terrarium-eco-system

Amino acid-dependent cell type differentiation

mTORC1 is a protein complex that functions as a nutrient/energy/redox sensor and controls protein synthesis.
MCRS1 Binds and Couples Rheb to Amino Acid-Dependent mTORC1 Activation” reported as:

Oncogene regulated by nutrients identified

A protein that is a molecular link connects Rheb-GTP to mTORC1 activation, lysosomes, and amino acid responses. Depletion of the protein links a chain of interactions to mTORC1 inactivation. The authors address the complexity of the biophysically constrained chemistry of RNA-directed DNA methylation and RNA-mediated protein folding, which links ecological variation to ecological adaptation via amino acid sensing. Their findings can be placed into the context of my model of nutrient-dependent pheromone-controlled protein biosynthesis and ecological adaptations.
See this 5.5 minute-long video representation: Nutrient-dependent / Pheromone-controlled thermodynamics and thermoregulation. See also: Making sense of amino acid sensing.
Conclusion (with my emphasis): “The results presented by Rebsamen et al., Wang et al., Jewell et al., and Thomas et al. almost certainly foreshadow the complexity yet to be uncovered regarding amino acid sensing by mTORC1.”
The links from amino acid sensing to metabolic networks and genetic networks fit perfectly into my detailed model with its examples from different species.  The effects of amino acid substitutions on the stability of nutrient-dependent RNA-mediated protein folding can readily be differentiated from the effects of mutations, which cause physiopathology. Amino acid substitutions are linked to the increasing organismal complexity of nutrient-dependent biodiversity via thermodynamic cycles of protein biosynthesis and degradation that enable organism-level thermoregulation. The amino acid substitutions are fixed in the context of the nutrient-dependent physiology of reproduction. Mutations perturb protein folding, which is why they are not beneficial.
Theorists can now attempt to explain (and continue to fail to explain) how mutations are linked to biodiversity via the Evolution of High Mobility Group Nucleosome-Binding Proteins and Its Implications for Vertebrate Chromatin Specialization. This was reported as: Scientists unlock tangled mysteries of DNA
Excerpt: While today’s human body contains a variety of these proteins, Eirin-Lopez believes they evolved from a single ancestor millions of years ago. This finding, published recently in Molecular Biology and Evolution, is pivotal in unraveling the mysteries of DNA organization and regulation, and could someday lead to innovative biomonitoring strategies and therapies targeting a variety of diseases including cancer.
See my comments to the phys.org site. That belief has not been supported by any experimental evidence of biologically-based cause and effect.
Obviously, unsupported beliefs are not “…pivotal in unraveling the mysteries of DNA organization and regulation…” Experimental evidence that links top-down causation to biodiversity via RNA-mediated amino acid substitutions and cell type differentiation is pivotal.  See, for instance, this claim:  “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. Thus, currently, the most plausible hypothesis is that we are observing a universal, intrinsic trend that emerged before the last universal common ancestor of all extant organisms.
My comment: Any approach to cell type differentiation that does not include what is currently known about nutrient-dependent amino acid substitutions is an approach that is based on pseudoscientific nonsense. Ridiculous theories about evolution will NOT  lead to “…innovative biomonitoring strategies and therapies targeting a variety of diseases including cancer.”

Excerpt (with my emphasis): “MCRS1 was initially described as a nucleolar protein p120 interactor (Ren et al., 1998), associated with transcription regulation (Andersen et al., 2010; Ivanova et al., 2005; Lin and Shih, 2002; Wu et al., 2009). However, it participates in other processes, including cellular senescence (Hsu et al., 2012), cell division, and survival by interacting with the centrosomal protein Nde1 (Hirohashi et al., 2006) and is reportedly an essential RanGTP-regulated factor for bipolar spindle assembly protecting them from depolymerization (Meunier and Vernos, 2011) MCRS1 regulates mTORC1 independently of microtubule networks and its nuclear function argues that cells may contain several MCRS1 pools with different functions, without excluding a general role of MCRS1 in scaffolding small GTPase proteins.”
My comment: What aspect of evolution argues for the role of mutations in cell type differentiation? How are mutations linked to increasing organismal complexity via the physiology of nutrient-dependent reproduction? See for example: Was ribosome the first self-replicator? 
Excerpt: “…does it make sense to talk about dark variants of cell and cell membrane? Can one tell whether it was pro-cell or bio-molecules that emerged first? It seems that all these structures could have emerged simultaneously. What emerged was dark matter and its emergence involved the emergence of all the others. Hens and eggs emerged simultaneously.”
My comment: Who pays for research that reports the simultaneous emergence of hens and eggs? Who pays for research that links mutations to the evolution of biodiversity and also links mutations to cancer? Who pays the price that must be paid for touting pseudoscientific nonsense since the time that neo-Darwinism was invented? Why isn’t every serious biologist Combating Evolution to Fight Disease?
See, for comparison: Clinically Actionable Genotypes Among 10,000 Patients With Preemptive Pharmacogenomic Testing and Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults. See also, this 2.5 minute-long video: Pharmacogenomics at Mayo Clinic.
It is already past time to move forward from “Oncogene regulated by nutrients identified
Excerpt (with my emphasis) : “Although in our study we published the results obtained from these colorectal samples, we are also studying the relationship between this protein and diseases of the liver, the primary metabolic organ,” explains Djouder.
See also: Nutrient-dependent/pheromone-controlled adaptive evolution: a model.

Excerpt (with my emphasis): The recently detailed mouse model (Li et al., 2013) builds on what is known about olfactory/pheromonal communication in species from microbes to man and incorporates works from mammals that elucidate the molecular mechanisms that are clearly involved. Sex-dependent production of a mouse ‘chemosignal’ with incentive salience appears to have arisen de novo via coincident adaptive evolution that involves an obvious two-step synergy between commensal bacteria and a sex-dependent liver enzyme that metabolizes the nutrient chemical choline.

The result of this synergy is (1) a liver enzyme that oxidizes trimethylamine to (2) an odor that causes (3) species-specific behaviors. Thus, the complex systems that biology required to get from nutrient acquisition and nutrient metabolism to species-specific odor-controlled behavior is exemplified by adaptive evolution of an attractive odor to mice that repels rats (see for review Li et al., 2013).

