5th-6th Sept 2018 Dublin, Ireland

Ecological adaptations vs the randomness of evolution (3)

Summary: Fifty years later, only theorists and other pseudoscientists have failed to recognize the facts that link experimental evidence of differences in the energy of photons to the proton motive force, which links the potential of hydrogen (pH) to biophysically constrained viral latency and all biodiversity on Earth. In that context, Carl Zimmer serves as an important example of human idiocy each time he makes claims about evolution.
Serious scientists will meet during Schrödinger at 75 – The Future of Biology – September 2018 to discuss the overwhelming amount of human idiocy exemplified in the works of theorists who failed to learn that life is “All about that base.”
Without the quantized energy-dependent creation of the base pairs, viral latency could not be biophysically constrained and entropy would be used to explain the evolution of biodiversity manifested in sympatric speciation.
See for comparison: The costs of living at the edge: Seasonal stress in wild savanna-dwelling chimpanzees

Adaptations associated with shifting from a predominately forested habitat to a more open environment are considered a crucial step in hominin evolution.

The adaptations are food energy-dependent and biophysically constrained by the pheromone-controlled physiology of reproduction in species from microbes to humans. For example, higher levels of dehydroepiandrosterone in humans are an adaptation.
See:  Dehydroepiandrosterone – is the fountain of youth drying out?

…humans are unique in having adrenals that secrete large amounts of the prohormone, dehydroepiandrosterone (DHEA) and its sulfate, DHEA-S, into the bloodstream of males and females. Even non-human primates produce only ~10% of the DHEA found in humans

Carl Zimmer places everything known about how ecological variation must be linked to energy-dependent ecological adaptations into the context of human evolution.
See: Hints of Human Evolution in Chimpanzees That Endure a Savanna’s Heat

Millions of years ago, our apelike ancestors gradually moved from woodlands to savannas and began walking upright at some point. The Fongoli chimpanzees demonstrate just how difficult that transition would have been — and how that challenge may have driven some major changes in our evolution, from evolving sweat glands to losing fur and walking upright.

Before she graduated from her medical technologist course (circa 2014), I mentioned to Misty ______ the importance of  β-lactamase testing to understanding how the energy-dependent creation of microRNAs would soon be linked to all biophysically constrained biodiversity on Earth via antibiotic susceptibility testing in the hospital medical laboratory.
Shared strategies for β-lactam catabolism in the soil microbiome

A hydrolase from the put operon was found to degrade in vitro benzylpenicilloic acid, the β-lactamase penicillin product.

This clearly exemplifies how the virus-driven degradation of messenger RNA in β-lactamase positive organisms is linked to antibiotic resistance via what all serious scientists know about the molecular mechanisms of energy-dependent cell type differentiation.
The findings were reported in the ridiculous context of claims about How Bacteria Eat Penicillin

…some of the bacteria could, in fact, eat the drugs… As it turned out, they were everywhere. He also found examples of the phenomenon in the scientific literature going back to the 1960s.

In 1964, McEwen et al, linked the creation of the sun’s anti-entropic virucidal energy from Schrödinger’s claims in What is Life? (1944) to the creation of ATP and the creation of RNA. Now, others like McEwen know that RNA interference biophysically constrains viral latency.
In 1968, Frohlich speculated that the highly ordered storage of quantized energy in species from microbes to humans linked hydrogen-atom transfer to the functional structure of cell membranes via the hydrogen bonds of molecules, or other dipolar constituents, which he linked to the shared energy supply that biophysically constrains life.
Fifty years later, only theorists and other pseudoscientists have failed to recognize the facts that link experimental evidence of differences in the energy of photons to the proton motive force, which links the potential of hydrogen (pH) to biophysically constrained viral latency and all biodiversity on Earth. In that context, Carl Zimmer serves as an important example of human idiocy each time he makes claims about evolution.
See also: UTX-mediated enhancer and chromatin remodeling suppresses myeloid leukemogenesis through noncatalytic inverse regulation of ETS and GATA programs

By integrating proteomic and genomic analyses, we link these changes to UTX regulation of ATP-dependent chromatin remodeling, coordination of the COMPASS complex and enhanced pioneering activity of ETS factors during evolution to AML.

They linked the anti-entropic virucidal energy of sunlight from the creation of ATP to chromatin remodeling during the evolution of pathology, which all serious scientists know is biophysically constrained by the physiology of food energy-dependent pheromone-controlled reproduction.
See: [Pheromonal regulation of genetic processes: research on the house mouse (Mus musculus L.)] (1994)

A study of the influence of pheromone stressor(s) on proliferating germ and somatic cells was performed on laboratory lines of house mouse in the context of the physiological hypothesis of mutation process, proposed by M.E. Lobashev in 1947. Data from experiments are presented, and results obtained during last 10-15 years are discussed. The adaptive role of cytogenetic and other observed pheromonal effects is considered. The possible existence of interorganism systems of genetic regulation is discussed, the search for and study of which may help in more complete understanding of the regularities of functioning of genetic material.

The interorganism systems of genetic regulation have since been placed into the context of sympatric speciation by all serious scientists.
See: Direct estimation of mutations in great apes reveals significant recent human slowdown in the yearly mutation rate
See also: Analysis of 6,515 exomes reveals the recent origin of most human protein-coding variants


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.