient-dependent pheromone-controlled ecological adaptations lead to biodiversity manifested in the morphological and behavioral phenotypes of species from microbes to man via conserved molecular mechanisms (“Genome Dynamics Events”).
Excerpt 2) In 2008, for example, scientists raised stickleback fish on two different diets. One group of fish ate bloodworms squirming around at the bottom of their tanks. The other fish ate shrimp scooting around in the open water. The bloodworm-eating fish had to clamp down on the blood worms to eat them, while the shrimp-eating ones just needed to sneak up on their prey and swallow them with a quick slurp.
The result of these different movements was different heads: the bloodworm-feeders had short, wide mouths, and the shrimp-feeders had long, narrow ones.
My comment: Attributing differences in morphology to “different movements” in sticklebacks fed two different diets is akin to telling people that differences in C. elegans (grazing nematodes) and P. pacificus (predatory nematodes with teeth) is due to differences in their movements.
The differences in nematodes and sticklebacks are due to nutrient-dependent pheromone-controlled ecological, social, and neurogenic niche construction in all species with neuronal networks. How else would hundreds of different species of sticklebacks arise in one lake? See for review: Advances in Ecological Speciation: an integrative approach
See also: “It’s a series of adaptations that affect many aspects of the organism: the shape of the fish, its behaviour, diet and mating preferences,” says evolutionary biologist Greg Wray at Duke University in Durham, North Carolina, who was not involved in the study.”

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.

 

neuronal-plasticity

Ecologically linked adapted ants and brains

Ants Swarm Like Brains Think

A neuroscientist studies ant colonies to understand feedback in the brain.
By Carrie Arnold April 24, 2014
Excerpt: “The behavior of each individual in the group is set by the rate at which it meets other ants and a set of basic rules. Its behavior alters that of its neighbors, which in turn affects the original ant, in a classic example of feedback. The result is astonishing, complex behavior.”
My comment: The molecular mechanisms of nutrient-dependent intracellular, intercellular, and extracellular signaling appear to be conserved in species from microbes to man. In ants, the mechanisms are pheromone-controlled. If no other organism on this planet supports representations that mutations are somehow responsible for evolution, what could explain the lack of acceptance for the scientific truth?
Ecologically linked variation results in nutrient-dependent pheromone-controlled ecological adaptations via conserved molecular mechanisms.  Ecologically linked changes in nutrient-dependent morphology and pheromone-controlled species-specific behaviors does not seem like a difficult concept to grasp. That means it is time for those who cannot seem to grasp it to explain why they think mutations, or anything else, might be responsible for the behavior of any organism.
Odor memories regulate olfactory receptor expression in the sensory periphery of honeybees. It is unlikely that any other regulatory mechanisms cause differences in morphology and behavior in other model organisms, especially ants. Thus, the fact that “…olfactory receptor expression is experience-dependent and modulated by scent conditioning…” is one that should be considered in the context of the mechanism that appears to underlie the plasticity of signaling that involves nutrient-dependent pheromone-controlled changes in the microRNA/messenger RNA balance, DNA methlylation, and RNA-mediated amino acid substitutions that differentiate the cell types of individuals in species from microbes to man.
If others consider the possibility that mutations somehow cause controlled changes in morphology or behavior in any organism, they should provide reasons for such considerations so that their reasoning can be compared to what is known about biological facts that link ecological variation to ecological adaptation in all species.
Signaling Crosstalk: Integrating Nutrient Availability and Sex (microbes)
Feedback loops link odor and pheromone signaling with reproduction (vertebrates)
Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems (viruses to whales and humans)

Schrodinger conference

The birds and the bees; olfaction and pheromones

Product sales have been virtually eliminated by the pseudoscientific nonsense touted by neo-Darwinian theorists and Big Bang cosmologists. I may revisit their ridiculous claims here, but prefer to continue moving forward via my other domains: RNA-mediated.com and Autophagy.pro

Summary: 2018 Update: Sympatric speciation has been linked to species diversity as an example of an ecologically validated proof-of-concept in all living genera.