Excerpt 2) “… 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.”
My comment: If the link from nutrient-dependent microRNAs to amino acid substitutions and cell type differentiation and behavior in mammals is not yet clear, see:
Androgens regulate ovarian follicular development by increasing follicle stimulating hormone receptor and microRNA-125b expression
Alternative splicing of the androgen receptor in polycystic ovary syndrome
Search the presentation abstracts from SFN 2013 for  MicroRNA and GnRH and 2014 MicroRNA and GnRH
For example, see: Tuning fertility: miRNA regulation of GnRH genetic network
See also: Alternative RNA Splicing in Evolution (2012)
Excerpt:  “…alternative splicing is, perhaps, the most critical evolutionary factor determining the differences between human beings and other creatures.”

And see: From Fertilization to Adult Sexual Behavior
Excerpt: “Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.”
My comment: Evolutionary theorists have delayed scientific progress that might otherwise have led to rapid advances in disease prevention and treatment. Theorists still seem to know nothing about cell type differentiation. Yet, Eva Jablonka, who co-authored Evolution in Four Dimensions: Genetic, Epigenetic, Behavioral, and Symbolic Variation in the History of Life claims that “…we have learned that cells are very clever. They have a genetic-engineering kit within each cell, which it can use in all kinds of circumstances. Evolution has led to very clever and sophisticated systems, including systems that can direct their own evolution. There’s nothing wrong with it, and we shouldn’t be surprised at it. In fact, we would be surprised if it didn’t happen, in the long term. I don’t see why it is not evolution.” — See: Beyond Genetic Evolution. A Conversation With Eva Jablonka 
David Sloan Wilson then decides to move forward with “…the second dimension of evolution, epigenetics. Now we do have mechanisms, and we can begin to understand how epigenetics counts as an inheritance system.”
Theorists have ignored the mechanisms. In the molecular epigenetics section of our 1996 Hormones and Behavior review, we detailed the mechanisms of RNA-mediated cell type differentiation. Clearly, the conserved molecular mechanisms have been known to serious scientists for almost two decades. The conserved molecular mechanisms have not been addressed by most evolutionary theorists. Alternatively, the mechanisms have been placed into the context of ridiculous theories.  See page 327  of  Evolution in Four Dimensions.
Excerpt (with my emphasis): “…where there were networks of RNA-mediated interactions, natural selection could have led to some RNA molecules responding to changes in conditions in a way that inhibited the activities of other molecules with a similar sequence. They might have modified the structure of these molecules by base-pairing with them, for example. Later in evolutionary history, as the division of labor between nucleic acids (eventually DNA) as information carriers and proteins as the main enzymes and regulatory molecules increased, vestiges of earlier RNA control systems may
have remained. These could have become modified to fit the new information system and defend it against foreign RNA and DNA sequences.

What we have just said is very vague and speculative, and based on no evidence whatsoever.”

My comment: Our evidence-based approach to RNA-mediated cell type differentiation linked the nutrient-dependent pheromone-controlled physiology of reproduction in species from microbes to primates. It led to accurate representations of how cell type differentiation occurs in the context of the biophysically constrained chemistry of protein folding in all genera. For example, Sabatini’s group appears to have linked “Nutrient-sensing mechanisms and pathways” from the light-induced de novo creation of amino acids to the RNA-mediated stability of all organized vertebrate genomes via insertion of glycine in the GnRH decapetide.
See: Evolution of Constrained Gonadotropin-releasing Hormone Ligand Conformation and Receptor Selectivity
Abstract excerpt: “…substitution of glycine for a chiral amino acid in GnRH during evolution allows a more constrained conformation for receptor binding and that this subtle single amino acid substitution in a site remote from the ligand functional domains has marked effects on its structure and activity.
Kochman (2012) wrote: “The discovery of the fact that one decapeptide molecule, among the GnRHs, was constructed perfectly at the beginning of 400 million years evolution and that it is not possible to improve its physiological potency using the any natural amino acid is, in my opinion, important, fascinating and beautiful” (p. 19).
See also: “SHMT2 drives glioma cell survival in ischaemia but imposes a dependence on glycine clearance.
I can only speculate on what these findings mean in the context of everything currently known to serious scientists about links from physics to chemistry and the conserved molecular mechanisms the enable all extant and extinct biodiversity on this planet. I think it is likely that the balance of viral microRNAs and nutrient-dependent microRNAs is nutrient-dependent and epigenetically inherited as a system of control that enables fixation of other nutrient-dependent amino acid substitutions via the physiology of reproduction, which is controlled by the metabolism of nutrients to species-specific pheromones in species from microbes to humans.
I cannot prove that mutations do not link evolution to biodiversity. I was not taught to believe in ridiculous theories, so the thought never occurred to me that I would need to prove that the idea of mutation-driven evolution is pseudoscientific nonsense. I became a medical laboratory scientist who performed diagnostic testing on people. For example of the latest information on diagnostic testing see:
New blood test can predict future breast cancer
The link from nutritional epigenetics and pharmacogenomic profiles is apparent. Both predict outcomes via metabolic networks and genetic networks during life history transitions.
The networks link nutrient-dependent amino acid substitutions from RNA-directed DNA methylation to the stability of organized genomes in all genera.
Now that nutrient excess has been linked to colorectal cancer, it will be interesting to see how long it takes to link mTORC1 signaling from nutrient sensing to epigenetically-effected sex differences in hormone-organized and hormone-activated physiopathology.
Again, see: Scientists identify an oncogene regulated by nutrients See also: Brain development suffers from lack of fish oil fatty acids, study finds
The amount of experimental evidence that supports my model of RNA-mediated cell type differentiation is overwhelming. I can barely finish one new blog post before at least one more journal article is published as a refutation of evolutionary theory.  What’s worst is that the evolutionary theorists have continued to tout their pseudoscientific nonsense, and they don’t comment on the fact that their theories continue to be ridiculed by serious scientists.

terrarium-eco-system

The miRNA/mRNA balance: a suboptimal strategy?

