diseases-disorders

Your indifference is killing you and others

Summary: Coherence-inducing mechanisms is double-speak for mechanisms that are nutrient-dependent and pheromone-controlled.
Feedback loops link odor and pheromone signaling with reproduction has been presented in double-speak as Looplessness in networks is linked to trophic coherence

We are currently studying the entropy of the coherence ensemble we defined for this work. “In general, higher trophic coherence would be associated with lower entropy states, which means that if networks are more coherent than the random expectation there must indeed be some kind of negentropic process at work.” Johnson notes that the impact in this case relative to trophic coherence would be found in quantifying the extent to which different empirical networks have been driven from their maximum entropy state. “This might be the best way of discovering when there are coherence-inducing mechanisms at work, how much energy must be involved, and ultimately identifying the nature of such processes.”

Feedback loops link the sun’s anti-entropic virucidal energy from the food that organisms eat to the physiology of pheromone-controlled reproduction in all living genera. The virucidal effect of ultraviolet light biophysically constrains viral latency. Energy-dependent RNA-mediated amino acid substitutions in supercoiled DNA are fixed in organized genomes via the physiology of reproduction and supercoiled DNA protects all organized genomes from the virus-driven degradation of messenger RNA that links mutations to all pathology.
Coherence-inducing mechanisms is double-speak for nutrient-dependent and pheromone-controlled in the context of Nutrient-dependent/pheromone-controlled adaptive evolution: a model. 
Despite the validity of the model, it has not been accepted by neo-Darwinian theorists or “Big Bang” cosmologists. Ridiculous beliefs about emergence and evolution are pervasive and the pseudoscientific nonsense of their theories leads to claims about coherence-inducing mechanisms.
That is why I changed the FB page description at RNA-mediated after a series of posts (see below).

It took 20 years for others to realize that all life on Earth is food energy-dependent. Now, most people are indifferent to that fact. They refuse to learn anything about where the food energy comes from.

Differences in the energy of photons have been linked to quantized energy-dependent fixation of RNA-mediated amino acid substitutions. The substitutions biophysically constrain supercoiled DNA via the physiology of pheromone-controlled reproduction.

Virus-driven energy theft links the degradation of messenger RNA to mutations via amino acid substitutions in viruses. The substitutions in the viruses have been linked to all pathology via changes in the energy-dependent microRNA/messenger RNA balance.

For comparison, the pseudoscientific nonsense of neo-Darwinian theories links mutations from natural selection to the evolution of new species. In reality, light energy is quantized information. The information links physics, chemistry, and molecular epigenetics from the speed of light on contact with water and hydrogen-atom transfer in DNA base pairs in solution to learning, memory, and behavior via RNA-mediated events such as the energy-dependent creation of enzymes and the the de novo creation of G protein-coupled receptors such as olfactory receptor genes.

Top-down causation and de novo gene creation are exemplified by energy-dependent differences in the microRNA/messenger RNA balance that link natural selection for codon optimality to amino acid substitutions that link the physiology of reproduction to supercoiled DNA. Supercoiled DNA protects all organized genomes from virus-driven energy theft. That fact supports the beliefs of young earth creationists, which may be the only existing basis for discussion of quantum biology and refutations of neo-Darwinian theories that have linked olfaction to quantum souls. If there is another basis for the link from quantum physics to quantum souls, no one has detailed in in the context of top-down causation, which must include information about the creation of genes.

Most people seem unwilling to accept experimental evidence that attests to how genes are created or information that shows how virus-driven energy theft is linked to all pathology. Discussion of the energy-dependent paradigm shift would lead others away from pseudoscientific nonsense about emergence and/or beneficial mutations and evolution.

Only via discussion of facts about the paradigm shift will others learn what is currently known to serious scientists about the biophysically constrained nutrient energy-dependent chemistry of RNA-methylation and all biophysically constrained RNA-mediated protein folding chemistry. Simply put, the protein folding chemistry must be linked to all biodiversity by the physiology of energy-dependent pheromone-controlled reproduction in all living genera.

Your indifference to that fact is killing people.

See for comparison: Looplessness in networks is linked to trophic coherence (May 16, 2017)

Our theory correctly classifies a variety of networks-including those derived from genes, metabolites, species, neurons, words, computers, and trading nations-into two distinct regimes of high and low feedback and provides a null model to gauge the significance of related magnitudes. Because trophic coherence suppresses feedback, whereas an absence of feedback alone does not lead to coherence, our work suggests that the reasons for “looplessness” in nature should be sought in coherence-inducing mechanisms.

Reported August 14, 2017 as Trophic coherence explains why networks have few feedback loops and high stability

The researchers are also investigating whether negentropy – the opposite of entropy, and in which a physical, thermodynamic or biological process creates order – are affected by trophic coherence. “The modern concept of entropy,” Johnson points out, “comes from statistical physics and is a property of ensembles, as described above – that is, the entropy of an ensemble is simply a function of the number of elements it contains.” Moreover, he adds, graph ensemble entropy has proven to be a powerful tool for understanding various network properties. We are currently studying the entropy of the coherence ensemble we defined for this work. “In general, higher trophic coherence would be associated with lower entropy states, which means that if networks are more coherent than the random expectation there must indeed be some kind of negentropic process at work.” Johnson notes that the impact in this case relative to trophic coherence would be found in quantifying the extent to which different empirical networks have been driven from their maximum entropy state. “This might be the best way of discovering when there are coherence-inducing mechanisms at work, how much energy must be involved, and ultimately identifying the nature of such processes.”

See for comparison: Feedback loops link odor and pheromone signaling with reproduction

These studies also indicate that GnRH neurons are likely to influence numerous brain functions. They appear to transmit signals to as many as 30,000 or more neurons in 34 brain areas, consistent with previous studies showing GnRH+ fibers and GnRH receptors in multiple brain regions (Badr and Pelletier, 1987; Jennes et al., 1988; Jennes et al., 1997). BL+ neurons likely to receive synaptic input from GnRH neurons were seen in areas associated with numerous different functions, including odor and pheromone processing, sexual behavior, appetite, defensive behavior, motor programs, and the relay of information to higher cortical areas. These results may reflect a strategy wherein GnRH neurons can modify diverse functions in order to coordinate the internal state of the animal and its behavior with reproduction in order to optimize reproductive success.

See my posts on Discovering Vismodegib in the Fight Against Skin Cancer: The First Approved Inhibitor of the Hedgehog Pathway
No one I know is likely to understand this link from the anti-entropic virucidal energy of sunlight to prevention of all pathology because they must first understand the fact that proteins do not create themselves. There is no need for this inhibitor of the Hedgehog pathway or inhibition of any other pathway if cancer is prevented. But most people are not willing to learn about prevention because they think they can rely on medical practitioners to effectively treat their diseases. Do you think that your physician knows anything about light scattering characterization of glycoproteins and their interactions with other proteins and antibodies?
Absolute Characterization of Glycoproteins and their Interactions with Proteins and Antibodies by Light Scattering
Light scattering can now be linked to the characterization of glycoproteins and their immune system interactions in all species on Earth. That suggests the speed of light on contact with water links energy as information to the de novo creation of the glycoproteins,
If so, the physiology of reproduction links pheromones to biophysical constraints on the creation of more glycoproteins in the context of morphological and behavioral differences in species from microbes to humans. That suggests the refutation of neo-Darwinism is complete, since the virus-driven degradation of messenger RNA has been linked to all pathology in bacteria that become archaea before virus-driven energy theft causes them to become L-forms.
Simply put, Carl Woese was wrong. There is only one domain of life and virus-driven energy theft is what destroys all life on Earth.

 

Cytosis

The Origin of Information (3)

Summary: I presented two poster sessions during the Labroots virtual conference “Neuroscience,” March 16-17, 2016
One linked sunlight to energy as the origin of information. The other linked energy as information to biophysically constrained viral latency via the pheromone-controlled physiology of reproduction in all living genera.
Additional experimental evidence of top-down causation has since confirmed that the creation of sunlight can be linked from energy as information to all biodiversity via its anti-entropic virucidal effects. The direct quantitative measurement of top-down causation supports the claims made by all serious scientists, and also refutes all the claims made by evolutionary theorists and “Big Bang” cosmologists.
See:  The Origin of Information (1) 7/28/16 From hydrogen atom transfer in DNA base pairs to ecosystems

The Origin of Information (2) 7/28/16 RNA mediated molecular epigenetics and virus driven entropy (working title: The Origin of Information)
 
A good model predicts. See also: Direct quantitative measurement of the C═O⋅⋅⋅H–C bond by atomic force microscopy

The direct measurement of the interaction with a hydrogen atom paves the way for the identification of three-dimensional molecules such as DNAs…

Reported on 7/31/17 as: Scientists Decode DNA; See and Touch the Force That Gives Us Life
My summary: Hydrogen (H) t is the most abundant energy source in the Universe. It is also an indispensable source of the energy that is required for life. The energy links nucleic acids (DNA, RNA) and proteins to the creation of life via hydrogen bonds between molecules.
Energy as information is crucial for encoding the secrets of life. Those who cannot understand the concept of energy as information cannot understand anything about the energyd-dependent creation of life or the energy-dependent physiology of pheromone-controlled reproduction, which links energy as information to all biodiversity.
For instance, the biodiversity of all morphological and behavioral phenotypes is food energy-dependent. Richard Feynman put that fact into the perspective of something that many people are intuitively able to understand.

Feynman also presciently placed the measurement of energy into its current context. He somehow knew that technological advances would someday allow serious scientists to measure the energy in a hydrogen atom and link what organisms eat to all biodiversity.
See also: Hydrogen bonds directly detected for the first time

The measured forces and distances between the oxygen atoms at the tip of the atomic force microscope and the propellane’s hydrogen atoms… show that the interaction clearly involves hydrogen bonds. The measurements mean that the much weaker van der Waals forces and the stronger ionic bonds can be excluded.

The fact that experimental evidence established the primacy of the hydrogen bond in the interactions that link energy-dependent changes from chirality to autophagy and from angstroms to ecosystems in all living genera can be placed into the context of the food energy-dependent physiology of reproduction for comparison to: Mutation-Driven Evolution, which was published on the same day in 2013 as Nutrient-dependent/pheromone-controlled adaptive evolution: a model
The good news is that neo-Darwinian theories have been replaced with Darwin’s energy-dependent “conditions of life.” That is bad news for all theorists.
For example, yesterday, Jay R. Feierman again threatened to ban me from participation on the Human Ethology Yahoo Group. Our history of friction began in 1995 but it was amplified in 2013, when I wrote:

Evolution by natural selection cannot be the outcome if something is not first selected. Selection is always for nutrients. It is as simple as that.

Feierman responded:
7/25/13
Jay R. Feierman: Variation is not nutrient availability and the something that is doing the selecting is not the individual organism. A feature of an educated person is to realize what they do not know. Sadly, you don’t know that you have an incorrect understanding [of] Darwinian biological evolution.
7/26/13
Jay R. Feierman: 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.
As first author of the award-winning review Human pheromones: integrating neuroendocrinology and ethology, I may be the only former member of the International Society for Human Ethology (1) who still participates on the yahoo group they own (2). See also their FB page (3).

  1. The International Society for Human Ethology (ISHE) promotes ethological perspectives in the scientific study of humans worldwide. We aim to achieve this goal through:
    • Encouraging empirical research in the field of human behavior, using the full range of methods developed in biology and the human behavioral sciences, and operating within the conceptual framework provided by evolutionary theory.
    • Promoting the exchange of ethological knowledge and opinions with the other empirical sciences of human behavior.
  2. The International Society for Human Ethology (ISHE), http://www.ishe.org/, a not-for-profit scientific organization, is the owner of this listserv, whose purpose is to facilitate communication among persons interested in human ethology and to attract new persons to the field. The language is English. The current moderator is Jay R. Feierman.
  3. The International Society for Human Ethology (ISHE) aims at promoting ethological perspectives in the scientific study of humans worldwide. ISHE encourages empirical research in all fields of human behavior.