I have neglected this domain during the past 7 years because it became clear that pseudoscientists were not going to let people know that all aspects of sympatric speciation have been detailed in the context of food energy-dependent pheromone-controlled reproduction, which is required to biophysically constrain viral latency.

That fact was placed into the context of the cell biology game “Cytosis,” which was delivered to backers in October 2017.

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

See also: A transmissible RNA pathway in honey bees (2018)

The authors link my model of food energy-dependent pheromone-controlled biophysically constrained sympatric speciation from atoms to ecosystems in all living genera via my 2013 published review and my unpublished invited review of nutritional epigenetics.

Nutrient-dependent/pheromone-controlled adaptive evolution: a model (2013)

…the epigenetic ‘tweaking’ of the immense gene networks that occurs via exposure to nutrient chemicals and pheromones can now be modeled in the context of the microRNA/messenger RNA balance, receptor-mediated intracellular signaling, and the stochastic gene expression required for nutrient-dependent pheromone-controlled adaptive evolution. The role of the microRNA/messenger RNA balance (Breen, Kemena, Vlasov, Notredame, & Kondrashov, 2012; Duvarci, Nader, & LeDoux, 2008; Griggs et al., 2013; Monahan & Lomvardas, 2012) in adaptive evolution will certainly be discussed in published works that will follow.

2018 Update: Sympatric speciation has been linked to species diversity as an example of an ecologically validated proof-of-concept in all living genera.

For a historical perspective, see: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems (2014 preprint)

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.

The facts about sympatric speciation for comparison to the neo-Darwinian pseudoscientific nonsense about mutation-driven evolution have been placed in to the context of 3 more recently published works.

A 360 degrees view of circular RNAs: From biogenesis to functions (2018)

Circular RNAs: Unexpected outputs of many protein-coding genes (2017)

The Output of Protein-Coding Genes Shifts to Circular RNAs When the Pre-mRNA Processing Machinery Is Limiting (2017)

It is no longer possible to put the facts about sympatric speciation back into the context of ridiculous theories about the emergence of energy and evolution of all life on Earth. Anyone who returns to the links or to the published works I have posted here, will realize that pseudoscientists know virtually nothing about food energy-dependent RNA-mediated cell type differentiation in any species.

In 2011, I wrote:

A recent report says that homing pigeons depend on their sense of smell to find their way home. This report helps to confirm that olfaction is essential to behavioral development in species  from insects to vertebrates.

Several other articles also have recently reported on how pheromones are involved in

1. sexual arousal in birds, and

2. mate choice in birds.

The cause and effect that is missing from earlier works on avian behavior is addressed in these articles.

It has become obvious that visual and auditory signals are not the most salient cues involved in avian species, which suggests we quit comparing bird-brained behaviors that are driven by relatively insignificant cues (i.e., compared to pheromones) to human behavior. Research on birds has allowed us to be led to believe that our sexual behavior is based on visual and auditory input.  Supposedly, olfactory input and pheromones play lesser roles.  But no scientific data suggest this.

Nevertheless, as we approach the celebration of Valentine’s Day, you will no doubt read that humans are primarily visual creatures. The series of articles on love that appear each year in the mass media are a testament to the fact that we can easily led to believe that we are not like other animals, which helps to keep us blind as bats when it comes to love.

Even animals that have the visual acuity of  eagle-eyed avians depend on their sense of smell and pheromones to drive the neurophysiological mechanisms of behavioral development, sexual arousal, and mate choice. It’s the pheromones in every species from yeasts to you.

1. Ball, G. F. and J. Balthazart (in press). “Sexual arousal, is it for mammals only?” Hormones and Behavior In Press, Accepted Manuscript.

2. Whittaker, D. J., H. A. Soini, et al. (2010). “Songbird chemosignals: volatile compounds in preen gland secretions vary among individuals, sexes, and populations.” Behavioral Ecology 21(3): 608-614.

see also Caro, S. P. and J. Balthazart (2010). “Pheromones in birds: myth or reality?” J Comp Physiol A Neuroethol Sens Neural Behav Physiol 2010: 21.