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Attacking Young Earth Creationists

‘Residual diversity estimates’ do not correct for sampling bias in palaeodiversity data
Abstract excerpt:

Evolutionary dynamics such as speciation are inherently a phylogenetic process, and only an explicitly phylogenetic approach will correctly model this process.

Reported as: Flawed analysis casts doubt on years of evolutionary research

The method assumes that variations in the number of different fossils at any given time are a reflection of how much rock was available. It has been used in more than 150 published research papers since it was first used in 2007.

For comparison: No assumptions about the fossil record are include in more that 54,000 published articles that link energy-dependent changes in the microRNA/messenger RNA balance to all biodiversity via the physiology of reproduction in all living genera.
See: microRNA

See also:
Published on 3 May 2016

Abstract:

Olfaction and the innate immune system link energy as information from the epigenetic landscape to the physical landscape of supercoiled DNA. The sun’s biological energy is the source of the information that links angstroms to ecosystems via physics, chemistry, and molecular epigenetics.

RNA-mediated protein folding chemistry and amino acid substitutions link the anti-entropic quantized energy of sunlight from the virucidal effects of ultraviolet (UV) light to healthy longevity via biophysically-constrained energy-dependent hydrogen-atom transfer in DNA base pairs in solution and cell type differentiation.

Biomarkers link energy-dependent differences in base pairs and amino acid substitutions to biosignatures across the healthy life span. RNA-mediated amino acid substitutions also reveal the increasing complexity of interactions among cell types as pathology progresses. For comparison, successful reproduction links energy from supercoiled DNA to protection of all organized genomes from virus-driven energy theft and pathology.

This model links the sun’s biological energy from top-down causation in microbes to the most recent model of bottom-up gene activation and cell type differentiation in vertebrates. Citations to extant literature provide examples of what is currently known about how ecological variation leads to biophysically constrained cell type differentiation in the context of nutritional epigenetics and Precision Medicine, which clearly link metabolic networks and genetic networks to pharmacogenomics.

See for comparison: Published on 26 Aug 2016

Description:

On July 11th 2002, then-Representative Mike Pence testified before the House of Representatives that public schools should teach the theory of evolution as if it were only one of multiple hypotheses regarding the origins of species. Now that Trump the Chump has chosen Pence the Dense as his vice presidential running mate, I felt obliged to address now-Governor Pence’s willful ignorance and deliberate misrepresentation of evolution.


He claims there is no other theory, but he also ignores publication of my model on June 14, 2013 for comparison to the textbook misrepresentations published in Mutation-driven evolution on the same day.
Similarly, in his Criticisms of the nutrient-dependent pheromone-controlled evolutionary model,  Andrew Jones cites Mutation-driven evolution, but does not provide an alternative model of biologically-based cause and effect.
Excerpt:

Based on his writings, both published and unpublished, James Kohl presents an unsupported challenge to modern evolutionary theory and misrepresentations of established scientific terms and others’ research. It was a mistake to let such a sloppy review through to be published. Note: I concluded “…the model represented here is consistent with what is known about the epigenetic effects of ecologically important nutrients and pheromones on the adaptively evolved behavior of species from microbes to man. Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.

My comment: There is still no other model for comparison, and neo-Darwinian theory has been invalidated by all experimental evidence of biologically-based cause and effect. At every level of examination, serious scientists have linked energy-dependent changes from angstroms to ecosystems without the pseudoscientific nonsense about mutations and natural selection or evolution.
For comparison, this blog site focuses on mathematical models of observed phylogenetic differences. Reason Advocates.
If I were as biologically uninformed as this fool is, I would not have a blog site to advertise my ignorance via attacks on creationism.
He would only need to read one published work before he was forced to revise his ridiculous claims.
See: The phylogenetic utility and functional constraint of microRNA flanking sequences which was reported in advance as: All in the (bigger) family.
My comment:

The 2015 Society for Integrative and Comparative Biology (SICB) presenters may not recognize how much progress has been made since the 2013 ecological epigenetics symposium. For example, since then authors claimed “…ctenophore neural systems, and possibly muscle specification, evolved independently from those in other animals.” http://dx.doi.org/10.1038/nature13400

Six months later, other authors traced signaling factors found in vertebrates to the origin of nerve cell centralization via the diffuse nerve net of animals like the sea anemone. http://dx.doi.org/10.1038/ncomms6536 That fact suggests ecological variation is linked to ecological adaptations in morphological and behavioral phenotypes via signaling protein concentrations that differentiate various cell types in body axes and the central nervous system.

Links across species from the epigenetic landscape to the physical landscape of DNA in organized genomes appear to have their origins in the conserved molecular mechanisms of  RNA-directed DNA methylation and RNA-mediated protein folding. Two weeks after the publication that refuted ideas about independently evolved neural systems or muscle specification — and perhaps refuted the independent evolution of anything else, SICB presenters linked crustaceans to insects.

Apparently, they’ve learned that the same set of microRNAs controls expression of the genes for rate-limiting enzymes that control the hormone production of different hormones in insects and crustaceans.

Why were they left with  any questions about how crustaceans and insects could all be part of one big family? They linked RNA-mediated cell type differentiation to what we described in our section on molecular epigenetics in our 1996 Hormones and Behavior review. From Fertilization to Adult Sexual Behavior http://www.hawaii.edu/PCSS/biblio/articles/1961to1999/1996-from-fertilization.html

The report: Flawed analysis casts doubt on years of evolutionary research can be compared to what all serious scientists have claimed since 1964 or even earlier.
See for example: Biology, molecular and organismic

The notion has gained some currency that the only worthwhile biology is molecular biology. All else is “bird watching” or “butterfly collecting.” Bird watching and butterfly collecting are occupations manifestly unworthy of serious scientists! I have heard a man whose official title happens to be Professor of Zoology declare to an assembly of his colleagues that “a good man cannot teach zoology. A good man can teach, of course, only molecular biology.

Such pronunciamentos can be dismissed as merely ridiculous. They are, however, caricatures of opinions entertained by some intelligent and reasonable people, whose views deserve an honest and careful consideration and analysis. Science must cope with new problems that arise and devise new approaches to old problems. Some lines of research become less profitable and less exciting and others more so.
My comment: Flawed analyses during years of “evolutionary research” attest to the fact that there is no such thing as “evolutionary research” and no such thing as evolutionary biology. Clearly, as Dobzhansky claimed in 1964, “…the only worthwhile biology is molecular biology.” Molecular biologists have since linked energy-dependent changes from angstroms to ecosystems in all genera.
Isn’t it past time for evolutionary theorists to admit that millions of lives have been lost due to pseudoscientific nonsense and billions of dollars have been spent on nothing but ridiculous claims about the emergence of life and the evolution of all biodiversity?

See also: New trends in evolutionary biology: biological, philosophical and social science perspectives

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Nutrient-dependent pheromone-controlled autophagy (2)

See also: Nutrient-dependent pheromone-controlled autophagy

Autophagy: cellular and molecular mechanisms (2010)

Conclusion:

… autophagy has emerged as a new and potent modulator of disease progression that is both scientifically intriguing and clinically relevant.

My comment: Autophagy is energy-dependent and linked to supercoiled DNA by epigenetic effects on the innate immune system, which are linked to the physiology of energy-dependent reproduction. If you think that the innate immune system automagically “emerged,” you might also think that autophagy has automagically emerged as the only known link from the epigenetic landscape to the physical landscape of supercoiled DNA in all living genera. Emergence and evolution are terms that theoretical physicists and neo-Darwinian theorists use to link what they don’t know anything about to fertilization and adult behavior.
See for comparison: From Fertilization to Adult Sexual Behavior
Concluding sentence:

We see the primary contribution of this discourse, not to give answers but rather to broaden the scope of investigation. It would be helpful if some other investigators would similarly shed more light on a microanalysis of social-environmental factors impacting on sexual development.