Cells exercise suboptimal strategy to survive

Excerpt: “Learning the secrets of alternate molecular pathways could provide clues about how to use them to patients’ advantage, she said.”

My comment: The same molecular pathways control the nutrient-dependent physiology of reproduction in all genera. They link RNA-directed DNA methylation to RNA-mediated cell type differentiation via fixation of amino acid substitutions that determine cell types.

See also: Epistasis Among Adaptive Mutations in Deer Mouse Hemoglobin
“Mechanisms of epistasis are often best revealed through detailed examinations of interactions between amino acid mutations…”
See my comment: In my model species-specific epistasis is nutrient-dependent and pheromone-controlled. An additional example of this showed up earlier this week in the context of the epigenetically-effected microRNA/messenger RNA balance: “miR-124 controls male reproductive success in Drosophila
miR-14 acts in neurosecretory cells in the adult brain to control metabolism and miR-124 acts in the context of brain-directed neuroendocrine control of sexual differentiation and male pheromone production, which is controlled in mammals by gonadotropin-releasing hormone (GnRH) neurosecretory cells of the hypothalamus.
We can anticipate extension to mammals of the Drosophila model from the abstract of a forthcoming Science article: “MiR-200b and miR-429 Function in Mouse Ovulation and Are Essential for Female Fertility.” Given our earlier work in the context of molecular epigenetics and the concept of alternative splicings and sexual differentiation in Drosophila and C. elegans, I suspect we will see evidence for nutrient-dependent adaptive evolution of GnRH pulse frequency-controlled LH secretion and pheromone-controlled female fertility in mice.
If I’m correct, this evidence will link glucose and pheromones to feedback loops that control reproduction in invertebrates and vertebrates. (See Nutrient–dependent / pheromone–controlled adaptive evolution: a model). Model organisms exemplify these feedback loops in microbes, nematodes, insects, and other mammals. The mouse to human example that Kamberov et al., and Grossman et al., detailed is the most telling.
A single amino acid substitution appears to result in what seem to be nutrient-dependent changes in the thermodynamics of intracellular signaling, intranuclear interactions, stochastic gene expression, and selection for phenotype via organism-level thermoregulation in a human population that arose in what is now central China during the past ~30K years.
Using a model that integrates what is known about the common molecular mechanisms may help establish whether adaptive mutations lead to thermodynamic effects on organism-level thermoregulation and epistasis, or whether epigenetic effects of nutrients and their metabolism to species-specific pheromones that control reproduction via changes in the microRNA/messenger RNA balance are the driving force behind adaptive evolution in species from microbes to man.
My review was published on the same day as this article in Science. See: Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
So was Nei’s book: Mutation-Driven Evolution
The fact that scientists who study metabolism still cannot differentiate between mutations and amino acid substitutions attests to the overwhelming amount of ignorance among evolutionary theorists.
Mutations perturb protein folding.
Amino acid substitutions link metabolic networks to genetic networks in the organized genomes of all genera via the nutrient-dependent physiology of reproduction.
See also: The Human Condition—A Molecular Approach
Svante Pääbo includes discussion of the companion papers that link A single amino acid substitution to cell type differentiation in mice and in a modern human population, but fails to differentiate between the role of mutations and amino acid substitutions in the nutrient-dependent cell type differentiation of all cell types in all individuals of all species.

terrarium-eco-system

Too many targets for theories

Random mutations are the substrates upon which directional natural selection acts.” —  Jay R. Feierman.
Others have claimed that random mutations and natural selection somehow lead to the evolution of morphological phenotypes and behavioral phenotypes. They have not placed their claims into the context of what is known about ecological variation and ecological adaptations manifested as RNA-mediated sex differences in cell types of the human brain and all other cell type differences in all genera?
Ecological variation is the raw material by which natural selection can drive evolutionary divergence [1–4]. — Foote et al (2013)
For example, see: Model-guided quantitative analysis of microRNA-mediated regulation on competing endogenous RNAs using a synthetic gene circuit . It was reported as:

“Too many targets:” Scientists create model to analyze ceRNA regulation, validate results with synthetic gene circuits

This was reported by the same journalist who reported Seeing the (UV) light: Previously undetected difference in human mutation rate unique to Europeans. The differences between what has typically been attributed by theorists to mutations and the reality of facts about the biophysically constrained chemistry of RNA-mediated amino acid substitutions and protein folding can now be compared.
Too many targets” links the viral microRNA / nutrient-dependent microRNA balance from viruses and anti-entropic nutrients to the microRNA/messenger RNA balance and to RNA-mediated amino acid substitutions that enable cell type differentiation of all cells in all individuals of all genera via fixation of the RNA-mediated amino acid substitutions in the context of the physiology of reproduction.
Excerpt 1)  MicroRNA is a small non-coding RNA molecule containing about 22 nucleotides found in plants, animals, and some viruses, which functions in RNA silencing and post-transcriptional regulation of gene expression. Messenger RNA is a large family of RNA molecules that convey genetic information from DNA to the ribosome, where they specify the amino acid sequence of the protein products of gene expression
Excerpt 2) “When the miRNA level is high, the cells need more target transcripts to trigger a ceRNA effect.”
Excerpt 3) “… post-transcriptional regulation can be triggered by only 6-nt” (that is, six-nucleotide) “complementarity of the miRNA 5′-end so-called seed region to the target RNA. When miRNA perfectly matches the target RNA, the miRNA cleaves the target RNA and might be recycled to cleave the next target RNA; when miRNA imperfectly matches the target RNA, the miRNA binds to the target RNA, inhibiting translation or causing RNA destabilizing.”
Excerpt 4 “In addition to an appropriate molecular environment, ceRNA-crosstalk efficiency also positively correlates with the binding strength of miRNA to its MREs, including the number of MREs and the thermodynamic binding stability, while keeping the effective regime unchanged relative to target transcriptional level,”
My comment: Too many viral microRNAs appear to cause genomic instability via uncorrected errors in the stability of protein folding.  Genomic stability is maintained by the epigenetic effects of nutrient-dependent microRNAs and RNA-mediated amino acid substitutions. Parenthetically, that is why nutrient uptake is important to the survival of all ecologically adapted organisms of all genera.
In my atoms to ecosystems model of ecological adaptations, it is the balance of viral microRNAs to nutrient-dependent microRNAs that links nutrient-dependent thermodynamic cycles of protein biosynthesis and degradation to organism-level thermoregulation via everything currently known about the physics, chemistry, and the conserved molecular mechanisms of RNA-mediated cell type differentiation.
See for comparison: NIH’s Collins on Changing the Future of Medicine. See also these RNA society videos and the video representation from my 2013 poster session.
Attempts to compare UV-light induced mutations to what is currently known about the anti-entropic effects of the sun’s biological energy must eliminate the transfer of that energy as information. Not surprisingly, a new theory attempts to do that. See: Photon ‘afterglow’ could transmit information without transmitting energy.
The comments on this article attest to the fact that some theorists are willing to believe in virtually anything they are told until someone tells them something else. Then, only the biologically uniformed theorists will continue to believe in ridiculous untestable theories.
See also: Selective MicroRNA-Offset RNA Expression in Human Embryonic Stem Cells
Abstract excerpt: “…miRNA-offset RNAs (moRNAs) are similar in length to miRNAs…”
My comment: Use of the term moRNAs may prevent others from realizing the connection from the viral microRNA / nutrient-dependent microRNA balance to the microRNA/messenger RNA balance and nutrient-dependent RNA-mediated amino acid substitutions that differentiate the cell types of all genera via fixation of the substitutions in the context of the physiology of reproduction.
For examples of the link from viral microRNAs to amino acid substitutions, see: RNA Genes: Retroelements and Virally Retroposable microRNAs in Human Embryonic Stem Cells