If I am the only person who has detailed the facts about the Origin of Information, and Jay R. Feierman bans me from participation in the ISHE’s group, he will help to eliminate discussion of empirical research such as  Feedback loops link odor and pheromone signaling with reproduction.
There are a few other people like Jay R. Feierman, who have helped prevent the dissemination of accurate information about the Origin of Information and all biodiversity in the context of our visual perception of energy and mass, which has been placed into the context of everything known about the space-time continuum. See: Olfaction Warps Visual Time Perception.
But, to my knowledge, no one besides Jay R. Feierman has claimed that “Variation is not nutrient availability and the something that is doing the selecting is not the individual organism.” According to Feynman, Jay R. Feierman exemplifies “human idiocy.”
But, see also this comment from James Gray (August 1, 2017):

Jay,

I just want you to note my support for your warning to Jim Kohl.  Too bad that his attempts at comments are so incomprehensible.

After Feierman blocked another one of my posts to the group, I wrote:

It can only get worse from here, Jay. Even if you will not admit to the fact that you were dead wrong, others will learn that you caused the death of their loved ones via your ignorance and arrogance.
You are an example of what Feynman’s referred to as human idiocy.
 

Feierman responded (to the group)

This is warning #1. Say something equally offensive again to me in a personal email or on the group and you will be permanently banned from the Yahoo Human Ethology Group.
Sadly, no one ever responds to your posting because they are incomprehensible. I post them out of human compassion for you. But that does not give you license for being rude and flaming.
I’m copying this to the human-ethology group as well, so other members will know why you are gone from the group, if your flaming re-occurs.

Jay

Jay R. Feierman, Moderator Yahoo Human-Ethology Group

See for comparison: http://www.odedrechavilab.com/About.aspx

Our principle aim in the lab is to attack scientific dogmas. Mainly, we aim to use powerful genetic tools to discover novel biological principles by which RNA affects formation and inheritance of complex traits. While linking rare Mendelian traits to specific sequence variations has been accelerated, the genetic basis of many common diseases is not understood despite the undertaking of many genome wide association studies. It appears that our current genetic models fall short of faithfully explaining the inheritance of most complex traits.

Replaced by: Laboratory for radical science
See also: Principles of Transgenerational Small RNA Inheritance in Caenorhabditis elegans

…how these modifications regulate RNAi or small RNA inheritance was until recently unclear. Integrating the very latest literature, we suggest that changes to histone marks may instigate transgenerational gene regulation indirectly, by affecting the biogenesis of heritable small RNAs. Inheritance of small RNAs could spread adaptive ancestral responses.

The changes to histone marks are energy-dependent and they link hydrogen-atom transfer in DNA base pairs to the food energy-dependent fixation of RNA-mediated amino acid substitutions in supercoiled DNA, which prevents virus-driven energy theft from causing the degradation of messenger RNA that links mutations to all pathology.

On August 1, 2017 Jay R. Feierman wrote: 88186 “A genetic correlate of attachment and personality”

This is not a genetic correlate. The COMT VaL158Met amino acid substitution exemplifies the facts detailed in the context of: Hydrogen bonds directly detected for the first time The facts about hydrogen-atom transfer in DNA base pairs in solution have since been linked to all energy-dependent pheromone-controlled biodiversity in: Principles of Transgenerational Small RNA Inheritance in Caenorhabditis elegans

…how these modifications regulate RNAi or small RNA inheritance was until recently unclear. Integrating the very latest literature, we suggest that changes to histone marks may instigate transgenerational gene regulation indirectly, by affecting the biogenesis of heritable small RNAs. Inheritance of small RNAs could spread adaptive ancestral responses.
 

The changes to histone marks are energy-dependent and they link hydrogen-atom transfer in DNA base pairs to the food energy-dependent fixation of RNA-mediated amino acid substitutions in supercoiled DNA. The substitutions prevent virus-driven energy theft from causing the degradation of messenger RNA that links mutations to all pathology.

See for comparison: How to teach evolution when students hold creationist views

Teaching evolution is pointless.

See: Cytosis

A board game taking place inside a human cell! Players compete to build enzymes, hormones and receptors and fend off attacking Viruses!

Anyone ten years old or older will learn that natural selection for energy-dependent codon optimality is the key to healthy longevity and that the virus-driven degradation of messenger RNA links mutations to all pathology.

Light-induced-conformer-intercoversion-of-hydrogen-bond

Energy-dependent pheromone-controlled entropy (2)

See also: Energy-dependent pheromone-controlled entropy (1)
Let’s make peer review scientific

…peer review is often biased and inefficient. It is occasionally corrupt, sometimes a charade, an open temptation to plagiarists. Even with the best of intentions, how and whether peer review identifies high-quality science is unknown. It is, in short, unscientific.


The androgynous baby-faced boy or girl pictured among those wearing pink “crotch” hats appears to representing others at the March for Women. The sign may also be representing the intent of one of the organizers whose support for terrorists became better known after this March.
Next comes the March for Science, where anyone whose photo appears can be asked what area of scientific expertise most interested them. Attempts will be made to learn more about what they did to link energy-dependent changes in angstroms from sunlight to ecosystems in all living genera via hydrogen-atom transfer in DNA base pairs in solution.

See for example: Quantifying Intracellular Rates of Glycolytic and Oxidative ATP Production and Consumption Using Extracellular Flux Measurements

Abstract excerpt:

Measurement of ATP use revealed no significant preference for glycolytic or oxidative ATP by specific ATP consumers. Overall, we demonstrate how extracellular fluxes quantitatively reflect intracellular ATP turnover and cellular bioenergetics.

The energy-dependent extracellular fluxes link pheromone-controlled entropy from cellular bioenergetics to the physiology of reproduction. Virus-driven energy theft compromises the conserved molecular mechanisms of cellular bioenergetics.
See for example: Endothelial cell tropism is a determinant of H5N1 pathogenesis in mammalian species

…our study demonstrates that endothelial cell tropism is a determinant of the high virulence associated with HPAI H5N1 infection in mammalian hosts. By utilizing endogenous miRNA mediated restriction of viral tropism, we demonstrate that H5N1 infection of endothelial cells results in increased cytokine production in the lungs and loss of endothelial barrier function, which culminates in vascular leakage in the lungs. In addition, extrapulmonary spread of H5N1 virus likely occurs via the hematogenous route by infection of endothelial cells.

They link virus-driven energy theft from microRNAs in bacteria to messenger RNA degradation in archaea and L-forms (cells without walls). They fail to link energy theft to the substitution of nutrient energy-dependent amino acid substitutions in viruses, which links viruses to pathology in all living genera.
See for example: Identification of amino acid substitutions supporting antigenic change of influenza A(H1N1)pdm09 viruses

In conclusion, substitutions in or near the RBS can influence the antigenic properties of A(H1N1)pdm09 viruses. Based on the current and previous studies of antigenic change of influenza A viruses (11, 12), it is probable that emerging antigenic variants of A(H1N1)pdm09 viruses will escape from population immunity because of substitutions in or near the RBS. However, our results also suggest that the presence of antibodies directed to epitopes on seasonal A(H1N1) and A(H1N1)pdm09 viruses in much of the population limits the number of antigenic variants that can emerge to cause new epidemics.

Antigenic variants that are biophysically constrained cannot “emerge.” Nutrient stress or social stress must first break the biophysical constraints or there would be no new epidemics. That fact means that nutrient-dependent pheromone-controlled neurogenesis links the physiology of reproduction to ecological adaptations in all cell types of all individuals of all living genera, including organisms with no brain. If you start from neurogenesis in the human brain without realizing that it is pheromone-controlled, you may never learn how food odors and pheromones link the physiology of reproduction to the transgenerational epigenetic inheritance of all morphological and behavioral diversity via conserved molecular mechanisms of endogenous RNA interference.
See also from 6 years ago: Reproduction: A New Venue for Studying Function of Adult Neurogenesis?

Recent studies disclose that SVZ neurogenesis is under regulation of reproductive cues like pheromones.

Some recent debate about this fact was published to the Discover Magazine blog site in the context of accurate claims that Ben Carson made about learning and memory. A anonymous character with the screen name “Neuroskeptic” caused me to voice some concerns about the intelligence of people who accused Ben Carson, a pediatric neurosurgeon, of being wrong about anything.
See: Ben Carson and the Power of the Hippocampus 3/10/17

See also: Social phobia: Indication of a genetic cause — reported on “medicalxpress”
Excerpt: The cause of genetic illnesses often lies in the SNPs.
My comment: The energy-dependent differences in the SNPs is RNA-mediated. In this case, the differences link RNA methylation from endogenous RNA interference to learning and memory via experience-dependent cell type differentiation during life history transitions.
For example, one amino acid substitution (COMT Val158Met) was already linked to differences in the behavior of adolescents and adults. When will Neuroskeptic and others admit that they need to learn more about biologically-based cause and effect before they attack people like Ben Carson.

My comment from 3/11/17
See also:Reproduction: A New Venue for Studying Function of Adult Neurogenesis?” (2011) Cell Transplant

Excerpt: …the number of dividing neurons in the hippocampus of female sheep increased robustly (43), which is accompanied with a sharp increase in circulating luteinizing hormone. Additionally, luteinizing hormone level and hippocampal neurogenesis were also upregulated by the soiled bedding. With the use of prolactin and leutinizing hormone receptor knock-out mice, it was confirmed that the hippocampal neurogenesis is due to the increase of the luteinizing hormone but not prolactin; in contrast, prolactin is the regulatory factor of SVZ neurogenesis (69).

Neuroskeptic displayed the ignorance of all theorists and left them with no excuse to say anything more about Ben Carson, or anyone else who intends to help the President of the United States “Make America Great Again.” Only biologically uniformed liberals will continue their attempts to stop President Trump. The anti-entropic effect of pheromones on GnRH and luteinizing hormone links food odors and pheromones from feedback loops to the physiology of reproduction in all vertebrates via the substitution of the achiral amino acid glycine in position 6 of the GnRH decapeptide.

With co-authors, Donald Pfaff did this in the context of autism. For example, substitution of the achiral amino acid glycine in position 6 of the GnRH decapeptide also links food odors and pheromones from stress-linked changes and feedback loops to sex-specific gene–environment interactions via the hypothalamic-pituitary-gonadal axis.
See: Sex-specific gene–environment interactions underlying ASD-like behaviors

…we found a significant three-way interaction on corticotropin-releasing hormone receptor-1 (Crhr1) gene expression, in the left hippocampus specifically, which co-occurred with epigenetic alterations in histone H3 N-terminal lysine 4 trimethylation (H3K4me3) over the Crhr1 promoter. Although it is highly likely that multiple (synergistic) interactions may be at work, change in the expression of genes in the hypothalamic–pituitary–adrenal/stress system (e.g., Crhr1) is one of them. The data provide proof-of-principle that genetic and environmental factors interact to cause sex-specific effects that may help explain the male bias in ASD incidence.

This was reported as: Study tests the ‘three-hit’ theory of autism

…the researchers looked for molecular changes within these rodents’ brains that might help to explain the differences in behavior. They found an increase in the expression of a gene that helps to kick off stress responses, in a brain region called the left hippocampus. With help from C. David Allis’s lab, they looked for chemical alterations in the packaging of DNA that might explain this uptick in gene activity. This effort revealed one particular chemical change in the nerve cell nucleus that encourages the expression of this stress-relevant gene.

The chemical alterations are energy-dependent and RNA-mediated via methylation, which alters gene activation to help ensure that all organisms of all living genera have the best opportunity to ecologically adapt. If they fail to adapt, they die. They do not mutate and become another species.
See: Every amino acid matters: essential contributions of histone variants to mammalian development and disease  (2014) by senior author C. David Allis.
Conclusion:

…numerous histone variants seem to be restricted to specific cell lineages or tissue types, yet it remains unclear how such expression patterns are maintained and what the consequences are of increasing or reducing combinatorial variant deposition across cell types. Aberrations in these processes result in detrimental phenotypic outcomes across numerous mammalian systems, including humans. Although we are clearly still in the infancy of this ever-expanding and diverse field, we imagine that future endeavours related to histone variant biology will hold great promise for human health and disease.

The tag-team of Pfaff and Allis will continue to prevent others from what is known to all serious scientists about epigenetically-effected gene-environment interactions among all living genera. The interactions are nutrient-energy-dependent and pheromone controlled by the physiology of reproduction.
I posted this question to the CRISPR Cas 9 FB group and to the miRNA & siRNA FB group

Does any experimental evidence of biologically-based cause and effect suggest that microRNA-mediated host-induced gene silencing is not linked from biophysically constrained viral latency to energy-dependent RNA-mediated cell type differentiation via amino acid substitutions in the cell types of all living genera?