My comment: Nutrient stress and social stress have repeatedly been linked to all pathology via their effects on hormones that affect behavior. Suddenly, 20 years after we published our review of epigenetic effects on RNA-mediated hormone-organized and hormone-activated behavior, RNA-mediated “… autophagy has emerged as a new and potent modulator of disease progression that is both scientifically intriguing and clinically relevant.”
What makes autophagy more relevant now than it was when Dobzhansky (1973) linked it from RNA-mediated amino acid substitutions to all biodiversity in Nothing in Biology Makes Any Sense Except in the Light of Evolution
Excerpt:

For example, 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).”

See also: Non-coding portions of genome are found to play role in cancer
Excerpt:

We now have an innovative way of destroying RNA targets inside live cells and assessing whether a tumor is dependent on them for survival,” says Spector.

My comment: Virus-driven energy theft has always been an innovative way to cause pathology in all cell types of all living genera. Biophysically constraining the virus-driven pathology has always been the key to healthy longevity and the survival of all species.
See: Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution
Author’s comment:

The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.

My comment: The authors responded to my comment, which was removed. It is still available here.

See also: “Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution”

The idea of biophysical constraints seems antithetical to the idea of nature somehow selecting mutations that cause amino acid substitutions. However, I am not a biophysicist or evolutionary theorist.

The problem may be my focus on nutrient-dependent receptor-mediated amino acid substitutions in species from bacteria to humans (non-viral organisms). Since I am not a virologist or physicist, I’m not sure that the laws of physics apply to viruses and their replication.

If they do, natural selection for random mutations is not likely to result in amino acid substitutions because the thermodynamics of changes in organism-level thermoregulation preclude such randomness. Stability of protein biosynthesis and degradation that probably depends on protein folding must somehow be controlled. Besides, I don’t know how random mutations in viruses could be naturally selected for inclusion in the human virome (or in the virome of any organism capable of thermoregulating its thermodynamic intercellular signaling).

If the Second Law of Thermodynamics does not apply to viruses, which means the chemical bonds that enable the amino acid substitutions can form at random and somehow be naturally selected, the details of biophysical constraints in this article seems out of place, since I do not think in terms of constrained random mutations and natural selection in mutation-driven evolution.

Hopefully, someone with a background in biophysics will address my confusion in case others are confused. In addition, I wonder if the consequences of understanding the evolutionary mechanisms that govern viruses extend to consequences important to understanding the evolution of species from bacteria to humans via constrained random mutations and natural selection?

See: ‘Game-changing’ immunotherapy doubles head and neck cancer survival

The survival benefit was more pronounced in patients whose tumours had tested positive for human papillomavirus (HPV). These patients survived an average of 9.1 months with nivolumab and 4.4 months with chemotherapy.

My comment: Testing positive for virus-driven energy theft in the context of pathology is not a game changer. It is an admission of negligence on the part of others who should have changed the game sooner. Game-changing immunotherapy links what is known about physics and chemistry to biology via molecular epigenetics. That fact should help all serious scientists who are still waiting to claim that all pathology is caused by viruses.
But the game change could have occurred much earlier so that more winners than losers would have survived during the past two decades. Long before the advent of the “game-changing” therapy, all pathology, includes the pathological behaviors that develop throughout life could have been linked to the pathological behaviors that pseudoscientists have been trained to exhibit in their claims about emergence and evolution.
For comparison, early detection of the virus that causes the pathology in a species-specific tissue type will be the obvious link to effective treatment and cures. Unfortunately, there is not much funding for preventative medicine and even less funding is dedicated to finding how specific viruses such as the Zika virus cause craniofacial deformities. Similarly, changes in the development of the brain are caused by virus-driven genomic entropy in species that have not yet become extinct.
Some researchers still seem to think that we can save other species from virus-driven genomic entropy and extinction despite the fact that no experimental evidence of biologically-based cause and effect suggests we can save humanity from a similar fate. All experimental evidence links what is know about behavioral development in one species to behavioral development in all species.
Behavioral development is nutrient-dependent and pheromone-controlled via the physiology of reproduction in all living genera. That fact and the claims of all serious scientists tells us approximately how far from extinction we may be. Not far enough.

See for another example of that fact: Behavioral development in embryonic and early juvenile cuttlefish (Sepia officinalis)

Abstract excerpt:

S. officinalis is well-suited to addressing questions of behavioral ontogeny. As embryos, they can perceive and learn from their environment and experience no direct parental care. A marked progression in learning and behavior is observed during late embryonic and early juvenile development.

From Fertilization to Adult Sexual Behavior was cited in Organizational and activational effects of hormones on insect behavior (2000) and cited in Nutrient-dependent/pheromone-controlled adaptive evolution: a model

Excerpt:

Until recently, there was no direct evidence that human pheromones caused a definite behavior. In contrast, there was sufficient evidence to extend the mammalian model for epigenetic effects of nutrients and pheromones on GnRH and on hormonal organization and activation of behavior (Diamond et al., 1996) to invertebrates (Elekonich & Robinson, 2000). In that context, ‘From fertilization to adult sexual behavior’ (Diamond et al., 1996, p. 333) was extended to invertebrates with details from ‘egg to adult’ (Elekonich & Robinson, 2000, p. 1514).

My comment: How soon will the virus-driven energy theft that has been linked to the extinction of marine invertebrates and vertebrates be linked to the extinction of all terrestrial invertebrates and vertebrates?

See for example:  Past 5,000 years prolific for changes to human genome

Of 1.15 million single-nucleotide variants found among more than 15,000 protein-encoding genes, 73% in arose the past 5,000 years, the researchers report. 164,688 of the variants — roughly 14% — were potentially harmful, and of those, 86% arose in the past 5,000 years. More broadly, the results suggest that humans are carrying around larger numbers of deleterious mutations than they did a few thousand years ago. But this doesn’t mean that humans now are more susceptible to disease, says Akey.

My comment: Yes it does mean that humans now are more susceptible to disease. Only a theorist or someone who was equally biologically uninformed would make the claim that all humanity is not more susceptible to mutation-caused pathology than ever before.

The increasing number of deleterious mutations is killing us. Theorists have claimed that some mutations are beneficial because that claim supports their ridiculous theories.

See for comparison:

1) Role of olfaction in Octopus vulgaris reproduction

2) Olfactory organ of Octopus vulgaris: morphology, plasticity, turnover and sensory characterization

3) Neuroendocrine factors distinguish juvenile psychopathy variants

…two primary CU variants (aggressive and non-aggressive types) emerged with profiles characterized by low to average psychopathology and high DHEA levels. Findings contribute to a growing literature base suggesting that biomarkers may distinguish youth on separable developmental pathways to psychopathy.

See for comparison:
1) Phylogenetic plasticity in the evolution of molluscan neural circuits
2) The central pattern generator underlying swimming in Dendronotus iris: a simple half-center network oscillator with a twist
My comment: No experimental evidence of biologically-based cause and effect suggests that any central pattern generator “evolved” to link behavior to biophysically constrained energy-dependent RNA-mediated cause and effect. No experimental evidence of biologically-based cause and effect suggests that any mutation is beneficial.

See for comparison: A comprehensive transcriptional map of primate brain development

Excerpt:

Disparate cell populations exhibit distinct developmental timing of gene expression, but also unexpected synchrony of processes underlying neural circuit construction including cell projection and adhesion.

My comment: Virus-driven energy theft alters the distinct developmental timing of gene expression in disparate cell populations, and the developmental timing of RNA-mediated gene expression is the only known link from RNA-mediated amino acid substitutions to supercoiled DNA, which protects all organized genomes from virus-driven entropy.

amino acid homeostasis

Nutrient-dependent pheromone-controlled autophagy

See also: Nutrient-dependent pheromone-controlled autophagy (2)

The Excitable Mitochondria links 4 neurons from a nutrient energy-dependent pheromone-controlled network in a marine invertebrate to human brain development via the conserved molecular mechanisms that link the speed of light on contact with water to the de novo creation of G protein-coupled receptors (GPCRs).  Receptor-mediated species -specific chromatin remodeling links chromosomal rearrangements to all biodiversity via energy-dependent chemotaxis and phototaxis.

See: The central pattern generator underlying swimming in Dendronotus iris: a simple half-center network oscillator with a twist.