achiral-glycine

Anti-entropic solar energy

“We have a group trying to model the mitochondrion” — Ulla Mattfolk

Trash pickup problem

Excerpt: “The PGAM5 protein would be regulated by an allosteric mechanism, in which its biological function would switch from activation of the PINK1/PARKIN pathway for removal of damaged mitochondria to the FUNDC1 pathway for removal of damaged mitochondria,” according to Hannink. “Peptides behave like drug molecules; any time you can identify a biological process that is regulated by a peptide, that peptide becomes a leading candidate in the search for small, drug-like molecules that will act the same way.”

My comment: Antagonist Ricardo Lara Ramirez mentioned that “You could call DNA´s arrangement high-dimensional if you consider the entire chromosome. This is how DNA is packed to form chromosomes.”

His comment and misplaced focus on DNA caused me to wrongly think the discussion might benefit from including RNA-mediated events in the context of atoms to ecosystems. But Ricardo Lara Ramirez and other theorists don’t seem to like my attempts to discuss RNA. I think that’s because nutrient-dependent pheromone-controlled feedback loops link RNA-mediated amino acid substitutions to chromatin loops and protein folding.

The differences in protein folding are the link to chromosomal rearrangements and biodiversity in my model. My model takes their ridiculous theories about “emergence” and places them into the context of biologically-based cause and effect.  See, for example:

All in the (bigger) family

Excerpt: “Jerome Hui of the Chinese University of Hong Kong found that in both insects and crustaceans, the same set of micro RNAs control expression of the genes for those enzymes.”

My comment: Antagonist Ricardo Lara Ramirez is familiar with the works by Jerome Hui. But they don’t seem to know that the anti-entropic energy of the sun links nutrient-dependent microRNAs  and viral microRNAs from entropic elasticity to cell type differentiation via RNA-mediated amino acid substitutions. If they knew that, they might be able to link the pathway from nutrigenomics to pharmacogenomics, which I have detailed, and what is known about cell type differentiation of all cells in all individuals of all genera via the physiology of their nutrient-dependent reproduction.

Instead, Ulla Mattfolk claims my works and blog posts like this one are mere inferences. See: Quantum physics, quantum biology, and quantum consciousness

If not for Joseph Kover, I would have nothing to do with theorists, like Ulla Mattfolk and Ricardo Lara Ramirez. They are two of the most biologically uniformed antagonists I have ever encountered. Only Matti Pitkanen is worse. He placed everything I’ve detailed in the context of RNA-mediated cell type differentiation into the context of his ridulous theory about the simultaneous emergence of hens and eggs.

Was ribosome the first self-replicator?

Excerpt: Can one tell whether it was pro-cell or bio-molecules that emerged first? It seems that all these structures could have emerged simultaneously. What emerged was dark matter and its emergence involved the emergence of all the others. Hens and eggs emerged simultaneously.”

My comment: Among the other discussants I first encountered via Ulla Mattfolk, only Joseph Kover has been helpful. I think he directed my attention to Near-Infrared Laser-Induced Structural Changes of Glycine·Water Complexes in an Ar Matrix, which among other things, helps with Untangling the quantum entanglement behind photosynthesis.  Now, Joseph Kover claims he is planning to write something and discuss details that he has not mentioned in Facebook discussions.

Great. That’s what I did when I published Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors (2012) and Nutrient-dependent/pheromone-controlled adaptive evolution: a model (2013).  I’ve spent more than $2000 in the past two years to establish the domains PerfumingtheMind.com and RNA-Mediated.com, where I have continued to encourage discussion.

Ricardo Lara Ramirez has on several occasions chided me because both domains are “deserted” and I have been banned from discussion groups, like Ulla Mattfolk’s — and several others, like the Society for Integrative and Comparative Biology (SICB) group.  If not for the fact that one of the SICB 2015 presenters, who went to school with Ricardo Lara Ramirez just confirmed what I claimed in my 2014 invited review on nutritional epigenetics, I would think that telling the truth about biologically-based cause and effect was of no use to theorists.

In my 2013 review, I wrote: “The small non-coding RNA molecules are called microRNAs (miRNAs). MiRNAs alter intercellular signaling by changing the balance between miRNAs and messenger RNA (mRNA) . The changes are linked to health and to pathology (Mori et al., 2014).” Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems.
Sorry, I used intercellular when I meant intracellular. Hopefully, the context makes that clear. Intercellular means “between the cells” and intracellular means “inside the cells”.