For example, could host-induced gene silencing occur outside the context of natural selection for energy-dependent codon optimality and endogenous RNA interference and the physiology of reproduction?

See also: What’s Next for Diagnostic Patents After Ariosa v. Sequenom

…we should use language that highlights the inventive piece of the invention rather than the natural law underlying it.
 
The natural law underlying all links from ecological variation to ecological adaptation could be applied to the patent for RNA-Guided Human Genome Engineering. If so, the examiners will find that host-induced gene silencing is the obvious link from nutrient energy-dependent RNA methylation to the pheromone-controlled physiology of reproduction in all living genera via Kohl’s Laws of Biology.
 
Simply put, Kohl’s Laws includes two facts:
 
1) all organisms must eat or they die.
2) all species must reproduce or they become extinct.
 

Can you imagine what the value of future patents on drugs will be if researchers continue to deny what is known about those two natural laws?

Alternative splicing of pre-mRNA

Did evolution autophosphorylate your kinases? (3)

Did evolution autophosphorylate your kinases? (1)
Did evolution autophosphorylate your kinases? (2)
See also:

N6-Methyladenosine in Flaviviridae Viral RNA Genomes Regulates Infection

Reported as: Chemical tags affect ability of RNA viruses to infect cells

Dynamics of Human and Viral RNA Methylation during Zika Virus Infection

Reported as:  Zika virus infection alters human and viral RNA

My comment: Virus-driven hecatombic evolution of all pathology is linked from the failure of energy-dependent phosphorylation to biophysically constrain the RNA-mediated damage to DNA via fixation of amino acid substitutions in the cell types of all living genera.

It is now perfectly clear to all serious scientists that evolution did not autophosphorylate their kinases.

See how nutrient energy-dependent phosphorylation must occur to regulate transcription in the context of chromatin remodeling, linked to supercoiled DNA and to chromosomal rearrangements that link RNA-mediated amino acid substitutions to all biodiversity via differences in energy-dependent morphological and behavioral phenotypes.

For example: Chromatin Kinases Act on Transcription Factors and Histone Tails in Regulation of Inducible Transcription
Excerpt:

Chemical inhibition of MSKs selectively targets inducible transcription

My comment: Even C. David Allis has been forced to admit to the facts about chemical ecology that I placed into the context of this model.
Nutrient-dependent/pheromone-controlled adaptive evolution: a model

THIS MODEL DETAILS HOW CHEMICAL ECOLOGY DRIVES ADAPTIVE EVOLUTION VIA: (1) ecological niche construction, (2) social niche construction, (3) neurogenic niche construction, and (4) socio-cognitive niche construction. This model exemplifies the epigenetic effects of olfactory/pheromonal conditioning, which alters genetically predisposed, nutrient-dependent, hormone-driven mammalian behavior and choices for pheromones that control reproduction via their effects on luteinizing hormone (LH) and systems biology.

Everything published by serious scientists since then attests to the facts that link polycombic ecological adaptations from our 1996 review with its section on molecular epigenetics.
See: From Fertilization to Adult Sexual Behavior
Unfortunately, pseudoscientists and supporters of the evolution industry have tried to prevent the dissemination of accurate information about nutrient-dependent RNA-mediated cell type differentiation in the context of the pheromone-controlled physiology of reproduction in species from microbes to humans.
Others went so far as to invent the term oncohistone in an attempt to link virus-driven hecatombic evolution to beneficial mutations rather than admit that virus-driven energy theft is the link to all pathology in all living genera.
See: Histone H3K36 mutations promote sarcomagenesis through altered histone methylation landscape
Reported as: Gene regulatory mutation linked to rare childhood cancer
Excerpt:

Because the DIPG mutation always changed the same amino acid in the same location in the histone gene, Lewis knew something was special about it.

My comment: Unfortunately, Lewis did not seem to know that energy-dependent changes in RNA-mediated amino acid substitutions are linked to healthy longevity in all living genera or that virus-driven energy theft links amino acid substitutions in viruses to all pathology.

amino acid homeostasis

Base pairs, olfaction and RNA thermometers

Excerpt:

The stem-loop can be stabilized by strengthening the base pairing between the fourU element and SD sequence through the substitution of G-C base pairs, and this results in an elevated melting temperature (10).

Conclusion:

RNA thermometers represent a simple yet elegant mechanism for controlling temperature-dependent gene expression and may be more widespread among pathogenic bacteria that interact with mammalian hosts than is currently known.

See also:  MicroRNA Stability in FFPE Tissue Samples: Dependence on GC Content

Excerpt:

GC-poor miRNAs (GC<40%) were shown to be more degraded than GC-rich miRNAs. Although miRNAs are more robust than mRNAs, the deep sequencing data obtained using FFPE samples cannot be directly compared with the data obtained using fresh frozen tissue samples. The miRNA read counts in FFPE specimens are comparable only if the samples are prepared under the constant fixation conditions, and using the same sequencing protocol.

My comment: Energy-dependent changes link thermodynamic cycles of protein biosynthesis and degradation via the microRNA/messenger RNA balance. The balance links hydrogen-atom transfer in DNA base pairs in solution to microRNA flanking sequences, which have been linked from the de novo creation of olfactory receptor genes and other G protein-coupled receptors (GPCRs). The GPCRs are linked to all healthy longevity in all living genera. Loss of the GPCRs links virus-driven energy theft to all pathology via loss of functional structures in the olfactory glomeruli in the Drosophila antennal lobe.

See for instance: Elucidating the Neuronal Architecture of Olfactory Glomeruli in the Drosophila Antennal Lobe
Conclusion:

… our study demonstrates that each glomerulus is a unique morphological and functional unit whose significance regarding odor detection and odor-guided behavior can be predicted. Future studies dedicated to elucidating the synaptic connectivity in more detail will reveal whether ultrastructural characteristics of individual glomeruli are also correlated with functional properties.

Reported as: The basic units of the olfactory system in the fly brain provide references to their function and ecological relevance
Excerpt:

Because these new insights are not limited to the vinegar fly, and may also apply to other animals or even humans, they have far-reaching significance.

My comment: Anna Di Cosmo’s group has linked the far-reaching significance from all invertebrates to all vertebrates via the conserved molecular epigenetics of biophysically constrained energy-dependent cell type differentiation in species from microbes to humans.

See: Role of olfaction in Octopus vulgaris reproduction

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).

See also: Olfactory organ of Octopus vulgaris: morphology, plasticity, turnover and sensory characterization

Excerpt:

Olfactory sensory cells in all vertebrates are characterized by cycles of birth, maturation, and death (Graziadei and Monti Graziadei, 1978). This proliferation is remarkable given that the olfactory receptor cells are neurons, cells that are not generally considered to undergo neurogenesis in adults. The same labeling technique used to document turnover in vertebrates shows that OSNs in the anterior tentacles (olfactory organs) of snails also turn over (Chase and Rieling, 1986). Functional constancy in diverse groups of animals argues that turnover is a common adaptive property of OSNs. We verify the presence of OSNs proliferation in O. vulgaris based on the presence and distribution of PCNA immunoreactivity.

My comment: Thermodynamic cycles of RNA-directed DNA methylation link energy-dependent amino acid substitutions to cell type stability in all cell types of all individuals of all living genera via the physiology of reproduction.

See: Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors

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, and diseases of the X chromosome (Honeybee Genome Sequencing Consortium, 2006). Included among these different aspects of eusocial species survival are learning and memory, as well as conditioned responses to sensory stimuli (Maleszka, 2008; Menzel, 1983).

See also: DNA Methylation Adjusts the Specificity of Memories Depending on the Learning Context and Promotes Relearning in Honeybees

Following olfactory reward conditioning proteins catalyzing DNA methylation (i.e., DNA methyltransferases, Dnmts) and demethylation (i.e., ten–eleven translocation methylcytosine dioxygenase, Tet) are upregulated and DNA methylation levels change in memory-associated genes (Biergans et al., 2015).

My comment to the  “Frontiers site”

Re: …that epigenetic regulation of memory specificity might be conserved across animals.

Anna Di Cosmo’s group addressed that fact in the context of the Octopus model organism.

See: Role of olfaction in Octopus vulgaris reproduction http://www.ncbi.nlm.nih.gov/pubmed/25449183

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).

See also: Olfactory organ of Octopus vulgaris: morphology, plasticity, turnover and sensory characterization http://bio.biologists.org/content/early/2016/04/06/bio.017764

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

This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent pheromone-controlled ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity in species from microbes to man.

My comment: All conditioning paradigms are energy-dependent and they link the energy from the innate immune system to learning and memory. RNA methylation is linked from RNA-directed DNA methylation and energy-dependent fixation of RNA-mediated amino acid substitutions. Transgenerational epigenetic inheritance of biologically-based cause and effect links the physiology of reproduction to supercoiled DNA, which protects all organized genomes from virus-driven entropy.

See also: The Buzz about Honey Bee Viruses

See also: Distinct Circuits for the Formation and Retrieval of an Imprinted Olfactory Memory

See also: Rockefeller neuroscientist Cori Bargmann to lead science work at Chan Zuckerberg Initiative

See my attempt to discuss this on the Neuroscience FB group.

Scientists at the Max Planck Institute for Chemical Ecology in Jena, Germany, have now quantified and mapped the functional units of the olfactory center in the brains of vinegar flies responsible for the perception of odors.

Alternative splicing of pre-mRNA

Chromatin: The structure of DNA (2)

A Genetically Encoded Probe for Live-Cell Imaging of H4K20 Monomethylation
Excerpt (with my emphasis):

Highlights
•    A histone H4K20me1-specific live-cell probe, H4K20me1-mintbody, was developed.
•    Dynamics and replication timing of Xi were visualized.
•    Critical amino acids for the stability and/or folding of the mintbody were revealed.

Reported as: Catching histones by the tail: A new probe to track histone modifications in living cells

Excerpt:

H4K20me1 is most likely associated with the tight packing of a redundant (inactivated) female X chromosome (Xi) into heterochromatin. In a roundworm Caenorhabditis elegans model, Prof. Kimura and colleagues showed that the H4K20me1-mintbody could be used to monitor changes in H4K20me1 over the cell cycle and localization of dosage-compensated X chromosomes without disrupting cell function.

Also reported as: New Probe Detects Histone Modifications in Live Cells

Excerpt:

Using genetic analysis and X-ray crystallography, the new work has also identified amino acids that are critical to the solubility and conformational stability of the H4K20me1-mintbody. Aberrant folding of the antibody fragments in the cellular cytoplasm usually causes solubility problems…

My comment: The nutrient-dependent pheromone-controlled cell cycle and localization of dosage-compensated X chromosomes links  Max Tegmark’s claims about reorganized food and consciousness via the physiology of reproduction in Caenorhabditis elegans and other model organisms. The research results reported above link RNA methylation, learning and memory to RNA-directed DNA methylation via the addition of a methyl group or groups to histone H4 at the lysine 20 position (H4K20).

That energy-dependent change in methylation links biophysically constrained biologically-based cause and effect from yeast to humans. For instance, X-inactivation is closely linked from chromosomal rearrangements to sex differences in morphological and behavioral phenotypes in humans.

In the most recent report, they did not jump to humans from sex differences in the cell types of yeasts. Instead, they used the nematode, Caenorhabditis elegans as a link between the H4K20me1-mintbody and changes in methylation (i.e., H4K20me1) during the cell cycle at the cellular location of X-inactivated chromosomes. That’s how increasing orgaanismal complexity from yeasts to humans was again placed into the context of fixed RNA-mediated amino acid substitutions. I will reiterate this claim:

•    Critical amino acids for the stability and/or folding of the mintbody were revealed.

They identifies the amino acids that are critical to the solubility and conformational stability of the H4K20me1-mintbody and critical to cell type differentiation in all cell types of all individuals of all species. They linked X-inactivation and chromosomal rearrangements from aberrant RNA-mediated protein folding biochemistry to the solubility problems caused by antibody fragments in the cellular cytoplasm and found a potential solution to the problem.