See also: A quorum-sensing signal promotes host tolerance training through HDAC1-mediated epigenetic reprogramming

Reported as: Bacterial molecule trains the immune system to tolerate infection without inducing illness

Excerpt:

More work needs to be done to understand the molecular mechanisms allowing this mutually beneficial adaptation of both host and pathogen…

My comment: More people need to learn what is known about how the energy-dependent de novo creation of G protein-coupled receptors is linked from RNA-mediated amino acid substitutions to cell type differentiation. Receptor-mediated behaviors link links the epigenetic landscape to the physical landscape of DNA via natural selection for codon optimality in the context of autophagy. Fixation of the amino acid substitutions in supercoiled DNA protects organized genomes from virus-driven entropy and all pathology.

SARCASM ALERT If I told you more about that, the information could get me killed, so… Never mind. Virus-driven pathology will kill you and everyone you love, instead.

— in memory of Robin Williams

Few researchers use sarcasm or humor to make their point, which mean that sometimes they don’t make it.

See for example: Endolysosomal trafficking of viral G protein-coupled receptor functions in innate immunity and control of viral oncogenesis

See also: Epigenetic regulation of G Protein Coupled Receptor signaling and its implications in psychiatric disorders

With no sarcasm or humor they linked everything known about G protein-coupled receptors to all healthy longevity compared to all virus-driven energy theft and all pathology.

For comparison: How is social “evolution” linked to all pathology without acknowledging the role of G protein-coupled receptor signaling in the context of the structure and function of receptors that link chemotaxis and phototaxis in all living genera? Are these researchers joking?

Chemotaxis: Social Evolution Selects for Redundancy in Bacterial Quorum Sensing

Phototaxis across kingdoms: Microbiology: Here’s looking at you, squid

Link to the innate immune system: A model symbiosis reveals a role for sheathed-flagellum rotation in the release of immunogenic lipopolysaccharide

Link to weekend evolution of the bacterial flagellum: Evolutionary resurrection of flagellar motility via rewiring of the nitrogen regulation system

My comment: Neo-Darwinian nonsense links nothing to anything. Resurrection of something means it existed before the resurrection. Therefore, what ever existed before must be linked from chemotaxis and phototaxis to its origins and to its resurrection. Instead, the researchers claimed that two amino acid substitutions were mutations, and they linked the mutations to the weekend evolution of a new flagellum.

For comparison, here’s a link to everything known about biophysically constrained RNA-mediated protein folding chemistry in all living genera:

Feedback loops link odor and pheromone signaling with reproduction

Here’s a link to delivery of a “billion dollar baby” RNA-Guided Human Genome Engineering
Finally, here are some links from physics to chemistry and the molecular mechanisms that link nutrient-dependent pheromone-controlled autophagy from RNA-mediated amino acid substitutions to supercoiled DNA, which protects all organized genomes from virus-driven energy theft and genomic entropy.
Press Release: The Nobel Prize in Chemistry 2016

See also: The tiniest Lego: a tale of nanoscale motors, rotors, switches and pumps

…they predict that the basic components of molecular machines will be used in diverse areas of science: as light-activated switches that can release targeted drugs, for example, or as smart materials that can store energy or expand and contract in response to light.

…the bonds could be readily formed and broken, much like zipping and unzipping the hydrogen bonds that link the two strands of DNA.

A plethora of other switches soon followed. Some were controlled with light or changes in temperature, whereas others worked by binding specific ions or molecules from solution, in a similar way to how ion channels work in cell membranes, opening or closing in response to chemical signals.

See also: World’s tiniest machines win chemistry Nobel

Filtering light through a prism to identify tissue type

Hydrogen-atom energy in DNA base pairs

See also: Consciousness is simply food rearranged
Role of Double Hydrogen Atom Transfer Reactions in Atmospheric Chemistry
Abstract excerpt: 

Hydrogen atom transfer (HAT) reactions are ubiquitous and play a crucial role in chemistries occurring in the atmosphere, biology, and industry.

My comment: The link from physics to chemistry and the conserved molecular mechanisms of biologically-based RNA-mediated cell type differentiation has been the focus my works for more than 20 years, even before I knew what I would need to explain about the energy-dependent links from angstroms to ecosystems via hydrogen-atom energy in all living genera.
See also: For first time, researchers see individual atoms keep away from each other or bunch up as pairs
Excerpt:

Different configurations of electrons give rise to specific elements, making carbon atoms, for instance, distinct from hydrogen atoms.

My comment: Without the different configurations of electrons,  energy-dependent changes in angstroms could not be linked from hydrogen-atom transfer (HAT) in DNA base pairs in solution to all biodiversity in all ecosystems. Simply put, the sun’s biological energy must be linked from atmospheric chemistry to biophysically constrained protein folding chemistry on Earth.
When these interactions are seen for the first time the experimental evidence must confirm theories. Otherwise physicists will try to come up with new untestable theories to stall scientific progress.  Serious scientists make progress when experimental evidence is accepted. Chemists typically know what to accept. So do molecular biologists.
What do evolutionary theorists or other social scientists know about physics, chemistry, or molecular epigenetics? How do pseudoscientists known what to accept when they already have accepted only theories?
For comparison, serious scientists know that angstroms measure distance, and every angstrom is dynamic in the context of energy-dependent RNA-mediated cell type differentiation. How can any serious scientist understand the claims of theorists made in the context of articles like this:
Humans and Neanderthals had sex. But was it for love? An investigation
Excerpt:

We know for sure humans and Neanderthals had sex because of a Swedish scientist named Svante Pääbo, who “more or less invented the field of paleogenetics,” Elizabeth Kolbert wrote in a terrific New Yorker article in 2011.

My comment:  Elizabeth Kolbert lied and used Svante Pääbo’s works to support her ridiculous claim:

We know for sure humans and Neanderthals had sex…

Serious scientists know that Svante Pääbo is the senior author of two articles. The two articles linked Natural Selection on the Olfactory Receptor Gene Family in Humans and Chimpanzees and Loss of Olfactory Receptor Genes Coincides with the Acquisition of Full Trichromatic Vision in Primates.
Natural selection for the de novo creation of olfactory receptor genes and the loss of genes is not an indicator that humans and Neanderthals had sex. It is an indicator that natural selection for energy-dependent codon optimality occurred in the context of the physiology of reproduction in all primates. For contrast, all serious scientists know that members of two different species do not have sex. Chromatin remodeling and chromosomal rearrangements limit fertility among species via their nutrient-dependent pheromone-controlled physiology of reproduction and their behavior. The behavior is linked to energy-dependent codon optimality via the physiology of reproduction, not by sex between consenting humans and Neanderthals.
Is is silly to ask questions about sex for love without consideration of fertility, since the sexual interactions must be linked to survival of the species via biophysically constrained RNA-mediated protein folding chemistry in the context of the physiology of reproduction. The biophysical constraints are energy-dependent, but the theorists’ and journalists’ preference for fiction is clear.
Excerpt:

Robert Sawyer is a science fiction author who won the Hugo Award — one of sci-fi’s highest honors — for his 2002 book Hominids, a story that imagines a parallel world where Neanderthals survived and we didn’t. In the book (which spawned a trilogy), a Neanderthal physicist opens up a rift between the worlds and falls in love with a human.

For comparison, see this presentation text about Greg Bear’s novels in which he detailed for his non-technical audience how the nutrient energy-dependent pheromone-controlled physiology of reproduction is linked from RNA-amino acid substitutions to all cell type differentiation in all individuals of all species. The Darwin Code
See also: Structural and Functional MRI Differences in Master Sommeliers: A Pilot Study on Expertise in the Brain
Excerpt:

This study identified enhanced structural and functional patterns in the olfactory network of sommeliers. These findings are consistent with the learning they undergo in achieving the status of Master Sommelier. Furthermore, the volume of a region of the brain involved in olfactory memory was associated with experience, suggesting that the continued training results in morphological changes of the brain. These results speak to the plasticity of the adult brain in response to sensory expertise.

Reported as: Smelling Lots Of Wine Makes Your Brain Alzheimer’s Resistant

Overall, these differences suggest that specialized expertise and training might result in enhancements in the brain well into adulthood,” the study states. “This is particularly important given the regions involved, which are the first to be impacted by many neurodegenerative diseases.