In January 2015, Jerome Hui reported that the same enzymes in both insects and crustaceans were linked by the same set of microRNAs , which control expression of the genes for those enzymes.

On March 17, 2015, I read this report: ‘Junk DNA’ Used To Sort Species
Excerpt: Non-coding RNAs such as microRNAs (miRNA) are now recognized as important regulators of gene expression. Now, a team of researchers led by Professor Jerome Hui from the Chinese University of Hong Kong has found another use for miRNA—to understand the evolutionary relationship between different species. They first compared non-coding sequences between human, chimpanzee, gorilla, orangutan, and macaque, and successfully recovered the evolutionary history of human and our close relative, showing that chimpanzees share the closest common ancestor with human, followed by gorilla, orangutan, and then macaque being the more distant relatives.
My comment: In the journal article, they claim “This study establishes a new approach for resolving animal species relationships, building markedly on ideas first noted in Field et al. [9], and suggests that the flanking sequences of miRNAs are under strong functional constraint after speciation events.”
Dobzhansky (1973) was the first to note 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” (p. 127).
In our 1996 Hormones and Behavior review, we placed the differences in the cell types of primates and other species into the context of RNA-mediated pheromone-controlled species-specific cell type differentiation, which is functional constrained after speciation by nutrient-dependent species-specific pheromones.
In my 2013 review, I noted that “…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 claim that their findings build “…markedly on ideas first noted in Field et al. [9]…” (2014) suggests they are 18-41 years behind the extant literature on RNA-mediated amino acid substitutions and cell type differentiation in all cells of all individuals of all genera, which occurs in the context of their biophysically constrained chemistry of nutrient-dependent protein folding.
The context of my attempt to discuss RNA-mediated cell type differentiation is this report: NASA Is Amazed By A Huge, Unknown, Energy Field. See also: Correctly modeling biological energy I doubt the ability of theorists to understand anything about biologically-based cause and effect until they learn that solar energy is the energy that fuels the nutient-dependent physiology of reproduction on this planet.
 
 

human-evolution

Mimicking claims and ignoring facts

Summary: Last week, researchers reported they had caught up to “Nature” despite their inability to link viral microRNAs and nutrient-dependent microRNAs from the nature of non-living viruses to the nature of cellular life and to cell type differentiation via RNA-mediated amino acid substitutions, metabolic networks, and genetic networks. Today, we see the “billions of years” claim, with no mention of the over-the-weekend re-evolution of the bacterial flagellum or 1.8 billion years of epistasis in bacteria at the bottom of the ocean.

Mimicking nature’s chemistry to solve global environmental problems

Excerpt: “Nature has evolved over billions of years to convert nitrogen from the atmosphere into fertilizer or to harness solar energy to split water into oxygen and protons and electrons,” he explains. “As chemists, we’re trying to catch up in order to do those transformations ourselves.”
My comment: Last week, researchers reported they had already caught up to “Nature” despite their inability to link viral microRNAs and nutrient-dependent microRNAs from the nature of non-living viruses to the nature of cellular life and to cell type differentiation via RNA-mediated amino acid substitutions, metabolic networks, and genetic networks. See: Chemists claim to have solved riddle of how life began on Earth
Again, we see the “billions of years” claim, but no information on the over-the-weekend re-evolution of the bacterial flagellum or 1.8 billion years of epistasis in bacteria at the bottom of the ocean.

On March 18, in discussion of Chemists claim to have solved riddle of how life began on Earth, I wrote:
Excerpt: “Virus-driven thermodynamic cycles of protein biosynthesis and degradation clearly link ecological variation from entropic elasticity to nutrient-dependent anti-entropic ecological adaptations and organism-level thermoregulation via the biophysically constrained physiology of reproduction, which enables changes in the microRNA/messenger RNA balance. The changes link amino acid substitutions to cell type differentiation in all cells of all individuals of all species.”
My comment: That fact has been confirmed across disciplines. The first indication of that fact came from science fiction novelist Greg Bear. See this book review: Substantial excerpt from a review published in NATURE, March 2, 2000.
In the 2003 sequel, he integrated the nutrient-dependent pheromone-controlled physiology of reproduction and communication. Arguably, the fact that an English major with no science background could predict the fall of neo-Darwinism may be an embarrassment to theorists. If not, it should be.
For example, how embarrassing is this? Nutrient-dependent / Pheromone-controlled adaptive evolution: (a mammalian model of thermodynamics and organism-level thermoregulation)
Jon Lieff just placed the 5.5 minute video representation (linked above) into the context of his question: How can small pieces of DNA and RNA demonstrate such intelligent behavior? As is typical of Lieff, he informs others about what is known about biologically-based cause and effect. He adds plenty of common sense.
Here’s the obvious answer to the question How can small pieces of DNA and RNA demonstrate such intelligent behavior? It involves the creation of a nutrient-dependent thermodynamically controlled system for protein biosynthesis and degradation. It includes amino acid substitutions that stabilize the organized genomes of all genera via RNA-mediated events. The RNA-mediated events link non-living viruses to cellular life and cell type differentiation / proliferation via the biophysically constrained chemistry of protein folding and physiology of reproduction.
But this is not “Nature” at work across billions of years. It is the anti-entropic epigenetic effect of the sun’s biological energy. See: Short-wavelength near-infrared spectra of sucrose, glucose, and fructose with respect to sugar concentration and temperature.

Abstract excerpt: “The major spectral effect of decreased temperature or increased sugar concentration was a decrease in absorbance at 960 nm and an increase in absorbance at 984 nm, interpreted as an increase in the degree of H bonding.”