The problem they are trying to solve is different than mine.  I gave up trying to solve the problem of how to explain the origin of sex differences in cell types in species from yeasts to humans by putting the explanation in terms that educated laypersons might understand. Even other scientists won’t admit to knowing anything about amino acid substitutions and cell type differentiation. Meanwhile, neo-Darwinian theorists are trying to bury any explanation for the origin of sex difference in cell types so that evolution via mutations and evolution can continue to be used as an explanation for all biodiversity, including the diversity in male and female gametes.

However, no experimental evidence of biologically-based cause and effect suggests that X-inactivation “evolved” via mutations and natural selection. And no experimental evidence of biologically-based cause and effect suggests that sex difference in cell types “evolved.”

These researchers overcame the challenges involved in explaining that fact to biologically uninformed theorists by evaluating the performance of antibody fragments in live cells. Unfortunately, explaining the complexity of X-inactivation to an educated layperson may not be possible — especially if that person thinks that sex differences “evolved” via mutations and natural selection.

Until many others accept the fact that nutrient energy-dependent fixation of RNA-mediated amino acid substitutions in the context of the physiology of reproduction is the link to all biodiversity and all cell type, most theorists will not be encouraged to learn more about how virus-driven energy theft is linked to all pathology. If they don’t understand biologically-based cause and effect, they are not likely to understand the need to link thermodynamic cycles of protein biosynthesis and degradation to the molecular mechanisms of biodiversity.

See also:

My comment: The epigenetic effects of nutrients on intracellular signaling and stochastic gene expression appear to enable ecological adaptations in the context of tightly controlled organism-level thermoregulation in mammals. Nutrient-dependent single amino acid substitutions and de novo protein biosynthesis exemplify the involvement of the seemingly futile thermodynamic control of intracellular and intermolecular interactions in microbes that result in stochastic gene expression.
Thermodynamically “futile” cycles of RNA transcription and degradation also are responsible for changes in pheromone production that enable accelerated changes in nutrient-dependent adaptive evolution controlled by the microRNA/messenger RNA (miRNA/mRNA) balance. Environmental cues, like those that signal the availability of glucose, appear to cause changes in the miRNA/mRNA balance that enable gene expression during developmental transitions required for successful nutrient-dependent reproduction in species from microbes to humans.
The facts about protein biosynthesis and degradation show that the thermodynamic cycles are nutrient energy-dependent and the facts link virus-driven energy theft to all pathology via conserved molecular mechanisms of biophysically constrained RNA-mediated protein folding chemistry that prevent one species from evolving into another via mutations and natural selection.
See for comparison: Broad histone H3K4me3 domains in mouse oocytes modulate maternal-to-zygotic transition

Abstract excerpt:

Active removal of broad H3K4me3 domains by the lysine demethylases KDM5A and KDM5B is required for normal zygotic genome activation and is essential for early embryo development. Our results provide insight into the onset of the developmental program in mouse embryos and demonstrate a role for broad H3K4me3 domains in MZT.

My comment: They must think everyone knows the importance of amino acid substitutions that link lysine to biophysically constrained energy-dependent cell type differention or from mutations to pathogy. There is no mention of lysine demethylases outside the context of nutrient energy-dependent RNA-mediated amino acid substitutions and no mention of lysine in the context of virus-driven energy theft. The only indication that they know how important the difference may be is their citation to: Trapnell, C. et al. Transcript assembly and quantification by RNA-Seq reveals unannotated transcripts and isoform switching during cell differentiation. Nat. Biotechnol. 28, 511–515 (2010).

The isoform switching is energy-dependent and RNA-mediated.

That fact was missing from this report of their work: Breakthrough genomics technique can be used to map epigenetic marks across the genome using fewer cells

Excerpt:

Very soon after fertilization, the control of embryonic development shifts from pre-existing maternal gene products to the products of genes encoded by the early embryo (or zygote). This passing of the genetic baton, called the maternal-to-zygotic transition (MZT), is poorly understood because existing technologies have generally been too insensitive to capture the full scale of the epigenetic changes it entails across the zygotic genome.

See for comparison: From Fertilization to Adult Sexual Behavior
Excerpt:

The Genome, positioning, timings. There are major structural differences between the X and Y chromosomes; e.g., centromeric aiphoid repeats sequences and distribution of heterochromatin (Graves, 1995; Wolfe et al., 1985). These structural differences correlate with sexually dimorphic chromosomal positioning within the nucleus and with male/female differences in replication timing of the active X, the inactive X, and the Y chromosomes, e.g., Boggs and Chinault (1994), Clemson and Lawrence (1996); Hansen, Canfield, and Gartler (1995). Increasingly the structure and timings within the nucleus are realized as contributing to gene expression regulation (Manders, Stap, Strackee, van Driel, and Aten, 1996; Stein, Stein, Lian, van Wijnen, and Montecino, 1996).

My comment: Our next section title was Molecular distance and the one after that was Molecular epigenetics. In the section on molecular epigenetics, we wrote:

Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (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.

We did not link any aspect of RNA-mediated cell type differentiation from natural selection and evolution to sex differences in cell types or differences in somatic cell types. Why not? Because no experimental evidence suggests ecological variation can be linked to ecological adaptation via anything except energy-dependent fixation of RNA-amino acid substitutions in the context of the physiology of energy-dependent reproduction. All aspects of nutrient-dependent pheromone-controlled reproduction have been repeatedly linked from feedback loops to all biodiversity in all living genera. See: Feedback loops link odor and pheromone signaling with reproduction

See for comparison: Evolutionary learning of adaptation to varying environments through a transgenerational feedback

Excerpt:

The molecular basis of this learning mechanism could be searched for in model organisms showing epigenetic inheritance.

My comment: The transgenerational epigenetic inheritance of molecular mechanisms of learning is energy-dependent and transgenerational epigenetic inheritance is linked from RNA methylation to supercoiled DNA via the innate immune system in all model organisms. Simply put, transgenerational epigenetic inheritance is energy-dependent and controlled by the physiology of reproduction.
 
If individuals of a species cannot find food, or if virus-driven energy theft steals the energy they need to support biophysically constrained protein folding chemistry and error-free reproduction, the species is on its way to becoming extinct.

Zika virus damaged DNA is an example of how quickly one insect species can ecologically adapt to a virus that is transmitted to the humans with unrepaired DNA . The damage is manifested as changes in craniofacial morphology and brain development in the context of one base pair change and one amino acid substitution in the virus compared to failed ecological adaptation in primates.

Dobzhansky (1973) tried to put that fact into the context of primate ecological adaptation.

See: Nothing in Biology Makes Any Sense Except in the Light of Evolution

Excerpt:

…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: Combating Evolution to Fight Disease

Excerpt:

The evolutionary biologist Theodosius Dobzhansky famously noted that “nothing in biology makes sense except in the light of evolution,” but perhaps, too, “nothing in evolution makes sense except in the light of biology.” Although the latter might be an exaggeration, an important gap is being filled by molecular understanding of the genesis of variation that confers the ability to evolve.

My comment: RNA-mediated learning and memory link ecological variation to ecological adaptation. Nothing links the energy-dependent RNA-mediated genesis of variation to the ability to evolve. Ecological adaptation is energy-dependent and biophysically constrained. Neo-Darwinian theories were invented by people who did not know that, or refused to admit it. Why hasn’t everyone complained that their theories are ridiculous so that people do not keep adding to the pseudoscientific nonsense?

See also: Paul Allen’s Latest Surprising Revelation About The Human Brain

See also: The nexus of vitamin homeostasis and DNA synthesis and modification in mammalian brain

See also: Sex-biased chromatin and regulatory cross-talk between sex chromosomes, autosomes, and mitochondria

Excerpt:

Crudely defined molecular mechanisms, however, have prevented a better understanding of genetic variants mediating sexually dimorphic expression.

My comment: All definitions of molecular mechanisms are useless to serious scientists who have linked energy-dependent changes from angstroms to ecosystems by starting with the sun’s biological energy.

See also: Plant RNAs Found in Mammals

My September 20, 2011 comment to the Scientist about this fact now appears to be attributed to an anonymous source

This important finding in mammals is predicted by an insect model in which the diet of the honeybee queen and her pheromones determine everything about the success of the hive including the neuroanatomy of worker bee brains.

The honeybee already serves as a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, development, mental health, longevity, and diseases of the X chromosome. Included among these different aspects of eusocial species survival are learning and memory as well as conditioned responses to sensory stimuli, like food odors, and the social odors called pheromones. Thus, the honeybee model also predicts that the behavior of mammals will be influenced by food odors, nutrition, and pheromones to the same degree that chemical stimuli influence the behavior of every other species on the planet.

In mammals, of course, the epigenetic effects of pheromones in the mother’s milk are clearer, perhaps even to non-biologists.

See also: Sequencing Reveals Genomic Diversity of the Human Brain
Excerpt:

Researchers examine the role of long interspersed element-1 retrotransposition in neuronal mosaicism.

My comment: Somatic mosaicism is nutrient energy-dependent and controlled by the physiology of reproduction in plants and animals.
 Plant RNAs Found in Mammals (revisited)

MicroRNAs from plants accumulate in mammalian blood and tissues, where they can regulate gene expression.

Today’s comment: Energy-dependent changes in the microRNA/messenger RNA balance are linked to healthy longevity, and virus-driven energy theft is linked to all pathology via conserved molecular mechanisms.
See also: Abiogenesis: A Theory on The Origins of Life
My comment from last year:
See: Common origins of RNA, protein and lipid precursors in a cyanosulfidic protometabolism

Didn’t Sutherland’s group link the speed of light on contact with water to the de novo creation of nucleic acids and the biophysically constrained chemistry of nutrient-dependent RNA-mediated protein folding in accord with Schrodinger’s claim about the anti-entropic epigenetic effect of the sun?

See also: Study shows lack of interest in sex successfully treated by exposure to bright light

Excerpt:

The researchers also found that testosterone levels increased in men who had been given active light treatment. The average testosterone levels in the control group showed no significant change over the course of the treatment – it was around 2.3 ng/ml at both the beginning and the end of the experiment. However, the group given active treatment showed an increase from around 2.1 ng/ml to 3.6 ng/ml after two weeks.

See also: Chromatin: The structure of DNA (3)

diseases-disorders

The Aquatic Ape / Waterside Ape divergence

See also: The Aquatic Ape: New evidence? (9/8/16)
Walt Patrick 

Now that I’m semi-retired…. My major focus is the development of village-scale energy sovereignty.
I believe that sustainable community stands on an interlocking foundation of effective and sustainable energy systems, and I’m working to develop ways that a community can meet its energy needs without having to rely on multi-national energy corporations.

My comment: Thanks to Walt for introducing me to Elaine Morgan’s work. He loaned me his copy of “The Aquatic Ape” in 1982. Thanks to Janissa Wilson for introducing me to Walt Patrick. Thirty-four years have passed, and I remember their friendship and their influence as if it was only yesterday.
See (from yesterday and earlier today):
The Waterside Ape — Sir David Attenborough considers whether new evidence will help a once widely ridiculed theory of human origins move towards to mainstream acceptance.
My comment: He takes a giant step forward in an obvious attempt to keep biologically uninformed theorists from being subjected to ridicule because they missed the paradigm shift.
He then takes small steps backwards to put the “The Aquatic Ape” back into the context of ridiculous theories, which he uses to link his divergence from claims in the “The Aquatic Ape.” He needs an evolutionary theory to evolve one theory into a new theory that becomes “The Waterside Ape.” Otherwise, he gets credit for nothing more than finally acknowledging what serious scientists have known for several decades.
The reports on the efforts of the serious scientists are exemplary. So is the attempt to put them all into the context of evolutionary theory at a time when energy-dependent changes have been linked from angstroms to ecosystems in all living genera in the context of energy as information.
See also:  A Chat with Information Scientist Pedro Marijuán
I’ve commented twice on this article, which is  on Suzan Mazur’s blog site, and both comments were promptly removed.
See for comparison: Kalevi Kull: Censorship & Royal Society Evo Event
My Jul 31, 2016 11:51am comment has not yet been removed:

James Kohl Founder at RNA-mediated.com

This response may not, at first, appear to be directed against the claims you have supported with your series of interviews. But watch closely as they squirm under the weight of experimental evidence that collectively refutes their ridiculous theories and philosophy.