See also:  What Sensory Receptors Do Outside of Sense Organs
My comment to the Scientist (I have posted: 361 comments so far)

20 years ago, we published: From Fertilization to Adult Sexual Behavior, which was a review of RNA-mediated cell type differentiation. We included a section on molecular epigenetic in the Hormones and Behavior review.

Unfortunately, few people realize that natural selection for energy-dependent codon optimality links the de novo creation of genes from the creation of G protein-coupled receptors to chemotaxis and to phototaxis before biophysically constrained energy-dependent biodiversity via RNA-mediated protein folding biochemistry can be linked to all biodiversity by amino acid substitutions.
When others report that mutations are linked to pathology, they seem to miss the fact that virus-driven energy theft causes the mutations. Nutrient-energy dependent viral latency has gone missing from explanations that would otherwise link what is known about biologically-based cause and effect from physics to chemistry and everything known about molecular epigenetics.
See also: Olfactory organ of Octopus vulgaris: morphology, plasticity, turnover and sensory characterization
My comment: Pseudoscientists could challenge representations like this if they had experimental evidence for comparison. They don’t. They have only their ridiculous theories, which they report in the story about sex between modern humans and Neanderthals. It is unadulterated pseudoscientific nonsense and nothing more than an unsubstantiated fictional account. It is not science fiction. The theorists claims are not scientifically based.
See for comparison: Role of olfaction in Octopus vulgaris reproduction and Two fatty acyl reductases involved in moth pheromone biosynthesis
Both articles cite Kohl (2013) Nutrient-dependent/pheromone-controlled adaptive evolution: a model
See also: The Ancient Origins of Consciousness: How the Brain Created Experience
Excerpt:

12. Plotnick, Dornbos, and Chen (2010). Others who advocate smell-first are Lucia Jacobs (Jacobs, 2012), who says the building of smell maps of environmental space came first and James Kohl (Kohl, 2013), whose model says chemical ecology is the main driver of adaptive evolution.  — p. 263

My comment: Chemical ecology is the main driver of energy-dependent ecological adaptations. It is not not the driver of mutation-driven evolution, and so far there is no other model for comparison to my model of chemical ecology. I deliberately used the term adaptive evolution to see if someone would take the bait and offer another model for comparison. No one did.
See also: How Psychiatrist Jon Lieff Turned an Interest in Cellular Intelligence into Award-Winning Blogging!
My comment: Lieff still presents cellular intelligence in the context of evolution. He ignores what is known about hydrogen-atom energy in DNA base pairs in solution. That shows how successful a blogger can be if they simply fail to address what is known about biophysically constrained RNA-mediated cell type differentiation. His focus is on evolution! That means he does not need to explain anything about how evolution occurs, or explain what he thinks cellular intelligence is or where it came from!
See for comparison: Direct interrogation of the role of H3K9 in metazoan heterochromatin function
Reported as: Tight DNA packaging protects against ‘jumping genes,’ potential cellular destruction
Tight DNA is supercoiled DNA and it protects the orgnaized genomes of all living genera from virus-driven energy theft and genomic entropy. Simply put, supercoiled DNA biophysically constrains virus-driven energy theft, which is the only way to establish a link from ecological variation to ecological adaptation without inventing another ridiculous theory.

… viral latency is responsible for life-long pathogenesis and mortality risk…

Nutrient energy-dependent microRNAs are the obvious link from olfaction to biophysically constrained RNA-mediated protein folding chemistry, plasticity, and prevention of all pathology.
See for example: Olfactory organ of Octopus vulgaris: morphology, plasticity, turnover and sensory characterization

Supercoiled DNA is the link to viral latency, which is the link to healthy longevity.

See also, from the Neuroscience FB group “As simple as random can be”
See also:  Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults
My comment: There is no experimental evidence of biologically-based cause and effect that links anything except energy or energy theft to the species-specific COMT Val158Met amino acid substitution during life history transitions and the development of morphological and behavioral phenotypes.

COMT val158met polymorphism and molecular alterations in the human dorsolateral prefrontal cortex: Differences in controls and in schizophrenia
Excerpt:

…the COMT val158met polymorphism is not found in species other than humans (Palmatier et al., 1999).

My comment: That fact makes the COMT val158met polymorphism a “smoking gun” in the context of energy-dependent de novo gene creation and virus-driven energy theft that links gene losses to loss of function via differences in G protein-coupled receptors.
Dopamine Neuron-Specific Optogenetic Stimulation in Rhesus Macaques
G protein-coupled receptor kinases as regulators of dopamine receptor functions
Subsecond Regulation of Synaptically Released Dopamine by COMT in the Olfactory Bulb
Programmable RNA-binding protein composed of repeats of a single modular unit
Excerpt from the conclusion:

… Pumby may present a simplified context in which to insert Pumilio modules to study how specific amino acids contribute to the emergent properties of modular RNA binding, independent of position-specific effects.

See also: Another gate-keeping attempt by Feierman

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Thermotolerance and longevity (2)

See also: Thermotolerance and Longevity

This article is part of the Research Topic Brain nutrient sensing in the control of energy balance: new insights and perspectives

Excerpt:

It is well established that nutrients act as signaling molecules in synergy with nervous and hormonal signals to inform the brain about the nutritional status of the body. The integration of these signals within the hypothalamus and other brain regions triggers behavioral and physiological responses through efferent autonomic nerves, hypothalamic-pituitary-Adrenal and thyroid axis in order to maintain energy homeostasis. In particular, the roles of glucose, fatty acid and amino acid sensing in the control of food intake and peripheral glucose metabolism have been extensively studied. Cellular and molecular mechanisms by which circulating nutrients act on the brain have become a highly competitive field with outcomes leading to several strategies to prevent or treat obesity and its co-morbidities.

In the past decade the field of brain nutrient-sensing has seen a profound evolution with, for instance, the predominant role for an interplay between homeostatic and non-homeostatic control of food intake and energy balance. The latter takes place in the mesolimbic system and recapitulates the rewarding and motivational aspects of feeding. In addition, other brain regions known for their role in memory (hippocampus), olfaction (olfactory bulbs) and circadian clock (suprachiasmatic nucleus) have emerged as nutrient sensitive areas contributing to feeding behavior and energy homeostasis. Finally, growing evidence suggests that the interplay between glial cells and neurons is fundamental in nutrient sensing.

In parallel to these new developments, several novel methodologies have emerged to dissect the neurocircuitries regulating feeding behavior and energy homeostasis, including optogenetics, DREAD, cell specific deletion… Together, these approaches will help to better understand the interplay between brain regions and circuits involved in nutrient sensing.
This Frontiers Research Topic aims to focus on new insights and perspectives in brain nutrient sensing (both in physiological and pathophysiological conditions) with a special attention to the multi-scale deciphering of cell inner mechanisms. In this regard contributors are encouraged to submit reviews, mini-reviews, commentaries, perspective articles, original research articles and method articles.

My invited review of nutritional epigenetics and microRNA-mediated cell type differentiation was returned without review by the journal editors at “Nutrients.”

See: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems

See also: Mitochondrial Ultrastructure and Glucose Signaling Pathways Attributed to the Kv1.3 Ion Channel

Thanks to Nerissa Belcher for calling this to my attention. I have followed the works of Debra Fadool for several years, but  might have missed this one.

For other examples of her progress, see:

Mammalian Pheromones (2005)

See also: Olfaction Under Metabolic Influences (2012)

See also: Hyperlipidemic Diet Causes Loss of Olfactory Sensory Neurons, Reduces Olfactory Discrimination, and Disrupts Odor-Reversal Learning (2014)

See for comparison:

A quantum theory for the irreplaceable role of docosahexaenoic acid in neural cell signalling throughout evolution (2013)

Periodic Scarred States in Open Quantum Dots as Evidence of Quantum Darwinism (2010)

Stress-induced structural plasticity of medial amygdala stellate neurons and rapid prevention by a candidate antidepressant

Reported as: New Signs of Stress Damage to the Brain: Mouse Study

Excerpt:

Nasca and her colleagues’ experiments included mice at high risk of developing anxiety- and depression-like behaviors in response to stress. Treatment with acetyl carnitine also appeared to protect these mice, suggesting that a similar preventative approach might work for depression-prone people.

