Finding odor and taste receptors everywhere

Bitter taste receptor agonists elicit G-protein-dependent negative inotropy in the murine heart

was published in October 2014 and reported in May 2015 as:

Researchers find bitter taste receptors on human hearts


“While the underlying physiology behind this phenomenon remains unclear, this is now a major area of ongoing investigation.”

For a historical perspective on this major area of ongoing investigation, see also: From ion channel to organismic phenotype: An example of integrative translational research into cardiac electromechanics (2013) and Systems Biology: An Approach (2010)
Excerpt (from 2010):

There is no basis for supposing that we can always correctly infer the existence of particular DNA sequences from observations based on the phenotype because the relations between genotypes and phenotypes are massively multifactorial (Figure 3). In cross-species cloning, for example, cytoplasmic networks can even influence phenotypes…

My comment: Experimental evidence of RNA-mediated thermodynamic cycles of protein biosynthesis and degradation continues to link the biophysically constrained nutrient-dependent de novo creation of odor and taste receptors to RNA-mediated cell type differentiation of all cells in all individuals of all genera via amino acid substitutions. Fixation of the amino acid substitutions occurs via the physiology of reproduction.  If odor receptors were not fixed in the cell types of human heart tissue there would be no link to their nutrient-dependent receptor-mediated fixation in any other tissue.  Instead, it is now perfectly clear to some serious scientists that:

Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans (Keller et al., 2007; Kohl, 2007; Villarreal, 2009; Vosshall, Wong, & Axel, 2000). — Kohl (2012)

Claims that “…the underlying physiology behind this phenomenon remains unclear…” suggest that other scientists have not yet considered the overwhelming amount of experimental evidence that links amino acid sensing to RNA-mediated amino acid substitutions and cell type differentiation. See, for example: Making sense of amino acid sensing

…cells residing in bodily tissues are normally bathed in nutrients, including more than one mTORC1-activating amino acid.


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.

My comment: mTORC1 links the immune system and self vs. non-self recognition via the systems complexity, which has historically been placed into the context of ridiculous theories about the evolution of biodiversity. Biodiversity is obviously nutrient-dependent and pheromone-controlled in species from microbes to man.  See Mutation-Driven Evolution, and compare the theory to the facts about amino acid substitutions and cell type differentiation in Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
Evolutionary theorists have no model. They know that the lack of a model is their biggest problem, but they are still trying to convince others that their ridiculous theories are reasonable. See: Beyond Genetic Evolution. A Conversation With Eva Jablonka.

The desperate attempt by Wilson and Jablonka to make it appear that epigenetics can be considered the “second dimension of evolution” flies in the face of everything known to serious scientists about how the epigenetic landscape is linked to the physical landscape of DNA in the organized genomes of species from microbes to man.
See my comment: Sabatini’s group appears to have just linked “Nutrient-Sensing Mechanisms across Evolution” 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 “SHMT2 drives glioma cell survival in ischaemia but imposes a dependence on glycine clearance.”
See also Nutrient-dependent RNA interference:

Feedback loops link the nutrient-dependent physiology of reproduction to chromatin loops in the context of nutrient-dependent pheromone-controlled epigenetically-effected biodiversity.RNA-mediated.com See also: rnasociety.org

My comment: The links from the feedback loops to the chromatin loops are known to serious scientists and must be considered across disciplines.
See for example: Mars astronauts risk brain damage from cosmic rays, say scientists

“It could develop into performance-based decrements and elevated anxiety and affect the ability to problem solve. These effects are likely to be subtle, however, and would not preclude our efforts to plan future manned deep space missions.”

My comment: If not for the anti-entropic epigenetic effects of nutrient-dependent microRNAs, virus driven entropic elasticity would lead to the extinction of life on this planet via viral microRNAs that perturb the biophysically constrained chemistry of nutrient-dependent RNA-mediated cell type differentiation. Claims that epigenetics is the second dimension of evolution are ridiculous in the context of what is known about biologically-based cause and effect.
A 3D Map of the Human Genome at Kilobase Resolution Reveals Principles of Chromatin Looping

As our understanding of the physical connections between DNA loci continues to improve, our understanding of the relationships between these broader phenomena will deepen.