The Origin of The Extended Evolutionary Synthesis: An Interview with Massimo Pigliucci

Moving forward:

Claims linked to the Extended Evolutionary Synthesis have since run out of “wiggle room”. Listen to: The Waterside Ape, which closes the case on how the nutrient-energy-dependent pheromone-controlled physiology of reproduction links ecological variation to ecological adaptation via RNA methylation and RNA-mediated amino acid substitutions in supercoiled DNA, which differentiates all cell types in all living genera.

part 1
part 2
Ongoing attempts have failed to place everything known about biophysically constrained RNA-mediated protein folding chemistry and epigenetic effects on supercoiled DNA into the context of evolution. The attempts will continue to fail until researchers and theorists stop trying to make what is known fit into their theories about millions of years of evolution. No experimental evidence of biologically-based cause and effect links what is known about energy-dependent changes from angstroms to ecosystems in all living genera.
See also: Elaine Morgan is a tenacious proponent of the aquatic ape hypothesis: the idea that humans evolved from primate ancestors who dwelt in watery habitats. Hear her spirited defense of the idea — and her theory on why mainstream science doesn’t take it seriously.

See for comparison: Study Links RNA Alterations to Stomach Cancer  September 14, 2016

Written By: Xuan Pham Science Writer, PhD LabRoots

Description: I am a human geneticist, passionate about telling stories to make science more engaging and approachable.

For comparison: I am a medical laboratory scientist who has followed the literature on biologically-based cause and effect since 1982.

The historical perspective on the current literature clearly states this:

For several years it has been apparent that an ecological approach is imperative for all studies in population genetics, including those pertaining to man. It also offers a potentially useful point of view to the physical anthropologist, the ethnologist, and the archeologist, and it should provide an important integrative bridge between the various fields of anthropology. — Blood, Bulbs, and Bunodonts: On Evolutionary Ecology and the Diets of Ardipithecus, Australopithecus, and Early Homo

See also: Unravelling the genetic mystery behind mitochondrial disease

Excerpt:
Mitochondrial disease is an illness that robs its sufferers of energy, and damages muscles and major organs like the brain and heart. About one in 5000 babies – or one Australian baby born each week – are born with a severe form of the disease, which can often lead to an early death.

My comment: Virus-driven energy theft of quantised energy is the cause of all pathology. That fact is not a genetic mystery. It is fact known to all serious scientists who understand why Church et al., (2015) applied for this patent RNA-Guided Human Genome Engineering.

Viruses steal the energy that all cell types require for cell-type differentiation, which links ecological variation to ecological adaptation and healthy longevity in the absence of excess nutrient-stress and/or excess social stress. Stress-linked pathology is manifested when changes in hydrogen-atom transfer in DNA base pairs in solution facilitate codon usage in codon usage that enables their proliferation and prevent cell type differentiation.

The energy stolen by viruses is quantised energy:

See: A quantum theory for the irreplaceable role of docosahexaenoic acid in neural cell signalling throughout evolution

My comment: This is not a quantum theory of neural cell signalling throughout evolution. It exemplifies what is know to serious scientists about the obvious links from ecological variation to ecological adaptation, which is nutrient-energy-dependent and pheromone-controlled in species from microbes to humans.

See also: Two fatty acyl reductases involved in moth pheromone biosynthesis 7/18/16

Studies over the last two decades have pinpointed that the epigenetic effect of pheromone-driven adaptive evolution is one of the major factors driving the successful diversification of Lepidopteran insects10. In moths, a few substitutions in critical amino acids in the key pheromone biosynthetic enzymes are sufficient to create a novel pheromone component11,12.

See also: Role of olfaction in Octopus vulgaris reproduction 1/1/15

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).

Kohl (2013) Nutrient-dependent/pheromone-controlled adaptive evolution: a model is also cited in Two fatty acyl reductases involved in moth pheromone biosynthesis.

In my 2013 review, 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’.

The criticisms of my 2013 review may be of interest in the criticisms of Elaine Morgan’s works, since there is still no other model that links ecological variation to ecological adaptation.

In his Criticisms of the nutrient-dependent pheromone-controlled evolutionary model, Andrew Jones wrote:

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.

Andrew Jones did not offer any other model for comparison. He seemed to think that he could support his criticisms via his claim in his thesis:

Despite their challenges, ribozymes have made an interesting niche for themselves in the field of abiogenesis. The evolution of a successful RNA polymerase ribozyme is a lofty goal. While its discovery would not be the be-all and end-all of abiogenesis research, it would represent an important stepping stone between prebiotic chemistry and life. The encapsulation of such a ribozyme is also an important step, as it would enable a system of heredity and evolution through natural selection. Based on progress in current research, it is only a matter of time before that ribozyme is discovered.

The current state of college education in the United States of American and perhaps elsewhere is reflected in the thesis by Andrew Jones as a continuation of the pseudoscientific nonsense that is used to support hypothesis-free science with claims that a system of heredity and evolution through natural selection may exist outside the context of any model that links energy-dependent changes from angstroms to ecosystems in all living genera.

See this invited review of nutritional epigenetics, for example: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems 4/10/14

Abstract:

This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent pheromone-controlled ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity in species from microbes to man. Species diversity is a biologically-based nutrient-dependent morphological fact and species-specific pheromones control the physiology of reproduction. The reciprocal relationships of species-typical nutrient-dependent morphological and behavioral diversity are enabled by pheromone-controlled reproduction. Ecological variations and biophysically constrained natural selection of nutrients cause the behaviors that enable ecological adaptations. Species diversity is ecologically validated proof-of-concept. Ideas from population genetics, which exclude ecological factors, are integrated with an experimental evidence-based approach that establishes what is currently known. This is known: Olfactory/pheromonal input links food odors and social odors from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man during their development.

In 2004, Elaine Morgan suggested it might be another 10 years before her concept of ecological adaptation gained more acceptance. If not for students like Andrew Jones, acceptance of historical works that link angstroms to ecosystems in all living genera via experimental evidence of biologically-based cause and effect would already be accepted. Until the experimental evidence is accepted and the theories are declared by all serious scientists to be ridiculous, you and your loved ones will suffer and die from virus-driven pathology. Why aren’t you already as sick of that as I am after 40 years experience as a medical laboratory scientist?

 

rp_levels-of-organization.jpg

Biophotonics, glycobiology, quantized biodiversity (2)

From Fertilization to Adult Sexual Behavior (1996)
In our section on Molecular epigenetics, we wrote:

Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.

My comment: Serious scientists have since learned that all cell type differences arise from alternative splicings of otherwise identical genes. Pseudoscientists still make claims about the emergence of life and link natural selection to structural biology and the function of genome organization.

See for comparison: A Big Bang in spliceosome structural biology (2016)

Excerpt:

Splicing cycles through a series of steps in which the spliceosome assembles on the intron-containing pre-mRNA, defining the boundaries between exons—the sequences ultimately retained in the mature mRNA—and introns (see the figure, panel A).

My comment: Energy-dependent changes in angstroms to ecosystems link the defined boundaries between exons and introns from ecological variation to ecological adaptation and all biodiversity.  The “Big Bang” in structural biology is a contextualized polite way to tell theoretical physicists and other theorists that energy-dependent changes in functional structures must link ecological variation to ecological adaptation via what is known to serious scientists about all the links from angstroms to ecosystems in all living genera. Others have been trying to tell theorists how to link biologically-based cause and effect for several years.

See for example (2007): The MicroRNA miR-124 Promotes Neuronal Differentiation by Triggering Brain-Specific Alternative Pre-mRNA Splicing
Excerpt:

Both microRNAs and alternative pre-mRNA splicing have been implicated in the development of the nervous system (NS), but functional interactions between these two pathways are poorly understood.

My comment: All serious scientists know that the functional interactions among microRNAs and alternative pre-mRNA splicing are nutrient energy-dependent and controlled by the physiology of reproduction. Do you know how energy-dependent RNA methylation links biophysically constrained protein folding chemistry to cell type differentiation via RNA-mediated amino acid substitutions? If not, you probably do not know why  information about amino acid substitutions was left out of the claim that linked chromatin to the control of behavior in this misrepresentation:
Chromatin controls behavior
Conclusion:

…the discoveries of Yang et al. are an important addition to an emerging literature implying a dynamic epigenome in the central nervous system (14, 15), which is contrary to the prevailing dogma in the epigenetics field.

My comment: There is no prevailing dogma in the epigenetics field. The dogma was eliminated when serious scientists linked energy-dependent changes from angstroms to ecosystems via epigenetic effects of sensory input on the innate immune system; the de novo creation of G protein-coupled receptors; the physiology of reproduction, and fixation of RNA-mediated amino acid substitutions that link supercoiled DNA to protection from virus-driven energy theft and genomic entropy in all organized genomes of all living genera.
See also: Chromatin remodeling inactivates activity genes and regulates neural coding.
Summary: Epigenetic regulation in the brain

The activity of neurons in the brain controls the transcription of genes that influence the pruning of dendritic connections between neurons, and such modifications can influence animal behavior. Yang et al. propose a role for chromatin remodeling by the nucleosome remodeling and deacetylase complex (NuRD) in the inactivation of such activity-dependent transcription in the mouse cerebellum (see the Perspective by Sweatt). Deposition of the histone variant H2A.z at promoters of activity-dependent genes required the NuRD complex. Loss of the NuRD complex function resulted in hypersensitivity of mice to sensory stimuli and excessive neuronal connectivity in animals performing a task on a treadmill.

This article was reported as: Ability to turn off genes in brain crucial for learning, memory
Excerpt (with my emphasis):

One process that controls chromatin structure and transcription is chromatin remodeling by energy-dependent protein complexes (4). Such complexes that depend on adenosine 5′-triphosphate (ATP) can control gene expression by moving, ejecting, or restructuring nucleosomes, the scaffolds around which DNA wraps. Each nucleosome contains a core particle of eight histone protein subunits (5). Remodeling events include posttranslational modifications, swapping individual One process that controls chromatin structure and transcription is chromatin remodeling by energy-dependent protein complexes (4). Such complexes that depend on adenosine 5′-triphosphate (ATP) can control gene expression by moving, ejecting, or restructuring nucleosomes, the scaffolds around which DNA wraps. Each nucleosome contains a core particle of eight histone protein subunits (5). Remodeling events include posttranslational modifications, swapping individual histone subunit isoforms into and out of the core particle, and facilitating the unbinding of DNA from the core particle.
into and out of the core particle, and facilitating the unbinding of DNA from the core particle.

My comment: Chromatin remodeling is energy-dependent. But, they buried the facts about how energy-dependent chromatin remodeling links sensory input from learning and memory to fixation of RNA-mediated amino acid substitutions. The substitutions differentiate all cell types of all individuals of all living genera, which explains why they invented the term histone subunit isoforms.
Serious scientists understand why pseudoscientists bury facts by stringing words together without telling others what a histone subunit isoform is, or what differentiates one histone subunit isoform from any other histone subunit isoform. In this case, the wordplay prevents others from learning that the availability of nutrients and nutrient energy-dependent changes links link fixation of RNA-mediated amino acid substitutions from learning and memory to chromatin remodeling and the control of behavior. Pseudoscientists tend to remove facts from consideration and remove the facts from the context of via well established pathways that link the epigenetic landscape to the physical landscape of supercoiled DNA  in all living genera.
See for example: Roles of Mutation and Selection in Speciation: From Hugo de Vries to the Modern Genomic Era
Excerpt:

…we will not consider geographical and ecological factors because of space limitation. Our primary purpose is to clarify the roles of mutation and selection in the evolution of reproductive isolation and show that the molecular basis of speciation is more complicated than generally thought at present. (p. 813)

My comment: Inventing the term histone subunit isoform outside the context of geographical and ecological factors is another way to dismiss the complexity of speciation.
See for example: This article mentions a subunit isoform in the context of Loss of the V-ATPase B1 Subunit Isoform Expressed in Non-Neuronal Cells of the Mouse Olfactory Epithelium Impairs Olfactory Function
Excerpt:

The present study is the first to indicate the relevance of the VATPase, and presumably of V-ATPase-mediated proton secretion, in olfactory function. Undoubtedly, further functional and behavioral studies will allow a more comprehensive assessment of the physiological and clinical significance of V-ATPase expression in sustentacular and microvillar cells of the olfactory epithelium. At this point, we can only speculate on such possibilities. For example, modulating olfactory H+ secretion could offer the ability of up- or down-regulating the threshold of detection for certain odorants. Moreover, since the NML plays a role as a barrier against inhaled pathogens, and microbial and chemical toxins, regulating mucus pH may be relevant for protection against various specific diseases.