Both humans and rodents naturally produce acetyl carnitine under normal conditions and several depression-prone animal models are deficient in acetyl carnitine. In a separate study, Nasca and colleagues are examining whether people with depression have abnormally low levels of the molecule.

The links from everything know to serious scientists about biophysically constrained RNA-mediated cell type differentiation can be compared to outcomes linked to healthy longevity or from virus-driven energy theft to mutations and all pathology via carnitine metabolism.

The journal article cites: Magarinos AM, McEwen BS. Stress-induced atrophy of apical dendrites of hippocampal CA3c neurons: involvement of glucocorticoid secretion and excitatory amino acid receptors. Neuroscience 1995; 69:89–98.

It does not link virus-driven energy theft to experience-dependent changes in RNA-methylation that have already been linked from RNA-directed DNA methylation to learning and memory during life history transitions by this group, and in the context of this report: Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults.

The likelihood that no one else has linked virus-driven energy theft to experience-dependent changes in RNA-methylation, which that have already been linked from RNA-directed DNA methylation to learning and memory during life history transitions, suggests that others have not followed the best advice I ever received. In the early 1990’s, I was told that my model could not be validated unless I could show that gene activation occurred in hormone-secreting neurons of the hypothalamus that all serious scientist know link energy-dependent RNA-mediated cell type differentiation to all biodiversity and also link virus-driven energy theft from mutations to all pathology via the physiology of reproduction in all living genera.

I did that, and co-authored a book, and have since published a series of articles with co-authors or as monographs. Most people remain uninterested and many are antagonistic because they don’t like the experimental evidence of biologically-based cause and effect that I included in my model. They prefer ridiculous theories.

 

poster-from-jesse

Teleophobes vs teleophiles: a recent history

 
Teleology is a reason or explanation for something in function of its end, purpose, or goal.
The teleological or physico-theological argument, also known as the argument from design, or intelligent design argument is an argument for the existence of God or, more generally, for an intelligent creator “based on perceived evidence of deliberate design in the natural or physical world”

My comment: Teleophobes make weak arguments peppered with logical fallacies.  They do not make physico-theological arguments, which can be supported with experimental evidence of biologically-based cause and effect.  Physico-theological are more likely to link atoms to ecosystems via energy and information.
The difference between a teleophobe and a teleophile is exemplified in the context of two works that were published on the same day: June 14, 2013

Mutation-Driven Evolution

Conclusion:

In other words, genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world. In this view of evolution there is no need of considering teleological elements.

Nutrient-dependent/pheromone-controlled adaptive evolution: a model

Conclusion:

…the model represented here is consistent with what is known about the epigenetic effects of ecologically important nutrients and pheromones on the adaptively evolved behavior of species from microbes to man. Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.

My comment: For comparisons between other teleophobes, like Nei, that have been placed into the context of my model, see:

Teleo-

Phobes:

  1. Roles of Mutation and Selection in Speciation: From Hugo de Vries to the Modern Genomic Era
  2. One crank dies, another rises to take his place
  3. I am absolutely certain that if you showed this statement to any professor of biology or genetics in any accredited university anywhere in the world that 100% of them would say that “Random mutations are the substrate upon which directional natural selection acts” is a correct and true statement.
  4.  We simply don’t know where the boundary between prespecified attraction and learned association lie in our own species, nor do we have compelling evidence for the primacy of one sense over another.
  5. Evolutionary resurrection of flagellar motility via rewiring of the nitrogen regulation system
  6. Large Numbers of Novel miRNAs Originate from DNA Transposons and Are Coincident with a Large Species Radiation in Bats

Teleo-

Philes:

  1. Evolution 2.0: Breaking the Deadlock Between Darwin and Design
  2. Stress dynamically regulates behavior and glutamatergic gene expression in hippocampus by opening a window of epigenetic plasticity
  3. Effect of two pyrazine-containing chemosignals on cells of bone marrow and testes in male house mice (Mus musculus L.)
  4. Role of olfaction in Octopus vulgaris reproduction
  5. Noncoding RNA –NORAD– Regulates Genomic Stability by Sequestering PUMILIO Proteins
  6. How Does Diet Influence Immunity
  7. Structural diversity of supercoiled DNA
  8. A quantum theory for the irreplaceable role of docosahexaenoic acid in neural cell signalling throughout evolution
  9. Molecular Vibration-Sensing Component in Human Olfaction

You may also want to stay informed on the issues that arise as Researchers attempt to uncover the origins of water’s unusual properties.
Excerpt:

…water’s anomalous properties are related to its hydrogen bonds, which cause liquid water to arrange itself in a highly ordered way because of the attraction between the hydrogen atoms in one water molecule and the oxygen atoms in adjacent molecules.

 

human-evolution

Ecological genomics: teleophobes respond (too late)

Forecasting Ecological Genomics: High-Tech Animal Instrumentation Meets High-Throughput Sequencing

Conclusion:

Twenty years ago, an essay about sequencing genomes and remotely tracking animals across the globe in real time would have been the subject of science fiction. In 2015, there are over 50,000 animals being tracked [12], and single research groups now sequence dozens, up to hundreds, of individual genomes [17,82]. By embracing new technology and integrating these data streams into an ecological genomic framework (Fig 1), we are now poised to inform, challenge, and develop biological theory.

My comment: Twenty years ago,  The Scent of Eros: Mysteries of Odor in Human Sexuality, developed the theme that Lewis Thomas (p. 732) used to challenge biological theory when he wrote:

I should think we might fairly gauge the future of biological science, centuries ahead by estimating the time it will take to reach a complete comprehensive understanding of odor. It may not seem a profound enough problem to dominate all the life sciences, but it contains, piece by piece, all the mysteries.

Review by Mark Sergeant
Reviewed by Ralph Underwager, Institute for Psychological Therapies.
Reviewed by Jan Peregrine
Note: At the Continuum editor’s insistence, co-author (the late) Robert T. Francoeur, included a few attestations to ridiculous theories about random mutations and/or mutations and evolution. These attestations were made to placate the teleophobes, which was required to publish a book that clearly portrayed how ecological variation was linked to ecological adaptation by the pheromone-controlled physiology of reproduction. Symbiotic Planet: A New Look at Evolution had not yet been published and few people knew that

[W]hat Haldane, Fisher, Sewell Wright, Hardy, Weinberg et al. did was invent…. Evolution was defined as “changes in gene frequencies in natural populations.” The accumulation of genetic mutations was touted to be enough to change one species to another….  Assumptions, made but not verified, were taught as fact.

See for comparison: 

Linking gene expression and DNA methylation in single cells

Excerpt:

Recent single-cell protocols also allow researchers to explore chemical modification of DNA (‘epigenetics’), for example DNA methylation, which is a driving force behind changes to gene expression.

My comment: Odor is driving force behind changes to gene expression. Since 1995, the driving force of odor has been placed into the context of experience-dependent nutrient-dependent RNA-directed DNA methylation.
See: Feedback loops link odor and pheromone signaling with reproduction
See also: From Fertilization to Adult Sexual Behavior
Excerpt: 

Molecular epigenetics. It is now understood that certain genes undergo a process called “genomic or parental imprinting.” Early in embryonic development attached methyl groups become removed from most genes. Several days later, methyl groups are reattached in appropriate sites. Fascinatingly, some such genes reestablish methylation patterns based upon whether the chromosomal segment carrying the gene came from maternal or paternal chromosomes. These sexually dimorphic patterns are labeled genomic or parental imprinting, and these imprintings are inheritable but non-genetic modifications of specific genes (Razin and Shemer, 1995; Reik, 1989; Surani, 1991; Zuccotti and Monk, 1995).