My comment: Biologically uniformed science idiots may continue to believe in theories that link H bonding to mutations and evolution. For example, see: Mutation-Driven Evolution conclusion: “… genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world” (p. 199). That may be the “Nature” of the best explanation they can offer for “…the enormous amount of biodiversity in this world.” But those who continue to claim “Nature has evolved over billions of years…” should probably stop to think how that might be possible given everything known to serious scientists and science fiction novelists (in 2003) about virus-driven entropic elasticity and anti-entropic light-induced biologically-based cause and effect via glucose metabolism.
See also: Elusive inheritance: Transgenerational effects and epigenetic inheritance in human environmental disease
Excerpt: Demonstrating whether transgenerational epigenetic inheritance occurs in mammals will require detailed genetic, epigenetic, transcriptomic, and metabolic profiling of well-controlled animal models with well-documented pedigrees.

My comment: They injected microRNA’s, which alter the microRNA/messenger RNA balance. That balance is linked to metabolic networks and genetic networks in all genera from RNA-mediated cell type differentiation. They claim that more evidence is required to demonstrate whether transgenerational epigenetic inheritance occurs in mammals. Simply put, they might as well claim that more evidence is required to demonstrate whether transgenerational epigenetic inheritance occurs in mammals via Feedback loops [that] link odor and pheromone signaling with reproduction via epigenetic effects on gonadotropin releasing hormone. They appear to not know there is a model for that: Nutrient-dependent/pheromone-controlled adaptive evolution: a model.

The model links viral microRNAs and the nutrient-dependent microRNAs to a finely-tuned balance, which is required for increasing organismal complexity to arise in the context of the nutrient-dependent physiology of reproduction. The increasing organismal complexity of bacteria the re-evolve their flagella “over-the-weekend” in the context of nutrients linked from RNA-mediated amino acid substitutions to cell type differentiation in species from microbes to man via their pheromone-controlled physiology of reproduction, suggests that something is wrong with reports about “Nature” that claim it has evolved across billions of years.

terrarium-eco-system

Rejecting what is known about viral microRNAs and nutrient-dependent microRNAs

Of Cells and Limits

Leonard Hayflick has been unafraid to speak his mind, whether it is to upend a well-entrenched dogma or to challenge the federal government. At 86, he’s nowhere near retirement.

By Anna Azvolinsky | March 1, 2015

Excerpt:

The rejection letter came from Francis Peyton Rous who received the Nobel Prize a few years later for his discovery of chicken tumor viruses.

My comment:
My 2014 invited review of nutritional epigenetics detailed how differences in the microRNA/messenger RNA balance link viral microRNAs from ecological variation to ecological adaptations via the RNA-mediated differentiation of all cell types in all individuals of all species. It was returned without review.
The problem appears to be the clear link from viruses to RNA-mediated cell type differentiation via amino acid substitutions that stabilize DNA in the organized genomes of all species. That clear link led to the invitation to submit the review.
The invitation came after publication of  Nutrient-dependent/pheromone-controlled adaptive evolution: a model and a series of other previously published works that detail the molecular epigenetics of biophysically constrained RNA-mediated protein folding.
Many of my “peers” still seem to think that mutations lead to the evolution of biodiversity. They won’t consider the fact that viral microRNAS cause entropy or that nutrient-dependent microRNAs link entropic elasticity from DNA repair to the physiology of reproduction.
That anti-entropic fact links the metabolism of nutrients to species-specific pheromones that control the physiology of reproduction. The pheromones link RNA-mediated fixation of nutrient-dependent amino acid substitutions from metabolic networks to genetic networks in species from microbes to humans. See for examples in humans: Clinically Actionable Genotypes Among 10,000 Patients With Preemptive Pharmacogenomic Testing.
Examples from more than 14,000 patients now show what serious scientists have learned during the past two decades. What they have learned is exemplified in the honeybee model organism and many other model organisms.
In 2013, I wrote: “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, diseases of the X chromosome, learning and memory, as well as conditioned responses to sensory stimuli (Kohl, 2012).”
In his 2003 presentation to the American Philosophical Society, Greg Bear told others about ancient viruses in the human genome that link sexual recombination and pheromonal interaction in multicellular organisms. The organisms communicate with each other, which links what is currently known about physics, chemistry, and molecular epigenetics to species-wide epigenesis and to the obvious anti-entropic examples of epistasis via metabolic and genetic networks.
Unfortunately, more than a decade after Greg Bear presented the facts about biodiversity in two of his science fiction novels, the accuracy of his claims about viruses goes largely unnoticed. Honeybee colony collapse is noticed. But, despite the fact that facts are facts and the fact that facts about viral microRNAs and nutrient-dependent microRNAs have replaced theories, theorists prefer their ridiculous theories.
Perhaps honeybee colony collapse has nothing to do with their nutrient-dependent pheromone-controlled reproduction. Perhaps Greg Bear was wrong when he claimed that “Networks from beehives to brains solve problems through the exchange and the selective cancellation and modification of signals. Species and organisms in ecosystems live and die like signals in a network.”
Perhaps evolutionary theorists like Masatoshi Nei are correct and “…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world.” Mutation-Driven Evolution (p. 199).
Is there a model for that?

poster-from-jesse

Nutritional epigenetics, exercise, and immune system integrity

Anti-inflammatory mechanism of dieting and fasting revealed

Summary: Researchers have found that a compound produced by the body when dieting or fasting can block a part of the immune system involved in several inflammatory disorders such as type 2 diabetes, atherosclerosis, and Alzheimer’s disease.

My comment: For the obvious link from nutrition and exercise to reproduction and RNA-mediated transgenerational epigenetic effects on the morphological and behavioral phenotypes of all species that must “move” to find food or to find mates see: Chapter 5: “Epigenetic Modulation of Gene Expression by Exercise in “Nutrition, Exercise and Epigenetics: Ageing Interventions” Use the search inside feature to see what will be published in April, 2015

Excerpt: Among the highlights are chapter-length discussion of such topics as: how anti-inflammatory action of calorie restriction underlies the retardation of ageing and age-related diseases (Chapter 3); epigenetic modification of gene expression by exercise (Chapter 5); the role of functional foods and their bioactive components…

See also: Acute Exercise Remodels Promoter Methylation in Human Skeletal Muscle

Excerpt: “…the unifying trigger that orchestrates the genomic response to exercise is incompletely defined.”