My comment: If you are unable to link the modulation of olfactory H+ secretion from hydrogen-atom transfer in DNA base pairs in solution to the de novo creation of G protein-coupled receptors and all energy-dependent biodiversity via RNA-mediated amino acid substitutions, please see:
Every amino acid matters: essential contributions of histone variants to mammalian development and disease.
Excerpt:

The introduction of these minor sequence variants into chromatin is physiologically relevant and fundamental to eukaryotic cellular plasticity. However, with the exception of substitutions towards modification permissive amino acids (for example, both H3.1A31 and H3.2A31 to H3.3S31, which can be phosphorylated), it remains unclear how histone variants acquire and/or differentially enrich for specific chemical modifications that are distinct from their canonical counterparts.

My comment: They just muddied the perfectly clear waters of how phosphorylation and fixation of RNA-mediated amino substitutions is links from biophysically constrained protein folding chemistry to all biodiversity via hydrogen-atom transfer in DNA base pairs in solution.   The claim that “every amino acid matters” is placed into the context of what is not known about biophysically constrained protein folding chemistry and biologically-based cause and effect. That is a way to help ensure these researcher get more funding. It’s a common tactic. If you focus on what is not known, people will think it’s not known to serious scientists who are funded to produce results that are supported by their experimental evidence of biologically-based cause and effect.

See also my comment on RNA and dynamic nuclear organization

Excerpt:

Moving forward, if RNA-mediated events organize the cell nucleus, mutations manifested in perturbed protein folding are not likely to lead to natural selection and the evolution of biodiversity. The requirement for DNA to be found in organized genomes is biophysically constrained via the conserved molecular mechanisms of protein biosynthesis and degradation in species from microbes to man.

For simplicity, see:

See also: Structural diversity of supercoiled DNA and m1A and m1G disrupt A-RNA structure through the intrinsic instability of Hoogsteen base pairs, which was reported as:

DNA’s dynamic nature makes it well-suited to serve as the blueprint of life.

My comment: The claim that DNA is the blueprint of life resurrects long-dead gene-centric theories. I expected others to make more rapid progress after the Zechiedrich lab linked energy-dependent changes from angstroms to ecosystems, but Al-Hashimi’s group is still reporting links in the context of pseudoscientific nonsense linked to neo-Darwinian theory. The theory does not address the need for biophysically constrained RNA-mediated protein folding chemistry in the context of the physiology of reproduction.
Perhaps Al-Hashimi’s group will be next to do that in RNA Structural Modules Control the Rate and Pathway of RNA Folding and Assembly, which supposedly is “In Press.” RNA methylation is clearly the link to all biodiversity. But, until then, they may fall behind even further, especially if they keep trying to placate the neo-Darwinists.
See: ‘Quantum jitters’ could form basis of evolution, cancer
Excerpt:

“This is a remarkable study that illuminates a fundamental mechanism responsible for the random mutations that drive evolution and contribute to cancer,” said Bert Vogelstein, M.D., a cancer researcher at Johns Hopkins University School of Medicine who was not involved in this research.

My comment: How did Vogelstein arrive at his ridiculous conclusion? Did Visualizing transient Watson-Crick-like mispairs in DNA and RNA duplexes inadvertently or deliberately lead him to it?
Excerpt:

These results, together with previous structural studies showing that WB and WC-like mispairs can exist within polymerase1–3 and ribosome5,6,13 active sites, strongly suggest that energetic competition between WB and WC-like mispairs is robust and is a key determinant of misincorporation probability during replication and translation (Supplementary Discussion 9).

My comment: How difficult would it have been to clarify the issues involved that suggest energetic competition causes the mutations, which means they do not randomly occur? I reiterate: Vogelstein thinks the “…study illuminates a fundamental mechanism responsible for the random mutations that drive evolution and contribute to cancer…”
Despite everything known to serious scientists about energetic competition for nutrients, I’m sure Vogelstein is not the only biologically uninformed cancer researcher who believes in neo-Darwinian theory. Others may also think that results framed in the context of energetic competition support ridiculous theories. Unfortunately, most people are not going to fight their way through an article like this one to discover that Vogelstein and all others like him are wrong.
Early myeloid lineage choice is not initiated by random PU.1 to GATA1 protein ratios
Excerpt:

These observed protein dynamics are incompatible with random and cross-regulatory PU.1–GATA1 co-expression acting as the central mechanism that initiates MegE versus GM lineage choice3.

My comment: Most people may miss the fact that they claimed “…observed protein dynamics are incompatible with random… co-expression, which initiates lineage choice. Simply put, they eliminated Vogelstein’s ridiculous idea about random mutations from any further consideration.
See also: A miR-155–Peli1–c-Rel pathway controls the generation and function of T follicular helper cells, which was reported as A potential new way to sway the immune system found
Excerpt:

“People know miRNAs are involved in immune response, but they don’t know which miRNAs and how exactly,” explained TSRI Research Associate Zhe Huang, study co-first author with Liu and Seung Goo Kang of TSRI and Kangwon National University.

See also: Regulation of B-cell development and tolerance by different members of the miR-17~92 family microRNAs
Excerpt:

In this experimental setting, the changes in the ratio of virus-transduced CD45.2+ cells (GFP+) versus WT competitors (CD45.1+) during the pro- to pre-B transition provided a measurement for the developmental defect. In the control WT:WT mix group, as no major difference existed between these two populations, the GFP+/CD45.1+ ratios remained unchanged during the pro- to pre-B transition, resulting in a pre-B/pro-B ratio close to 1 (Fig. 5b upper panels and Fig. 5c). In contrast, cells derived from the Mb1tKO HSCs, when transduced with control virus, underwent a severe developmental block in competition with WT cells. Therefore, the GFP+/CD45.1+ ratio shifted drastically as WT cells became dominant in the pre-B population, resulting in a pre-B/pro-B ratio below 0.2 (Fig. 5b middle panels and Fig. 5c).

My comment: All serious scientists know that nutrient energy-dependent microRNA flanking sequences link the innate immune system to differences in morphological and behavioral phenotypes via the physiology of reproduction in species from microbes to man via supercoiled DNA, which protects organized genomes of all living genera from virus-driven entropy.
Recent reports, which link specific families of miRNAs to healthy longevity or to pathology will obviously lead mroe researchers to discover the specific miRNAs that link virus-driven energy theft to all pathology.
See: The phylogenetic utility and functional constraint of microRNA flanking sequences and Role of olfaction in Octopus vulgaris reproduction
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).

See for comparison: (2016) Codon identity regulates mRNA stability and translation efficiency during the maternal-to-zygotic transition
Excerpt:

The bias between codons or amino acids, and mRNA expression levels has been previously recognized across species and is thought to result from selection for efficient, accurate translation, and folding of highly expressed genes (Ikemura, 1982; Akashi, 1994; Akashi & Gojobori, 2002; Drummond & Wilke, 2008; Kudla et al, 2009; Novoa & Ribas de Pouplana, 2012). The amino acid optimality code (Fig 6) provides an alternative perspective on sequence changes between paralogs in evolution and human disease.

My comment: These authors echo the claim that random mutations are not the source of energy-dependent cell type differentiation. They add that the across-species bias of RNA-mediated amino acid substitutions offers an alternative to ridiculous claims about mutation-driven evolution. For another example of facts about RNA-mediated amino acid substitutions, see how Dobzhansky (1973) framed his claims.
Excerpt:

…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).”

If you don’t like Young Earth Creationists, see also: (2016) Major Evolutionary Blunders: The ‘Degenerate’ Genetic Code?
Excerpts:

A detailed literature review in 2014 found that even if different codons prescribed the same amino acid in a protein, the codon differences still mattered in how the protein was made. The final folding shape of proteins is vital to their function. David D’Onofrio and David Abel documented that the DNA and its corresponding RNA sequence carried information not only for the proper amino acid sequence but also to control the timing of its folding. They “demonstrate that this TP [translational pausing] code is programmed into the supposedly degenerate redundancy of the codon table.”8 What this means is that the code of differing codons, even if they specify the same amino acid, still supplies important information, information that “purposely slows or speeds up the translation-decoding process….Variable translation rates help prescribe functional folding of the nascent protein. Redundancy of the codon to amino acid mapping, therefore, is anything but superfluous or degenerate.”8
…if synonymous codons can have important functional meaning, then the whole methodology goes out the window, and hundreds of studies that used these methods to infer “selection” during the supposed “evolution of genes” could be wrong.11

If you like neo-Darwinian theorists, see: Tempo and mode of genome evolution in a 50,000-generation experiment
Excerpt:

One line of evidence derives from the expectation that synonymous substitutions—point mutations in protein-coding genes that do not affect the amino-acid sequence—are neutral and should therefore accumulate at a rate equal to the underlying mutation rate20,35. This expectation is not strictly true owing to selection on codon usage, RNA folding, and other effects, but…

My comment: Let’s tell the truth with no buts, rather the invent more reasons to lie. Creationists and other serious scientists seem to arrive at the same conclusion by citing different literature that adds another level of epigenetic complexity in the context of non-random selection of RNA-mediated amino acid substitutions, which must be fixed in the organized genomes of all living genera to link the innate immune system to supercoiled DNA, which protects all organized genomes from virus-driven entropy.
The literature includes details about how the across species bias between codons or amino acids and microRNA or pre-mRNAs and mRNA expression levels links selection to efficient, accurate translation, and folding of highly expressed genes.   For comparison, no serious scientist has ever suggested that virus-driven energy theft is linked from mutations and selection to the evolution of one species from another. Thus, it has become perfectly clear that the amount of pseudoscientific nonsense people must believe to continue to believe in mutation-driven evolution is based on definitions and assumptions. Serious scientists do not rely on definitions and assumptions to support their claims.
See for comparison: Mutation-Driven Evolution (2013)

Excerpt:

Mutation is the change of genomic structure and includes nucleotide substitution, insertion/deletion, segmental gene duplication, genomic duplication, changes in gene regulatory systems, transposition of genes, horizontal gene transfer, etc. (2) Natural selection is for saving advantageous mutations and eliminating harmful mutations. Selective advantage of the mutation is determined by the type of DNA change, and therefore natural selection is an evolutionary process initiated by mutation. —

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.

See also: Replace the Modern Synthesis (Neo-Darwinism): An Interview With Denis Noble

[W]hat Haldane, Fisher, Sewell Wright, Hardy, Weinberg et al. did was invent…. The anglophone tradition was taught. I was taught, and so were my contemporaries, and so were the younger scientists. Evolution was defined as “changes in gene frequencies in natural populations.” The accumulation of genetic mutations was touted to be enough to change one species to another…. No, it wasn’t dishonesty. I think it was wish fulfillment and social momentum. Assumptions, made but not verified, were taught as fact.

For more assumptions in the context of ridiculous theories, see: Phylogenetic plasticity in the evolution of molluscan neural circuits (2016)
Conclusion:

Molluscan neural circuitry represents a different evolutionary trajectory from vertebrates and even other lophotrochozoans. Using the same morphogenic genes as other phyla, molluscs have created novel nervous systems that control a wide variety of body forms. Yet the largest brained invertebrates, the cephalopods, have converged with insects and vertebrates on the organization of circuitry for learning and memory. Even with this cross-phyletic convergence, there are intra-phyletic differences between octopus and cuttlefish in the sites of plasticity. Phylogenetic plasticity is also found in gastropods where homologous neurons have been re-used for different functions and where neuromodulatory actions also display species-specificity. One outcome from this work is to show that there are many solutions to the same problem. The story of molluscs is about how looks can be deceiving; the same genes and neurons can be used and reused in different ways to create diverse nervous systems that sometimes converge on the same solution. I think it is more exciting to realize that octopus and mammals independently came up with a learning machine that has a fan-out/fan-in organization and LTP than to think that these similarities are just a family resemblance. Call me a splitter, but I believe that uncovering the many solutions that nature has found will tell us more about fundamental organizational properties than lumping them all together.