My comment: Anyone who starts with DNA methylation as their “driving force” excludes what is known about odors and hydrogen-atom transfer in DNA base pairs. The experience-dependent de novo creation of olfactory receptor genes links everything currently known about nutrient-dependent non-genetic modifications of specific genes.
See: An Epigenetic Trap Stabilizes Singular Olfactory Receptor Expression
My comment: The epigenetic trap stabilizes hydrogen-atom transfer in DNA base pairs.
See also: How keeping active pays off in the olfactory system
In an attempt to discuss this, I wrote:

Is what’s being elucidated the bottom-up epigenetic effects on stochastic gene expression via chromatin remodeling, which is controlled by the top-down epigenetic effects of pheromones on reproduction in species from microbes to man?
Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338. DOI: 10.3402/snp.v2i0.17338.

Stavros Lomvardas echoed my claim but refused to discuss it further.

  • The article elucidates how the environment can broadly influence gene expression through an epigenetic effect chromatin – the way DNA is package and organized. This allows the environment to influence sensory function, to tune the olfactory sense to better suit the surrounding environment, because these environmentally regulated chromatin changes are coupled to cell longevity. This results in a change in the distribution of cells in the tissue that have made particular stochastic choices, where the stochastic choice is which olfactory receptor to express, without affecting the mechanism of stochastic gene expression.

My comment: Most people who exclude nutrient energy-dependent non-genetic modifications in DNA base pairs appear to be teleophobes who want others to believe in the pseudoscientific nonsense of neo-Darwinian theories. Their theories start with mutations, not with experience-dependent epigenetic traps that link stochastic choice to gene expression and feedback loops that link odor and pheromone signaling with reproduction.
In the context of those epigenetic traps and feedback loops, nutrient-dependent microRNAs typically repair the mutations. That is why teleophobes do not start with ecological variation and nutrient-dependent RNA-directed DNA methylation and DNA repair. They known that the microRNA/messenger RNA balance is linked from RNA-mediated events to teleophobic theory killers.
In the past 20 years more than 46,000 indexed publications from the NIH PubMed database, link microRNAs to biophysically constrained RNA-mediated cell type differentiation in the 50,000 animals being tracked. In 2016, serious scientists expect to see the tipping point reached. There will be more publications that explain how cell type differentiation occurs than publications that track the observations of researchers who Dobzhansky (1964) referred to as bird watchers and butterfly collectors. Teleophobic theories will finally be dismissed with extreme prejudice against those who invented or touted them.
See: Biology, molecular and organismic (p. 443)
Excerpt:

The notion has gained some currency that the only worthwhile biology is molecular biology. All else is “bird watching” or “butterfly collecting.” Bird watching and butterfly collecting are occupations manifestly unworthy of serious scientists!

See also: A Fear of Pheromones and The Great Pheromone Myth
Excerpt:  

…it is erroneous to infer that a plurality of mammalian behaviors and endocrine responses is uniquely determined in an invariant way by single or small sets of chemical stimuli and to apply a generic and misleading name to the presumptive agents in support of such an inference.

My comment: No serious scientist is afraid of the facts about human pheromones. No serious scientist has ever inferred that atoms and ecosystems could be linked to mammalian behaviors and endocrine responses in an invariant way by anything else. For comparison, most teleophobes have continued to make claims like this:

…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world. In this view of evolution there is no need of considering teleological elements” (p. 199).

My comment: Mutations are linked from perturbed protein folding to pathology. Claims by teleophobes fail to address everything known to serious scientists about physics, chemistry, and the conserved molecular mechanisms of biophysically constrained RNA-mediated protein folding chemistry and cell type differentiation in all individuals of all species of all living genera. The teleophobes link mutations to the enormous amount of biodiversity in this world.
See also: Extensive Gains and Losses of Olfactory Receptor Genes in Mammalian Evolution
Excerpt:

Why then did the number of OR genes change so dramatically in mammals but not in Drosophila? One possible explanation is the difference in the mechanism of gene expression system between mammals and Drosophila.

My comment: There is no difference in how the molecular mechanisms of gene expression link atoms to ecosystems in species from microbes to humans. The epigenetic landscape must be linked to the physical landscape of supercoiled DNA by nutrient-dependent changes in the microRNA/messenger RNA balance. The changes link the physiology of reproduction to the stability of organized genomes in all living genera.
For example, see: Secreting and Sensing the Same Molecule Allows Cells to Achieve Versatile Social Behaviors
Excerpt:

Evolution appears to favor efficient circuits and signaling elements that can accomplish many different tasks (13, 14). The diverse social behaviors that are enabled by the functional flexibility of the secrete-and-sense circuits (Fig. 5C) may explain the frequent occurrence of this class of circuits in nature.

My comment: Evolution favors nothing. The key phrase is that it appears to favor efficient circuits and signaling elements. That suggests evolution favors itself and that favoritism enabled weekend evolution of the bacterial flagellum.
See: Evolutionary resurrection of flagellar motility via rewiring of the nitrogen regulation system
Excerpt:

Genome resequencing revealed a single-nucleotide point mutation in ntrB in strain AR2S, causing an amino acid substitution within the PAS domain of the histidine kinase sensor NtrB [Thr97→Pro97 (T97P)] (13). The fast-spreading strain AR2F had acquired an additional point mutation in the σ54-dependent EBP gene ntrC, which alters an amino acid (R442C) within the DNA binding domain (Table 1 and table S2).

My comment: These researchers seem to think mutations cause nutrient-dependent RNA-mediated DNA methylation, which they linked to the two amino acid substitutions. Apparently, they have not learned anything about the biophysically constrained chemistry of RNA-mediated protein folding. Thermodynamic cycles of protein biosynthesis and degradation are perturbed by mutations and linked by RNA-mediated amino acid substitutions to cell type differentiation and healthy longevity.
See also: Intelligent Microbe Secretory Weapons
Conclusion:

It is absurd to think that this occurs randomly. Doesn’t the microbe need to have some way of knowing what needs to be built and what its uniquely produced effector molecules will do in the distant host cell.
How can anyone not think that these microbes exhibit extremely intelligent behavior?

Excerpt:

…when we eat food nucleic acids can get into our cells. Also, there is a theory that our cells in the body keep sending out nucleic acids and one theory has it that it seems to correct the mistakes that other cells have suffered from mutations. . .

My comment: All serious scientists know that RNA-mediated DNA repair of mutations is required to prevent virus-driven genomic entropy.  Nutrient-dependent RNA-mediated DNA repair is linked to the pheromone-controlled physiology of reproduction by supercoiled DNA.
See: Structural diversity of supercoiled DNA
Conclusion:

Our data provide relative comparisons of supercoiling-dependent twisted, writhed, curved, and kinked conformations and associated base exposure. Each of these structural features may be differentially recognized by the proteins, nucleic acids, and small molecules that modulate DNA metabolic processes.

Reported as: How Strange Twists in DNA Orchestrate Life
Excerpt:

Simply twisting DNA can expose internal bases to the outside, without the aid of any proteins. Additional work by David Levens, a biologist at the National Cancer Institute, has shown that transcription itself contorts DNA in living human cells, tightening some parts of the coil and loosening it in others. That stress triggers changes in shape, most notably opening up the helix to be read.