Conclusion: Our finding that the patterns of DNA methylation change in differentiated nondividing somatic cells provides further evidence that the epigenetic marks across the genome are subject to more dynamic variations than previously appreciated.

My comment: In my model, RNA-directed DNA methylation and RNA-mediated amino acid substitutions link the anti-entropic effects of nutrient-dependent survival of individuals to the survival of species. Species adapt to ecological variation in the availability of food. Entropic plasticity is linked from the availability of food to the nutrient-dependent physiology of reproduction via the metabolism of nutrients to species-specific pheromones.

The link from viral microRNAs to entropy and from nutrient-dependent microRNAs to their anti-entropic effects on cell type differentiation in the context of the required entropic elasticity has been fully detailed. All examples from all model organisms attest to the fact that species arise in the context of nutrient-dependent pheromone-controlled reproduction. Other attempts to explain extant biodiversity fail to include what is currently known about physics, chemistry, and conserved molecular mechanisms that link epigenetic effects of the sun’s biological energy to cell type differentiation in plants and to the animals that eat the plants or that eat other animals to ensure their nutrient-dependent pheromone-controlled survival.

See also: An integrative analysis reveals coordinated reprogramming of the epigenome and the transcriptome in human skeletal muscle after training

Abstract excerpt: “A transcriptional network analysis revealed modules harboring distinct ontologies and, interestingly, the overall direction of the changes of methylation within each module was inversely correlated to expression changes. In conclusion, we show that highly consistent and associated modifications in methylation and expression, concordant with observed health-enhancing phenotypic adaptations, are induced by a physiological stimulus.”

My comment: RNA-directed DNA methylation is consistently linked to health-enhancing phenotypic adaptations via RNA-mediated amino acid substitutions. The epigenetically effected microRNA/messenger RNA balance is the determinant of alternative splicings that link the RNA-mediated substitutions to the stability of DNA. When viral microRNAs accumulate due to nutrient stress and/or social stress, they may lead to mutations that perturb protein folding and lead to the instability of DNA if the DNA is not repaired. This links the accumulation of viral microRNAs across the life history of humans to age-linked physiopathology.

For example, see: A molecular chaperone breaks the catalytic cycle that generates toxic Aβ oligomers  reported as: Molecular inhibitor breaks cycle that leads to Alzheimer’s

Excerpt: Alzheimer’s disease is one of a number of conditions caused by naturally occurring protein molecules folding into the wrong shape and then sticking together – or nucleating – with other proteins to create thin filamentous structures called amyloid fibrils. Proteins perform important functions in the body by folding into a particular shape, but sometimes they can misfold, potentially kick-starting this deadly process.

My comment: Thermodynamic cycles of protein biosynthesis and degradation are nutrient-dependent. Nutrient-stress and social stress are linked to perturbed protein folding via RNA-mediated events. The molecular inhibitor that breaks the cycle that leads to Alzheimer’s probably inhibits misfolding via the prevention of “heat shock.” That’s what some molecular chaperones do.

See: Emergency Alert in the Cell

Excerpt: “During the heat shock response, different stress proteins are synthesized. Their task is to prevent permanent damage to the organism.”

My comment: All of the above attests to what is currently known about how cell type differentiation occurs during life history transitions, and what leads to perturbed protein folding and physiopathology. Everything currently known about Epigenetic Modulation of Gene Expression by Exercise in “Nutrition, Exercise and Epigenetics: Ageing Interventions can be placed into the context of evolutionary theory by simply ignoring it.

If you ignore what’s currently known about physics, chemistry, and the conserved molecular mechanisms of nutrient-dependent RNA-directed DNA methylation and RNA-mediated amino acid substitutions that differentiate all cell types in all individuals of all species during their life history transitions, you will not be on the side of those who are Combating Evolution to Fight Disease.

Excerpt: “Another mechanism involves chaperones such as heat shock protein 90 (Hsp90), proteins that massage subideal (mutant) proteins into functional conformations but abandon their regular client proteins during heat and other stresses that destabilize proteins. This causes a stress-inducible release of phenotypic diversity, which may drive evolution (with phenotypes ultimately stabilized by subsequent genetic changes). Both of these molecular mechanisms of protein-based inheritance are major departures from the modern synthesis views of solely mutation-directed variation, solely genetic inheritance, and independence of the generation of variation from environmental conditions.”

My comment: If you are not on the same side as those who are Combating Evolution to Fight Disease, you may wish to join those who believe in the pseudoscientific nonsense about Mutation-Driven Evolution.

Alternatively, you can wait until the combat ends and join the winners simply by claiming that you knew all along that ecological adaptation was nutrient-dependent and pheromone-controlled and that the theorists were simply biologically uninformed science idiots who caused the suffering and death of millions.

See also: Evolution evolves: physiology returns to centre stage (with my emphasis)

Conclusions: “The wide-ranging set of articles published in this issue reveal a major challenge both for the physiological sciences and for evolutionary biology. As the integration between the two proceeds, neither can remain unchanged. Evolutionary theory requires extension or even replacement, while physiological science needs to address the exciting possibilities opened up for the future. We hope that our article, and those published here, will enable both disciplines to respond effectively to that challenge.”
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

Pattern recognition and conserved receptors (TAARs)

Olfactory Receptor Patterning in a Higher Primate

Excerpt: We found that TAARs are also expressed in the macaque OE, suggesting that these receptors may also function as chemosensory receptors in the human nose.
My comment: The article links the senior author’s prior works from nutrient-dependent RNA-mediated events and the de novo Creation of odorant receptor (OR) genes to her 2005 co-authored work on the hormone-organized control of these RNA-mediated events:

Feedback loops link odor and pheromone signaling with reproduction.