Inching toward the 3D genome

The metaphors for DNA keep multiplying. It is a string of code, a spiral staircase, and, now, something very like origami. Just as folding a flat sheet of paper can transform it into a crane or lotus flower, researchers have come to realize that a complex pattern of loops and folds helps transform our genome into something meaningful. The twists and turns bring particular genes into close contact with distant stretches of DNA that regulate those genes’ activity, spurring the gene expression that makes a bone, muscle, or brain cell—or fuels a cancer.


NIH’s 4D Nucleome program aims to provide that. This 5-year, $24-million-a-year effort, announced in July 2014, will improve the existing techniques and, possibly, come up with new ones. It’s called 4D because the nucleome structure changes as cells age, differentiate, and divide, and researchers want to understand how and why. “The object is to make these techniques widely available,” says Rafael Casellas, a molecular biologist at the National Institute of Arthritis and Musculoskeletal and Skin Diseases in Bethesda, Maryland. They are sorely needed, Dekker says. Just as origami paper comes to life only when folded, he says, “nothing in our genome makes sense except in 3D.”

My comment to the Science Magazine site:
Re: “…the nucleome structure changes as cells age, differentiate, and divide, and researchers want to understand how and why.”
Cell type differentiation is nutrient-dependent. RNA-directed DNA methylation links RNA-mediated amino acid substitutions to cell type differentiation via protein folding during life history transitions. Amino acid substitutions stabilize protein folding; mutations perturb it, during nutrient-dependent theromodynamic cycles of protein biosynthesis and degradation.
Life is physics and chemistry and communication
The metabolism of nutrients links metabolic networks to genetic networks via species-specific pheromones that control the physiology of reproduction. Simply put, pheromones link nutrient-dependent life via physics, chemistry, and the conserved molecular mechanisms of communication in species from microbes to man.
Until nutrient-dependent protein folding is linked via the conserved molecular mechanisms of amino acid substitutions and pheromone-controlled DNA stability in organized genomes, which links the epigenetic landscape to the physical landscape of DNA, researchers must take a piece-meal approach to integrating the requirements for life and successful life history transitions — despite the fact that life history transitions have been detailed in the context of the honeybee model organism. See: Honey bees as a model for understanding mechanisms of life history transitions
See: Nutrient-Sensing Mechanisms across Evolution

Are different amino acids differentially important in the cytosol versus lysosome? The lysosome is enriched for basic amino acids, hinting that these amino acids may matter more than others in sensing that initiates from this organelle (Harms et al., 1981), which is consistent with the specific defect of cells lacking SLC38A9 in sensing arginine (Wang et al., 2015). Finally, how well conserved the sensors are between organisms will hint at how different or similar the amino acid and nutrient inputs are that drive mTORC1/TORC1 signaling in diverse organisms.

My comment: Theorists who tout epigenetic as the “second dimension of evolution” seem to have failed to realize that epigenetic effects link ecological variation to cell type differentiation and ecological adaptation via the conserved molecular mechanisms of biophysically constrained protein folding in all genera. If they wish to claim that evolution exemplifies ecological adaptation, they must do so without mention of the experimental evidence that links the de novo creation of amino acids to amino acid substitutions that differentiate all cell types of all individuals of all species and ignore claims that “nothing in our genome makes sense except in 3D” and facts that link RNA-mediated protein folding to the NIH’s 4D nucleome program via facts about how the nucleome structure changes as cells age, differentiate, and divide.
For details on how the nucleome changes during life history transitions, see the molecular genetics section in: From Fertilization to Adult Sexual Behavior. Remember “nothing in our genome makes sense except in 3D.” Try to get an evolutionary theorist to make sense of neo-Darwinism, and you will find your way back to Dobzhansky (1973) Nothing in Biology Makes Any Sense Except in the Light of Evolution.  He noted 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). That’s why others are Combating Evolution to Fight Disease.
Intelligent researchers know that mutations cause disease, and they are trying to be heard at the same time theorists claim that Mutation-driven evolution makes sense, and that epigenetics is the second dimension of evolution. The theorists have never made sense of how ecological variation is linked to ecological adaptations.
See for comparison my invited review of nutritional epigenetics: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems. No one claims that an atoms to ecosystems approach does not make sense. Evolutionary theorists simply ignore that fact.

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