My comment: Anyone who makes a ridiculous statement like the one above should be ‘called out’ and questioned to learn how he or she has managed to maintain their overwhelming ignorance despite the availability of publications like this one:
The phylogenetic utility and functional constraint of microRNA flanking sequences and this one The octopus genome and the evolution of cephalopod neural and morphological novelties
Excerpt:

Among the octopus complement of ligand-gated ion channels, we identified a set of atypical nicotinic acetylcholine receptor-like genes, most of which are tandemly arrayed in clusters (Extended Data Fig. 7). These subunits lack several residues identified as necessary for the binding of acetylcholine26, so it is unlikely that they function as acetylcholine receptors. The high level of expression of these divergent subunits within the suckers raises the interesting possibility that they act as sensory receptors, as do some divergent glutamate receptors in other protostomes27. In addition, we identified 74 Aplysia-like and 11 vertebrate-like candidate chemoreceptors among the octopus GPCR superfamily of ~330 genes (Extended Data Fig. 6).

My comment: The GPCR superfamily links receptor-mediated signaling from chemotaxis to phototaxis and all energy-dependent biophysically constrained biodiversity via RNA methylation and RNA-directed DNA methylation, histone acetylation and every aspect of the energy-dependent physiology of reproduction. Taken together, everything known about the energy-dependent receptor-mediated physiology of reproduction links the innate immune system to supercoiled DNA.
Those who tout neo-Darwinian theories for comparison must continue to use definitions and assumptions as if that approach was acceptable to anyone else who was not also a pseudoscientist.
See also: (2016) 33. Octopus Signals
Excerpt:

We define a ‘signal’ as any act or structure which alters the behavior of other organisms, which evolved because of that effect, and which is effective because the receiver’s response has also evolved.

My comment: Via the bastardization of everything known to serious scientists about biologically-based cause and effect, the definition of signal is linked to its evolution via an effect, which is not linked from any epigenetic effect on hormones to any affect on behavior. That makes it impossible to link food odors to the energy-dependent de novo creation of olfactory receptor genes, which are GPCRs. The de novo gene creation of GPCRs links metabolic networks to genetic networks via the pheromone-controlled physiology of behavior in the context of epigenetic effects of pheromones on hormones. The hormones affect the species-specific behaviors of all invertebrates and vertebrates.
Definitions lead to confusion about the use of the terms “effect” and affect, which link epigenetic effects on hormones the the affects of hormones on behavior. Neo-Darwinian theorists skip everything known to serious scientists about the differences between effect and affect and link the definition of a ‘signal’ to species-specific behaviors and all biodiversity.
See for comparison: Feedback loops link odor and pheromone signaling with reproduction

Conclusion:

It appears that GnRH neurons integrate a variety of information about the internal state of the animal and its external environment. 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.
These studies also indicate that GnRH neurons are likely to influence numerous brain functions. They appear to transmit signals to as many as 30,000 or more neurons in 34 brain areas, consistent with previous studies showing GnRH+ fibers and GnRH receptors in multiple brain regions (Badr and Pelletier, 1987; Jennes et al., 1988; Jennes et al., 1997). BL+ neurons likely to receive synaptic input from GnRH neurons were seen in areas associated with numerous different functions, including odor and pheromone processing, sexual behavior, appetite, defensive behavior, motor programs, and the relay of information to higher cortical areas. These results may reflect a strategy wherein GnRH neurons can modify diverse functions in order to coordinate the internal state of the animal and its behavior with reproduction in order to optimize reproductive success.

My comment: Have neo-Darwinian theorists found a species in which feedback loops do not link what the organism eats to its physiology of reproduction? If not, what do they claim links energy-dependent changes in angstroms to ecosystems in all living genera?
Who cares?

See also: The scent of a hatchling: intra-species variation in the use of chemosensory cues by neonate freshwater turtles

The 5300-year-old Helicobacter pylori genome of the Iceman
Abstract excerpt:

The “Iceman” H. pylori is a nearly pure representative of the bacterial population of Asian origin that existed in Europe before hybridization, suggesting that the African population arrived in Europe within the past few thousand years.

See also: Evolution of gut bacteria in humans and hominids parallels ape evolution
See also: Rapid evolution of microbe-mediated protection against pathogens in a worm host

My comment: Taken  together, these two articles link the difference in the bacteria that nematodes eat to the morphological and behavioral diversity of C. elegans for comparison to the predatory nematode with teeth, P. pacificus. From there, the conserved molecular mechanisms link the gut bacteria of the “Iceman” to the morphological and behavioral diversity of all human populations.

See also:

Special Report on Cell Biology: Sweetening the pot

Glycosylation in cellular mechanisms of health and disease

Glycomics: A rapidly evolving field with a sweet future
Excerpt 1)

Glycans play many critical roles in both the normal function of cells and in disease. They assist in the folding of many proteins, aid in protein trafficking, mediate cell adhesion, differentiate blood groups, modulate the immune system, are implicated in many signaling pathways, and provide a protective extracellular matrix for many types of cells. Glycans are also implicated in the process of infectivity for many pathogenic bacteria (2) and most viruses (3), including those that cause the common cold, influenza, and HIV/AIDS.

Excerpt 2)

Glycomics is now being used in combination with genomics, epigenomics, proteomics, lipidomics and metabolomics to provide a more holistic view of how cellular pathways function and how they change in response to disease.

It has become nearly impossible for me to keep up with the information that refutes neo-Darwinian pseudoscientific nonsense at the same time more articles are published that tout the nonsense.
See for comparison: The role of microRNAs in metabolic interactions between viruses and their hosts
Lineage tracing of human B cells reveals the in vivo landscape of human antibody class switching
Conclusion:

epigenetic inheritance of active and repressed chromatin state during mitosis has been demonstrated (Cavalli and Paro, 1998; Grewal and Klar, 1996). Our measurements suggest that the timescale on which the relative accessibility of IGHC loci persists is ~10 somatic mutations. Calibration of the mutational clock should allow recovery of information about epigenetic state and phenotypic dynamics in units of time and cellular generations. Together with recent studies of mammalian (Spencer et al., 2009) and bacterial cells in culture (Hormoz et al., 2015), our work suggests that phenotypic correlations between sister cells due to shared inheritance are widespread. We predict that such correlations often will be detected when genealogical relationships between individual cells can be resolved. We propose that inheritance of epigenetic state provides a mechanism for orchestrating cellular behavior without the need for signaling.

My comment: Attempts to define the term “signal” will fail because everyone knows what a signal is and all serious scientists know that food odors and pheromones are signals that link feedback loops from the innate immune system to chromatin folding and supercoiled DNA, which protects organized genomes from virus-driven entropy. The proposal the “…inheritance of epigenetic state provides a mechanism for orchestrating cellular behavior without the need for signaling” exemplifies the ignorance of all neo-Darwinian theorists who have failed to link energy-dependent signals to biophysically contrained protein folding chemistry via RNA methylation and RNA-mediated amino acid substitutions that differentiate all cell types in all individuals of all living genera.
Finally,  see:Downstream Antisense Transcription Predicts Genomic Features That Define the Specific Chromatin Environment at Mammalian Promoters
It was reported on August 4, 2016 by Engaging Epigenetic Experts as:

…the authors say that they suspect such antisense transcription plays an important role in “in the regulation of gene expression and the maintenance of a promoter-associated chromatin environment.”

My comment: This site started removing my comments after several weeks of allowing me to accurately link articles like this one to what is known about RNA-mediated cell type differentiation. Others have already invented terms like oncohistones and histone subunit isoforms in attempt to continue obfuscating the links from energy-dependent RNA-mediated amino acid substitutions to healthy longevity because they know virus-driven energy theft has been linked to all pathology.

Engaging Epigenetics Experts appears to be caught in the crossfire. They’ve supported too much neo-Darwinian nonsense to suddenly admit that it never made sense, but that’s what antisense transcription confirms. There are many other sources of what should have been “Science” news but the news was placed into the context of pseudoscientific nonsense touted by neo-Darwinian theorists who have trapped themselves in their ignorance.
In the article mentioned by Engaging Epigenetics Experts, this claim is substantiated:

Despite differences in epigenetic features, tendency for association with transregulatory factors, and capacity to produce stable RNA transcripts, all three classes of TSS described in this work display similarities in sequence content, including enrichment for GC content and Pol II-associated sequence motifs (Fig 2). As such, antisense transcription appears to be encoded in genetic sequence. This connection between sequence content and epigenetic features provides the compelling suggestion that antisense transcription encoded by sequence may direct the positioning of nucleosomes and deposition of histone marks. Antisense transcription may also participate in signal-dependent modulation of epigenetic content where activation of sequence-encoded antisense TSS precedes nearby changes in chromatin structure. In this way, the collection of transcription initiation-associated sequence motifs near promoters may define regulatory potential for a given gene. This connection to sequence also provides a means to interrogate antisense transcription function. Future studies with selective mutation of associated sequence motifs may elucidate the function of antisense transcription and its coincidence with promoter-associated features. Directed mutagenesis could also establish the extent of the effect of antisense transcription on the chromatin environment at promoters.
We characterized downstream antisense transcription initiating near gene promoters in human T47D/A1-2 cells. daTSSs fall between regularly positioned nucleosomes downstream of gene TSSs. Histones within this region are enriched for marks closely associated with active promoter regions, such as H3K4me3 and H3K27ac modifications. Chromatin remodeling complexes show enriched binding upstream of observed daTSS positions, suggesting that antisense transcription contributes to the establishment and maintenance of a promoter-specific chromatin environment. Downstream antisense transcription is common to many human promoters, and daTSSs correlate with the downstream edge of promoter-associated chromatin features. Coincidence of daTSSs with these features suggests interplay between antisense transcription and regulatory pathways.

My comment: There are too many ways to obfuscate what is known about the epigenetically-effected links from energy-dependent changes in angstroms to ecosystems in all living genera. These two paragraphs are important to understand in that context. They link RNA methylation and RNA-mediated amino acid substitutions to cell type differentiation in all living genera via chromatin remodeling, but you will not be encourage to look at the facts because there is no mention of epigenetically-effected RNA-mediated amino acid substitutions in the context of chromatin remodeling.  That’s why I added emphasis to this claim: “…transcription initiation-associated sequence motifs near promoters may define regulatory potential for a given gene.” 
It links hydrogen-atom transfer in DNA base pairs in solution from energy-dependent changes in the microRNA/messenger RNA balance to gene regulation via everything known to serious scientists. It links RNA-mediated amino acid substitutions and morphological diversity by linking energy-dependent RNA methylation from learning and memory to behavior via chromatin remodeling. The chromatin remodeling occurs in the context of the physiology of reproduction and what is known about supercoiled DNA, which protects all organized genomes from virus-driven energy theft and genomic entropy.
But their claim that “…transcription initiation-associated sequence motifs near promoters may define regulatory potential for a given gene” is placed into the context of a theory about the fact that energy-dependent RNA-mediated amino acids substitutions, which are referred to in the context of  transcription initiation-associated sequence motifs may define the energy-dependent regulatory potential of different genes in different individuals of different species. All pseudoscientists know how to obfuscate facts about the energy-dependent regulatory potential of different genes, because they have been placing them into the context of virus-driven energy theft and mutation-driven evolution since the time that de Vries (1902) defined “mutation.”
Addendum: People complain that I am not explaining how quantum physics, quantum chemistry, quantum biology, and quantum consciousness in terms they can understand. See:

Double slit experiment and the REAL secret

Real-world explanation: Brian Greene : What’s Beyond The Double Slit Experiment ?

See also:
 Our Reality Is Information Tom Campbell
Probability & Uncertainty: The quantum mechanical view of nature Richard Feynman
New Experiments Show Consciousness Affects Matter Dean Radin

rp_levels-of-organization.jpg

The end of neo-Darwinism

Rapid bacterial infection test reduces antibiotic use

Excerpt:

The rapid tests detect C-reactive protein (CRP), a marker of infections caused by bacteria, in patients’ blood. A low level of CRP is suggestive of viral infection and therefore antibiotic treatment is not required.

