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


Behavior (2): All responses are RNA-mediated not genetically-determined

Diana Maria Petrosanu also asked: “who was the author of the article that had stolen your ideas?
I cannot recall claiming that anyone had stolen our ideas or my ideas.
See: Behavior: The first response is RNA-mediated not genetically-determined. In subsequent published works, I extended what we detailed about the molecular epigenetics of sex differences in cell types from yeasts to mammals via examples from model organisms of RNA-mediated cell type differentiation in different species. That is why I was surprised to see this title: The Biological Basis of Human Sexual Orientation: Is There a Role for Epigenetics?” I’ve requested a pdf reprint of the article from Dr. Vilain. I do not expect that he cited our 1996 review because I do not recall him even mentioning any works I have authored or co-authored in his publications? Is he ignoring my past publications?
For example, in our 1996 Hormones and Behavior review we (TB) wrote: “Parenthetically it is interesting to note even the yeast Saccharomyces cerevisiae has a gene-based equivalent of sexual orientation (i.e., a-factor and alpha-factor physiologies). These differences arise from different epigenetic modifications of an otherwise identical MAT locus (Runge and Zakian, 1996; Wu and Haber, 1995).”
The connection from RNA-mediated events to epigenetic modifications of the MAT locus should have been clear to any geneticist who did not know how mutations in DNA could lead to sex differences and to sexual orientation in different cell types. However, many of those who study human sexuality are like those who study evolutionary psychology. I think that is why this question was posed: Is There a Role for Epigenetics?
Anyone taught to believe an unknown evolutionary event might someday be linked to sex differences in cell types or to any and all other cell type differences in all cells of all individuals of all species has been taught to believe in pseudoscientific nonsense, and to ignore biological facts about RNA-mediated events that we (TB) detailed 18 years ago. Those who were not taught that mutations caused sex differences in cell types may have been left to wonder about how sexual orientation somehow ‘evolved.’ That’s just speculation on my part. Some people probably weren’t taught anything and never questioned the likely role of RNA-mediated events, or never questioned their teachers who probably still know nothing about molecular epigenetics and RNA-mediated events.
We wrote: “Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans. That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.” (p. 337)
Was anyone taught to believe the truth about the molecular epigenetics of cell type differentiation in species from microbes to man? When I saw the question “Is there a role for epigenetics,” I decided to look more at what Eric Vilain was telling people about how sex differences in cell types arise. See, for examples:
Sex Differences in Brain and Behavior: Hormones Versus Genes
Excerpt: “We hypothesize that one central neuronal pathway establishes sexual attraction to either males or females, usually to the opposite sex. However, a variety of genetic and nongenetic biological effects might intersect this pathway (p. 260).”
My comment: In my model, the GnRH neuronal pathway establishes classically-conditioned sexual preferences in the context of epigenetically-effected RNA-mediated events via the same pathway that links food odors to experience-dependent classically-conditioned food preferences.
The genetics of sex differences in brain and behavior
Excerpt: “Altogether, there is mounting evidence for a genetic role of human sexual orientation. The overwhelming dominance of heterosexual behavior in the animal kingdom points at a tight molecular regulation of this trait.”
My comment: In my model, nutrient-dependent pheromone-controlled effects on RNA-mediated events tightly regulate the molecular epigenetics of this trait throughout the animal kingdom. That means that human sexual orientation, like the sexual orientation of sexually-differentiation cell types in yeasts is genetically predisposed. There may be mounting evidence for a genetic role of human sexual orientation, but I haven’t seen any of it. All I’ve seen is increasingly more evidence that sexual orientation is epigenetically-effected by sensory stimuli that cause RNA-mediated events.
The effects of perinatal testosterone exposure on the DNA methylome of the mouse brain are late-emerging
Excerpt: “…methylation patterns particularly during adulthood and that the emergence of sex differences in the brain may be a gradual process that is cemented over the organism’s life. Our data provide a new perspective by showing that most sex differences in CpG methylation are dynamic and not the result of acute modifications in response to hormones.”
My comment: I do not know why anyone ever thought that “…the emergence of sex differences in the brain…” was not “…a gradual process that is cemented over the organism’s life.” Attributing the sex differences to dynamic modifications but not acute modifications in hormones that organize and activate sex differences in behaviors,which obviously develop during life cycle transitions, may be the only accurate attribution Vilain has ever linked to RNA-mediated events that are epigenetically-effected by olfactory/pheromonal input that alters hormones that affect the behavior of all vertebrates and invertebrates via conserved molecular mechanisms.
My comment (from our 1996 review): Molecular epigenetics. It is now understood that certain genes undergo a process called “genomic or parental imprinting.” Early in embryonic development attached methyl groups become removed from most genes. Several days later, methyl groups are reattached in appropriate sites. Fascinatingly, some such genes reestablish methylation patterns based upon whether the chromosomal segment carrying the gene came from maternal or paternal chromosomes.
Although Eric Vilain and his co-authors may think their “…data provide a new perspective…” the quote from our review should make others wonder what his group thinks is a “new perspective.”  Indeed, anyone who has followed the research on epigenetically-effected RNA-mediated events and hormones that affect behavior might wonder why anyone else ever might have thought that the RNA-mediated events did not occur across the life history transitions of species from insects to mammals.
For example, I never thought I was “Born to be Wild.” But, after I started my research on human pheromones in 1982, I gradually learned to accept the fact that my behavior was epigenetically-effected by human pheromones. From 1996 until today, I have never seen any experimental evidence of biologically-based cause and effect that links anyone’s behavior to anything that is not epigenetically-effected and RNA-mediated.
For reasons that should long ago have become obvious to all others, I am now sure that all their behavior occurs in the context of ecological variation that leads from epigenetically-effected RNA-mediated differentiation of cell types by nutrient-dependent amino acid substitutions. It is the amino acid substitutions that link behaviors manifested in ecologically adapted morphological and behavioral phenotypes to conserved molecular mechanisms in species from microbes to man.