My comment: The teleophobic claim about Strange Twists in DNA Orchestrate Life fails to address anything known to serious scientists about the questions posed by Schrodinger in What is Life? The teleophobes also fail to address Schrodinger’s answer.
Excerpt 1)

Indeed, in the case of higher animals we know the kind of orderliness they feed upon well enough, viz. the extremely well-ordered state of matter in more or less complicated organic compounds, which serve them as foodstuffs. After utilizing it they return it in a very much degraded form -not entirely degraded, however, for plants can still make use of it. (These, of course, have their most power supply of ‘negative entropy’ the sunlight)

My comment: All serious scientists understand why Schrodinger’s anti-entropic force is required.
Excerpt 2)

But about forty years ago the Dutchman de Vries discovered that in the offspring even of thoroughly pure-bred stocks, a very small number of individuals, say two or three in tens of thousands, turn up with small but ‘jump-like’ changes, the expression ‘jump-like’ not meaning that the change is so very considerable, but that there is a discontinuity inasmuch as there are no intermediate forms between the unchanged and the few changed. De Vries called that a mutation. The significant fact is the discontinuity. It reminds a physicist of quantum theory -no intermediate energies occurring between two neighbouring energy levels. He would be inclined to call de Vries’s mutation theory, figuratively, the quantum theory of biology.  We shall see later that this is much more than figurative. The mutations are actually due to quantum jumps in the gene molecule. But quantum theory was but two years old when de Vries first published his discovery, in 1902. Small wonder that it took another generation to discover the intimate connection! (page 33-34)

My comment: Since 1944, teleophobes have still not realized that the quantum jumps in DNA base pairs are nutrient-dependent. Nutrient energy-dependent changes in hydrogen atom transfers in DNA base pairs are not mutations.  The discontinuity is nutrient-dependent and controlled by the physiology of reproduction.  That is why, even to a teleophobe, the “strange twists” in DNA that orchestrate life can now be explained only in the context of Ecological Genomics.  A model of biologically-based cause and effect that links atoms to ecosystems is required.
The model must include the conserved molecular mechanisms of nutrient-dependent pheromone-controlled RNA-mediated events that link chromosomal rearrrangements to all biodiversity in all individuals of all living genera.
See also: Evolution’s Science Status
Excerpt: 

The problem stems from the absence of empirical evidence to scientifically supported these new concepts. Dawid argued that the essence and definition of science should be revised to allowing for three kinds of “non-empirical” evidences.

My comment: Non-empirical evidences are theories. Teleophobes are theorists, not serious scientists.

See also: A Single Blood Test For All Cancers? Illumina, Bill Gates And Jeff Bezos Launch Startup To Make It Happen

Excerpt:

Everything here is directed at being a pan-cancer test, something that is a universal test,” says Jay Flatley, who has been Illumina’s chief executive for sixteen years and has improved the power of DNA sequencing at a rate that exceeds improvements in microchips over the same period of time.

Conclusion:

The cancer world is changing, Nelsen says. “I think these things will converge pretty rapidly. If I was a big pharma with a minimally effective, medium toxicity chemotherapy drug I would be nervous. I think it’s going to be really a fascinating time.”

My comment: Nothing about the claims of teleophobes attests to the the power of DNA sequencing, or to the fact that hydrogen-atom transfers in DNA base pairs are the link between nutrient-dependent health and mutation-driven pathology. Claims like this one should make c nervous.

“It was really surprising,” Dr. Bernstein said. “Why would a metabolism gene cause cancer?”

For comparison, see: The convergent cancer evolution toward a single cellular destination

Excerpt:

Complex multicellular organisms, including humans, must possess sophisticated genetic constraints that suppress the fitness of individual cells in order to ensure the fitness of the whole organism 2. However, accidental events such as somatic mutations or viral infections can wipe out such constraints and reactivate the cell’s otherwise dormant capacity of seeking for its own fitness, often resulting in cancer 3-5.

Reported as: Dominant evolutionary theme emerges to better predict clinical outcomes for cancer

My comment: The dominant evolutionary theme did not include the role of viruses.

If it had, we would already have effective treatments for cancer and the focus would have been on prevention long before now. Neo-Darwinists are teleophobes who have stalled the “Precision Medicine Intiative” and will continue to do that for as long as serious scientists allow it.

The entire evolution of the microbial world and the virus world, and the interaction between microbes and viruses and other life forms have been left out of the Modern Synthesis… –Eugene Koonin (2015)

See for comparison: Distinct E-cadherin-based complexes regulate cell behaviour through miRNA processing or Src and p120 catenin activity

Conclusion:

Taken together, our data untangle the complicated roles of E-cadherin and p120 in the context of distinct junctional complexes, spatially separating their functions and providing an explanation for their conflicting behaviour in cell growth. In addition, they identify PLEKHA7 as a specific marker of ZA that mediates suppression of growth-related signalling. Finally, they reveal an interaction of the ZA with the microprocessor complex, and uncover a mechanism whereby the ZA regulates a set of miRNAs to suppress cellular transformation and maintain the epithelial phenotype.

Excerpt:
“LEDs are great things, and people should be buying them,” Soljačić says. “But understanding these basic properties” about the way light, heat, and matter interact and how the light’s energy can be more efficiently harnessed “is very important to a wide variety of things.”
 
My comment: Indeed, the anti-entropic epigenetic effects of virucidal UV light appear to link hydrogen-atom transfer in DNA base pairs to the answer to Schrodinger’s question: “What is Life?” Nutrient-dependent life and the physiology of reproduction are epigenetically-effected ways that supercoiled DNA traps energy to ensure organized genomes are protected from virus-driven entropy.

terrarium-eco-system

Amino acid substitutions, stress, and human behavior

Stress dynamically regulates behavior and glutamatergic gene expression in hippocampus by opening a window of epigenetic plasticity

Excerpt:

…33% of the human population present a BDNF Val66Met SNP that leads to a valine-to-methionine substitution in the BDNF protein at codon 66, and this SNP has been associated with increased susceptibility to development of stress-related disorders (21, 22).

Reported as: Newly discovered windows of brain plasticity may help with treatment of stress-related disorders
Excerpt:

The researchers also identified the molecule regulating the regulator, an enzyme called P300. By adding chemical groups to proteins known as histones, which give support and structure to DNA, P300 increases expression of mGlu2, they found.

My comment:  They linked a nutrient energy-dependent base pair substitution and the BDNF Val66Met amino acid substitution from ecological variation to ecological adaptations via a metabolic networks linked to a genetic network. The conserved molecular mechanisms can be compared in the context of life history transitions that link the honeybee model organism to humans. For example, the COMT Val158Met substitution links histones to supercoiled DNA, which appears to protect the organized genomes of all living genera from virus driven entropy.
See also: Additive Gene–Environment Effects on Hippocampal Structure in Healthy Humans
Excerpt: 

Similarly, BDNF Val66Met, a single nucleotide polymorphism (SNP) located in the brain-derived neurotrophic factor gene (BDNF), has been associated with stress susceptibility (Gatt et al., 2009; Alexander et al., 2010). Further, COMT Val158Met, a functional SNP located in the catechol-O-methyltransferase gene (COMT), has been implicated in HPA axis hyper-reactivity (Armbruster et al., 2012), altered μ-opioid neurotransmitter responses to pain stressors (Zubieta et al., 2003), and increased limbic reactivity (Smolka et al., 2005).

My comment: The links from nutrient energy-dependent base pair substitutions to RNA-mediated amino acid substitution and SNPs linked to behavior are clear and the amino acid substitutions are linked to morphological and behavioral phenotypes across all genera.
See the examples in: Nutrient-dependent/pheromone-controlled adaptive evolution: a model
Excerpt:

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).

See also: Human pheromones: integrating neuroendocrinology and ethology
Abstract:

The effect of sensory input on hormones is essential to any explanation of mammalian behavior, including aspects of physical attraction. The chemical signals we send have direct and developmental effects on hormone levels in other people. Since we don t know either if, or how, visual cues might have direct and developmental effects on hormone levels in other people, the biological basis for the development of visually perceived human physical attraction is currently somewhat questionable. In contrast, the biological basis for the development of physical attraction based on chemical signals is well detailed.

My comment: Our award-winning 2001 review has since been cited in these recently published works, which link atoms to ecosystems via the model of nutrient-dependent receptor-mediated events and examples of RNA-mediated amino acid substitutions.
See: Investigating biomolecular recognition at the cell surface using atomic force microscopy
Excerpt:

The fission yeast pheromone receptor is a kind of G protein-coupled receptor (GPCR), a typical membrane receptor protein on cell surface. These receptors are activated by pheromone binding and then enable cellular signal transduction (Kohl et al., 2001).

See also: Chemosignals from isolated females have antimutagenic effect in dividing the cells of bone marrow from male mice of the CBA strain

See also: Coding of Group Odor in the Subcaudal Gland Secretion of the European Badger Meles meles: Chemical Composition and Pouch Microbiota

Abstract excerpt:

As it is likely that the variation in metabolic activity is found at the species-, subspecies-, or even strain-level, future high-throughput sequencing can be expected to reveal more subtle differences in the microbial communities between social groups.

Excerpt:

Some Actinobacteria have been found to play a major role in the transformation of odorless steroids into odorous derivatives (e.g., Gower et al. 1986 , Kohl et al. 2001 ).