My comment: The level of one protein differentiates between a viral and a bacterial infection. That fact attests to claims that one RNA-mediated amino acid substitution in a virus increases its virulence.

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

Major antigenic changes are less likely to occur when the nutrient energy-dependent stability of the host microbiome already exemplifies ecological adaptation to the virus.  Ecological adaptation occurs via the pheromone-controlled physiology of reproduction in species from microbes to humans.

Based on the results of one test, all serious scientists who have linked energy-dependent changes from angstroms to ecosystems via RNA-mediated amino acid substitutions in all living genera may now be willing to reassert their claims. They can differentiate between mutations and amino acid substitutions and eliminate ridiculous neo-Darwinian theories from any further consideration whatsoever.
Pseudoscientists may still hope to publish in “Science” or in “Nature” until even the top supporters of the evolution industry are forced to withdraw their support.

For example, see these two citations from: Tempo and mode of genome evolution in a 50,000-generation experiment, in which ‘adaptation’ is mentioned 10 times in the body of the text.

Wichman, HA, et. al, (1999) Different trajectories of parallel evolution during viral adaptation. Science 285, 422–424.

Kvitek, DJ & Sherlock, G.  (2013) Whole genome, whole population sequencing reveals that loss of signaling networks is the major adaptive strategy in a constant environment. PLoS Genet. 9, e1003972 (2013).

My comment: Ecological variation must link the adaptations to viruses via energy-dependent RNA-mediated amino acid substitutions. Do authors who make claims about parallel genome evolution in the context of mutations but place them into the context of population-wide adaptations know that? The two citations suggest that these authors do not know enough about energy-dependent RNA-mediated cell type differentiation.

Olivier Tenaillon, Jeffrey E. Barrick, Noah Ribeck, Daniel E. Deatherage, Jeffrey L. Blanchard, Aurko Dasgupta, Gabriel C. Wu, Sébastien Wielgoss, Stéphane Cruveiller, Claudine Médigue, Dominique Schneider & Richard E. Lenski

Alternatively, they may be deliberately misrepresenting what is known to all serious scientists about energy-dependent biophysically constrained RNA-mediated protein folding chemistry by linking their results to genome evolution in Lenski’s long term evolution experiment (LTEE).
See for comparison: Changing Folding and Binding Stability in a Viral Coat Protein: A Comparison between Substitutions Accessible through Mutation and Those Fixed by Natural Selection (2014)
Excerpt 1)

Bloom and collaborators presented a thermodynamic framework to predict the probability that a protein retains its structure after one or more random amino acid substitutions, and highly simplified models of proteins were used to support their prediction that the substitutions tend to be destabilizing [4], [7], [8], [15], [22], [23].

Excerpt 2)

We find that there are unexpected differences between accessible and observed substitutions. Observed substitutions tend to have smaller effects on stability than expected by chance. Substitutions observed in high temperature adaptations tend to stabilize folding but slightly destabilize binding. Finally their cumulative stability effects in lab adaptations can be considerably greater than individual effects suggesting that selection is acting on local aspects of protein stability.

My comment: Holly A. Wichman, who is the first author of the 1999 article about parallel evolution during viral adaptation is  a co-author of the 2014 article about fixed substitutions, which are referred to as mutations. With news that C-Reactive Protein (CRP) is suggestive of viral infection, claims about fixed amino acid substitutions and mutations can be placed into their proper perspective.
For example, mutations may be fixed in a virus during replication, but only energy-dependent RNA-mediated amino acid substitutions can be fixed in the organized genomes of species from microbes to humans via the physiology of reproduction. Nutrient energy-dependent microRNAs allow fixation of RNA-mediated amino acid substitutions in C-Reactive Protein, which stabilizes the organization of the human genome.

See also: Posttranscriptional Regulation of the Inflammatory Marker C-Reactive Protein by the RNA-Binding Protein HuR and MicroRNA 637 (2015)

Conclusion:

The role of CRP as both a risk factor and a biomarker warrants investigation of its regulation by other molecular factors. We have discovered a posttranscriptional mechanism by which the RBP HuR and the miRNA miR-637 modulate CRP expression downstream of IL-6 signaling. We have identified HuR and miR-637 as new factors that may play an integral role in the development of the inflammatory state and may represent new valuable targets in the diagnosis, treatment, or prevention of inflammation and diseases with a major inflammatory component.

My comment: This suggests all virus-driven energy theft, which is linked to all pathology in all living genera, can be treated in the context of nutrient energy-dependent microRNA flanking sequences. The flanking sequences link hydrogen-atom transfer in DNA base pairs in solution from RNA methylation to cell type differentiation via RNA-mediated amino acid substitutions, the innate immune system, and the physiology of reproduction. The physiology of energy-dependent reproduction links fixation of the nutrient-dependent amino acid substitutions to supercoiled DNA, which protects all organized genomes from virus-driven entropy.

See also: New Perspectives on Ebola Virus Evolution also with Holly A. Wichman

Abstract excerpt:

We tested for positive selection and considered the placement of adaptive amino acid substitutions along the phylogeny and within the protein structure of GP1,2. We conclude that: 1) the common practice of rooting the phylogeny of EBOV between the first known outbreak in 1976 and the next outbreak in 1995 provides a misleading view of EBOV evolution that ignores the fact that there is a non-human EBOV host between outbreaks; 2) the N-terminus of GP1 may be constrained from evolving in response to the host immune system by the highly expressed, secreted glycoprotein, which is encoded by the same region of the GP gene; 3) although the mucin-like domain of GP1 is essential for EBOV in vivo, it evolves rapidly without losing its twin functions: providing O-linked glycosylation sites and a flexible surface.

My comment: They linked virus-driven energy theft to amino acid substitutions in the EBOV lineage between outbreaks. They link changes in the virus from a non-human host to the ability of human hosts to protect themselves via nutrient energy-dependent glycosalation sites and receptor-mediated behaviors that link glycobiology from energy-dependent RNA methylation to supercoiled DNA. But they also link virus-driven energy theft in the human host to all pathology via this report.

Epigenetics and Genetics of Viral Latency

Excerpt:

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

My comment: Rarely do researchers see the amount of confusion about biologically-based cause and effect that is exemplified in two articles published on the same day, albeit in different journals. However, in this case, the conclusions in Tempo and mode of genome evolution in a 50,000-generation experiment will make no sense to serious scientists who understand the claims in New Perspectives on Ebola Virus Evolution.

For example, the 50,000-generation experiment cannot be linked from energy-dependent amino acid substitutions in the virus carried by mosquitoes to mutations in the Ebola virus in humans. However, nutrient-dependent RNA-amino acid substitutions can be linked to prevention of Ebola virus-driven energy theft and the prevention of all virus-driven human pathology via what is known about the biophysically constrained chemistry of RNA-mediated protein folding in all living genera.

rp_levels-of-organization.jpg

Biophotonics, glycobiology, quantized biodiversity

Historical perspective: From Fertilization to Adult Sexual Behavior
Excerpt:

Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.

My comment: I do not know any serious scientist who claims that protein folding chemistry is not energy-dependent and RNA-mediated or that it does not involve alternative splicings of pre-mRNA.
See for comparison:

Protein folding video misrepresentation (4 minutes)

My comment: The most recent misrepresentation of protein folding chemistry links two mutations from amino acids to co-evolution.

There is no magic in protein folding; it is energy-dependent. All misrepresentations fail to link what is known about biophysically constrained energy-dependent protein folding chemistry to cell type differentiation via RNA-mediated amino acid substitutions. Instead, the misrepresentations are consistently used to support ridiculous theories about evolution outside the context of virus-driven energy theft and genomic entropy.

The ignorant masses of biologically uninformed pseudoscientists and laypersons are led to believe in the pseudoscientific nonsense of neo-Darwinian theory. And yet, few people respond to my  accurate representations of biologically-based cause and effect in my FB posts or blog posts about articles like this one:

Epigenetics and Genetics of Viral Latency

Excerpt:

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

My comment: I would like to be polite about the consequences of knowing that. Does everyone accept the fact that their ignorance is killing them?
If you don’t want to suffer and die from a preventable early death, see:

Special Report on Cell Biology: Sweetening the pot

My comment: This comprehensive report links nutritional epigenetics from energy-dependent metabolic networks to genetic networks in all living genera. It stops short of placing what’s known about energy-dependent RNA-mediated cell type differentiation into the context of links from the innate immune system to supercoiled DNA.
The supercoiled DNA protects all organized genomes from virus-driven entropy. Schrodinger’s claims from 1944 and the comment by Roger Penrose in the forward to the reprint of “What is Life?” can now be placed into the contest of information as nutrient-dependent energy that regulates the transgenerational epigenetic inheritance of mRNA stability and translation efficiency.
Finally, others have learned how to link energy-dependent changes in the microRNA/messenger RNA balance from RNA methylation to learning and memory via the function of the innate immune system. Proper function links the immune system from the physiology of reproduction to fixation of RNA-mediated amino acid substitutions in the supercoiled DNA that protects all organized genomes from virus-driven energy theft and genomic entropy.
See for examples: (2010) Mystery RNA spawns gene-activating peptides
Excerpt:

This finding has echoes of the paradigm-changing discovery of the small non-coding RNAs called microRNAs, which have direct gene-regulatory functions.

See also: (2014) Redundancy of the genetic code enables translational pausing
Abstract excerpt:

The codon redundancy (“degeneracy”) found in protein-coding regions of mRNA also prescribes Translational Pausing (TP). When coupled with the appropriate interpreters, multiple meanings and functions are programmed into the same sequence of configurable switch-settings.

See also: (2014) Identification of small ORFs in vertebrates using ribosome footprinting and evolutionary conservation

Excerpt:

Central roles of small peptides have been known for decades based on the importance of neuropeptides, peptide hormones (such as secretin or insulin) and secreted signaling molecules (such as FGF1). However, the majority of these small peptides are encoded as large pre‐proteins that undergo post‐translational cleavage and modification. By contrast, similar functional small peptides such as ELABELA/toddler (Chng et al, 2013; Pauli et al, 2014) (also identified in our set of smORFs; Supplementary Fig S3) are directly translated from small ORFs. Indeed, Pauli et al (2014) recently reported the independent identification of more than 300 previously unannotated zebrafish proteins. Small proteins are also found in viral genomes, where transmembrane proteins (often shorter than 50 aa) have been shown to play vital roles in virus replication and virulence (Dimaio, 2014).

See also (2016) Chromatin controls behavior

reported as: Ability to turn off genes in brain crucial for learning, memory
Excerpt:

One process that controls chromatin structure and transcription is chromatin remodeling by energy-dependent protein complexes (4). Such complexes that depend on adenosine 5′-triphosphate (ATP) can control gene expression by moving, ejecting, or restructuring nucleosomes, the scaffolds around which DNA wraps. Each nucleosome contains a core particle of eight histone protein subunits (5). Remodeling events include posttranslational modifications, swapping individual histone subunit isoforms into and out of the core particle, and facilitating the unbinding of DNA from the core particle.

My comment: Word choice and omissions are a form of wordplay for those who know better than to refute neo-Darwinian nonsense by substituting ‘histone subunit isoforms’ for claims about RNA-mediated amino acid substitutions.
Google:histone subunit isoform” in an attempt to find what you were just told linked energy-dependent changes in chromatin from learning and memory to behavior. For an even clearer indication of the games academics play with works, find the newly invented term.
Here, let me help:  An oncohistone deranges inhibitory chromatin
Excerpt:

Missense mutations (that change one amino acid for another) in histone H3 can produce a so-called oncohistone…

My comment: Mutations do not change one amino acid for another in organized genomes, which is why the result of a missense mutations is called an oncohistone.  They use a form of evolutionary double-speak to link mutations and RNA-mediated amino acid substitutions to a negative outcome because virus-driven energy theft causes the mutations, and nutrient energy-dependent RNA-mediated cell type differentiation prevents the mutations. If energy-dependent RNA-mediated DNA repair did not occur, the virus-driven energy theft would bring all life on Earth to a fast and very unpleasant end. All organisms would suffer to the degree that any species can suffer, and all species would become extinct.
See also: What is life when it is not protected from virus driven entropy