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.”


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”).
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.
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


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.”


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.



Pheromone-controlled thermodynamics and cancer

If you learnt evolutionary biology and genetics a decade or more ago you need to be aware that those debates have moved on very considerably, as has the experimental and field work on which they are based.” — Denis Noble

Can thermodynamics help us better understand human cancers?

Excerpt: “In a new study, UCLA researchers analyzed the gene-expression profiles of more than 2,000 patients and were able to identify cancer-specific gene signatures for breast, lung, prostate and ovarian cancers. The study applied an innovative approach to gene-array analysis known as “surprisal analysis,” which uses the principles of thermodynamics—the study of the relationship between different forms of energy—to understand cellular processes in cancer.”
My comment: This article “miRNA and mRNA cancer signatures determined by analysis of expression levels in large cohorts of patients” integrates what is known about RNA-directed DNA methylation and the RNA-mediated DNA/RNA protein synthesizing system and biological information with the thermodynamics of intercellular interactions. A robust microRNA/messenger RNA (miRNA / mRNA) balance exemplifies a finely tuned, calibrated, and standardized reference state. Deviation from the finely tuned miRNA / mRNA balance exemplifies the cancer-specific disease pattern. The deviation is “…a signature comprised of unique mRNAs and miRNAs capable of distinguishing diseased patient samples from normal controls.” Thus, the importance of Nutrient-dependent / Pheromone–controlled thermodynamics and thermoregulation to distinguishing between an atypical or typical miRNA / mRNA balance becomes more important to the diagnosis and treatment of cancer, or to prevention. For example, I wrote: “Disease is associated with mutations exemplified in cancer where perturbations of the glucose-dependent thermodynamic/thermoregulatory equilibrium are equally clear (Locasale, 2012).”
However, it is simply not possible to differentiate bottom-up nutrient-dependent epigenetic effects on thermodynamics and stochastic gene expression from top-down pheromone-controlled epigenetic effects on organism-level thermoregulation until others realize that common molecular mechanisms are involved across species and that only one neuronal signaling pathway is required in mammals. The gonadotropin releasing hormone (GnRH) neuronal system is responsible for thermodynamically controlled organism-level thermoregulation in mammals. Yet the origins of this neuronal system can be traced back to single-celled yeasts at the advent of sexual reproduction that predicts sex differences in hormone-linked cancers and other disease states. This means thermodynamics alone cannot help us better understand human cancers. Cancer must be understood in the context of organism-level thermoregulation and adaptive evolution by differentiating it from theories that incorporate mutation-initiated natural selection. Mutations perturb the thermodynamics of intercellular signalling, and no organism naturally selects for anything involved in cancer.

Researchers must begin to popularize biological facts and continue to fight against the popularity of mutations theory. We can then better teach others to understand the epigenetic effects of nutrient stress and social stress on cancer, which is not adaptive, and also help others to begin to better understand many things about adaptive evolution. See, for example, this 5.5 minute video representation from my 2013 International Society for Human Ethology Summer Institute Poster presentation:  “Nutrient-dependent / pheromone-controlled adaptive evolution: (a mammalian model of thermodynamics and organism-level thermoregulation)”


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.