We wrote:

The odors produced by humans are a function of the location on the body where the odor is being produced. The amount of available oxygen as well as water and skin gland secretions determine the type and number of cutaneous flora, which are present on different body areas. Moist areas of the body, such as the mouth, axillae, genital region, and feet, support greater varieties and numbers of bacteria because they are occluded, or are moist because of their function (e.g., mouth, vaginal barrel). The type and density of cutaneous microorganisms on different areas of the body interacting with skin and other glandular secretions give rise to a variety of odors from various body sites.

Citations by others
My comment: The links from the skin microbiome to individual-specific and species-specific pheromones have since been widely reported as have links from the gut microbiome. Every aspect of pheromone production links metabolic networks to genetic networks via the conserved molecular mechanisms detailed in the molecular epigenetics section of our 1996 Hormones and Behavior review. From Fertilization to Adult Sexual Behavior
 
 

 

terrarium-eco-system

Epigenetic (re)programming of behavior (3)

Bipolar drug turns foraging ants into scouts


Excerpt:

“DNA methylation has become nearly synonymous with epigenetics,” says Brendan Hunt, an insect geneticist at the University of Georgia in Griffin. “This research brings needed attention to the importance of other epigenetics marks, like histone modifications.”
“We finally have a mechanism to understand ‘nurture’ in molecular terms,” says Gene Robinson, a geneticist at the University of Illinois, Urbana-Champaign, who studies caste determination in honey bees. The ant study, he adds, highlights “how the environment gets under the skin to affect gene expression, and consequently, neural activity and behavior.”

My comment: Gene Robinson’s word choice reveals the amount of nonsense he included in his claim that “We finally have a mechanism to understand ‘nurture’ in molecular terms…” His claim about “how the environment gets under the skin to affect gene expression” was placed into the context of epigenetic effects on genes and hormones that affect behavior by Bruce McEwen.
See: Brain on stress: How the social environment gets under the skin and Correction for McEwen, Brain on stress: How the social environment gets under the skin
Excerpt: 

The authors note that on page 17184, right column, first paragraph, line 4, “effect” should instead appear as “affect.”

Robinson and McEwen know that we linked effect and affect in our 1996 Hormones and Behavior review in our section on molecular epigenetics. For example, Robinson, with Elekonich cited From Fertilization to Adult Sexual Behavior in Organizational and activational effects of hormones on insect behavior (2000).
Excerpt:

Effects of hormones on brain and behavior occur through three mechanisms: (1) behaviors both organized and activated by hormones, (2) behaviors only organized by hormones, and (3) behaviors only activated by hormones (reviewed in Arnold and Breedlove, 1985; Diamond et al., 1996).”

My comment: In Diamond, Bintock and Kohl (1996), we detailed everything known about the molecular epigenetics of RNA-mediated cell type differentiation in species from microbes to mammals and linked it to chromosomal rearrangements and to sexual orientation.
Excerpt 1)

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.
A potential ramification of epigenetic imprinting and alternative splicing may be occurring in Xq28, a chromosomal region implicated in homosexual orientation…

Excerpt 2) 

Parenthetically it is interesting to note even the yeast Saccharomyces cerevisiae has a gene-based equivalent of sexual orientation (i.e., a-factor and alpha-factor physiologies). These differences arise from different epigenetic modifications of an otherwise identical MAT locus (Runge and Zakian, 1996; Wu and Haber, 1995).

My comment: The epigenetically-effected molecular mechanisms that link RNA-mediated cell type differentiation in yeasts to humans via every aspect of behavior including those associated with sexual orientation were placed into the context of brain gene expression in the honeybee.
See also: Brain gene expression changes elicited by peripheral vitellogenin knockdown in the honey bee (2013) Co-authored by Gene Robinson
Excerpt 1)

Vitellogenin (Vg) is best known as a yolk protein precursor. Vg also functions to regulate behavioural maturation in adult honey bee workers, but the underlying molecular mechanisms by which it exerts this novel effect are largely unknown.

My comment: The yolk protein precursor links yeasts to invertebrates and egg-laying vertebrates, such as chickens via juvenile hormone (JH).
Excerpt 2)

…the tight coregulatory relationship that exists between JH and Vg in the regulation of honey bee behavioural maturation is manifest at the genomic level and suggest that these two physiological factors act through common pathways to regulate brain gene expression and behaviour.

My comment: Taken together, Gene Robinson and others have linked our model of hormone-organized and hormone-activated differences in behavior from the nutrient-dependent pheromone-controlled behavior of yeasts and all invertebrates to all vertebrates via the honeybee model organism. This brings out model current in the context of our claims about pre-mRNAs, which are now also called microRNAs.
See also: The gene vitellogenin affects microRNA regulation in honey bee (Apis mellifera) fat body and brain
Excerpt:

…we demonstrate a causal link between the Vg knockdown forager phenotype and variation in the abundance of microRNAs in different tissues with possible consequences for regulation of foraging behavior.

My comment: They demonstrate top-down causation linked from atoms to ecosystems to foraging behavior via the abundance of nutrient-dependent microRNAs in the different cell types of different tissues in different species. But they link the gene vitellogenin to an affect on microRNA regulation. They ignore everything known about epigenetics, metabolic networks, and genetic networks. They do not link atoms to ecosystems via the epigenetic effects of food odors and pheromones on the hormones that affect behavior.
The failure of researchers to link top-down causation to biologically-based cause and effect via any model that links atoms to ecosystems is catastrophic. It prevents others from understanding the difference between epigenetic effects on hormones and the affect of hormones on behavior in the context of all hormone-organized and hormone-activated behaviors in all vertebrates and invertebrates.
Their failure becomes evident in this report: Role of olfaction in Octopus vulgaris reproduction. This link opens the pdf
Excerpt:

Future work on O. vulgaris olfaction must also consider how animals acquire the odours detected by the olfactory organ and what kind of odour the olfactory organ perceives. The OL acting as control centre may be target organ for metabolic hormones such as leptin like and insulin like peptides, and olfactory organ could exert regulatory action on the OL via epigenetic effects of nutrients and pheromones on gene expression (Kohl, 2013; Elekonich and Robinson, 2000). — p. 61

My comment: I find it difficult to believe that only one group of researchers would link two decades of my published works from atoms to ecosystems in all living genera. However, others have virtually ignored the fact that we were the first to link the molecular mechanisms of all RNA-mediated cell type differentiation in our 1996 Hormones and Behavior review. Lest anyone think I am complaining about being ignored in the context of “sour grapes,” let’s look at the other links from atoms to ecosystems that Gene Robinson and others have ignored.
See: Bacteriophages isolated from chicken meat and the horizontal transfer of antimicrobial resistance genes reported as: Phage spread antibiotic resistance
Excerpt:

Until recently, transduction of antibiotic resistance via phage was assumed to be a very minor source of the spread of resistance, said Hilbert. “New information from the sequencing of bacterial DNA has shown that transduction must be a driving force in bacterial evolution, and thus, quite common.”

My comment: The claim that virus-driven “…antibiotic resistance via phage was assumed to be a very minor source of the spread of resistance…” can be linked to assumptions by neo-Darwinian theorists that antibiotic resistance was caused by mutations, which caused the evolution of one species from another. Those claims are not supported by any experimental evidence that links atoms to ecosystems or any that link what is known to serious scientists about biologically-based cause and effect.
Neo-Darwinian theorists fail to acknowledge what is known to all serious scientists about the molecular epigenetics of nutrient-dependent microRNA-mediated cause and effect. They ignore everything known about virus-driven genomic entropy. Nutrient energy-dependent DNA repair obviously occurs only in the context of nutrient-dependent microRNAs. The nutrient-dependent microRNAs are linked from energy-dependent base pair substitutions to RNA-mediated amino acid substitutions. The beneficial RNA-mediated amino acid substitutions are fixed in the context of the physiology of reproduction. The substitutions link microRNAs and adhesion proteins to supercoiled DNA. The supercoiled DNA protects organized genomes from virus-driven entropy in species from bacteria to all invertebrates and vertebrates.

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