Excerpt:”At least 10,000 neurons in 26 different brain areas appear to transmit signals directly to GnRH neurons. Among these are areas involved in odor and pheromone processing, sexual behavior, arousal, reward, and other functions. This suggests that GnRH neurons are poised to modulate reproductive physiology and behavior in accordance with the overall state of the animal.”
Nobel Laureate, Linda Buck has now linked the experience-dependent de novo Creation of another class of OR genes to primate behavior. But her most recent article does not mention the RNA-mediated events that are required to link nutrient uptake associated with food odors to amino acid substitutions that differentiate cell types in all the cells of all different species. Given what is known about these RNA-mediated events, I hope that others will make their refutations of evolutionary theory clearer.
Perhaps serious scientists don’t even consider the evolutionary theorist’s claims because the theorists have not described any biologically-based evolutionary events. Although that means their ridiculous claims can be compared to what is known, there may be no need for serious scientists to address the biologically-based RNA-mediated events that link nutrient-dependent amino acid substitutions to cell type differentiation in all cells of all individuals via conserved molecular mechanisms in species from microbes to man. Unless they are attempting to discuss biologically-based facts with a theorist, there isn’t much need to tell the theorist that evolutionary theory was invented and defined by population geneticists.
Sooner or later, the theorists will learn that conserved molecular mechanisms are responsible for the nutrient-dependent microRNA/messenger RNA-mediated events that differentiate cell types via amino acid substitutions. The differentiation of all other cell types appears to begin with food odor-induced epigenetic effects on the de novo Creation of olfactory receptor genes. However, unless a serious scientist like Linda Buck comments on the obvious refutations of theories touted by those who try to link mutations and natural selection to the evolution of biodiversity, the evolutionary theorists may not realize that the only evidence of biodiversity links ecological variation to ecological adaptations that occur in the absence of mutations and natural selection.
For example, in my 2013 review I noted that:

“The recently detailed mouse model (Li et al., 2013) builds on what is known about olfactory/pheromonal communication in species from microbes to man and incorporates works from mammals that elucidate the molecular mechanisms that are clearly involved. Sex-dependent production of a mouse ‘chemosignal’ with incentive salience appears to have arisen de novo via coincident adaptive evolution that involves an obvious two-step synergy between commensal bacteria and a sex-dependent liver enzyme that metabolizes the nutrient chemical choline.

The result of this synergy is (1) a liver enzyme that oxidizes trimethylamine to (2) an odor that causes (3) species-specific behaviors. Thus, the complex systems that biology required to get from nutrient acquisition and nutrient metabolism to species-specific odor-controlled behavior is exemplified by adaptive evolution of an attractive odor to mice that repels rats (see for review Li et al., 2013).

The mouse odor also repels humans. High excretion rates of trimethylamine-associated odor in humans cause ‘fish odor syndrome’. The aversive body odor has been attributed to a mutation (Dolphin, Janmohamed, Smith, Shephard, & Phillips, 1997). This attribution is not consistent with the portrayal of synergy in the mouse model, which enables both the production of the odor and the response to the odor.

This synergy requires at least two things to happen simultaneously: for example, (1) natural selection for nutrient chemicals and (2) sexual selection for odor production. Sexual selection for nutrient-dependent odor production is not likely to be achieved via one mutation involved in nutrient acquisition and another mutation that is involved in odor production because two mutations are not likely to simultaneously occur.”

We now can read about findings in Horowitz et al (2014) that “…raise the possibility that TAARs have been evolutionarily conserved due to a specialized ability to elicit innate responses, such as avoidance. The functional significance of these responses could vary among animals. For example, aversive responses of mice to 2-beta-phenylethylamine, a mouse TAAR4 ligand present in some carnivore urines, could aid in predator avoidance (Ferrero et al., 2011; Dewan et al., 2013). In contrast, the activation of human TAAR5 by spoiled fish might discourage the ingestion of foods that could harbor pathogenic microorganisms that pose a danger to health.”
In my model, the fish odor links sex differences in species-specific pheromone production from mice to primates via differences in the production of dehydroepiandrosterone (DHEA) in primates. DHEA is the most abundantly produced steroid hormone. The fact that Testosterone increases circulating dehydroepiandrosterone sulfate levels in the male rhesus macaque links its metabolism to sexually dimorphic species-specific ratios of androsterone and etiocholanolone, which were reported to vary with sexual orientation in human males.
Excerpt: “The finding that DHEA/S differs dramatically between males and females is highly consistent and is maintained throughout the lifespan in both humans and rhesus macaques (7, 20–22), but to date no theories as to the mechanism of this difference have been adequately investigated.”
My comment: I have suggested that the androsterone/etiocholanolone ratio is integrated into a blend of sex specific and individual specific indicators of nutrient-dependent reproductive fitness based on links from nutrient-stress and social stress that predictably might be manifested in the testosterone-dependent pheromone-signature of human males and females — along with other indicators of reproductive fitness like those associated with amine-like odors of chemicals called copulins in rhesus macaques. TAARs in the human nose appear to complete the model,  which appears to solve “… the “binding problem” of sexual attraction. By that I mean the problem of why all the different features of men or women (visual appearance and feel of face, body, and genitals; voice quality, smell; personality and behavior, etc.) attract people as a more or less coherent package representing one sex, rather than as an arbitrary collage of male and female characteristics. If all these characteristics come to be attractive because they were experienced in association with a male- or female-specific pheromone, then they will naturally go together even in the absence of complex genetically coded instructions.” (LeVay, 2011). See also: D’Scent of Man: A Comparative Survey of Primate Chemosignaling in Relation to Sex.
The latest from Nobel Laureate, Linda Buck, continues to support extension of what is known about nutrient-dependent RNA-mediated events from the pheromone-controlled reproduction of microbes to the nutrient-dependent pheromone-controlled behavioral development of man. Note, I did not claim that pheromones control human behavior or that food odors control human behavior because they obviously do not. If they did, we would always act like other primates or other animals in which Feedback loops link odor and pheromone signaling with reproduction.
However, the fact that most of us do not always act like other animals says nothing about the epigenetic effects of food odors and human pheromones on the hormones that affect our behavior. It would be odd if our species was the only one in which behavior was not conditioned to occur in the context of odor-induced de novo Creation of OR genes that link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to elephants via RNA-mediated events and species specific pheromones that control the nutrient-dependent physiology of reproduction. Besides, there’s no model for differences in the molecular epigenetics of species diversity, only for the similarities.

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)