An evolutionary theory killer

How to create biologically uninformed theorists

Summary: On March 2, 2018, Philip C. Ball and Nick Lane started making claims about proton gradients. Their claims are based on my model of quantized energy as information. This post includes added support for what is known to all serious scientists about the light-activated endogenous substrates that link molecular epigenetics to RNA-mediated autophagy.
See first: Energy as information and constrained endogenous RNA interference (audio/visual aid 2017)

Feedback loops link quantized energy as information to biophysically constrained RNA-mediated protein folding chemistry. Light induced energy-dependent changes link angstroms to ecosystems from classical physics to chemistry/chirality and to molecular epigenetics/autophagy.

The National Microbiome Initiative links microbial quorum sensing to the physiology of reproduction via endogenous RNA interference and chromosomal rearrangements. The rearrangements link energy-dependent fixed amino acid substitutions to the Precision Medicine Initiative via genome wide inferences of natural selection.

This detailed representation of energy-dependent natural selection for codon optimality links biologically- based cause and effect from G protein-coupled receptors to RNA-mediated amino acid substitutions and the functional structure of supercoiled DNA. Energy-dependent polycombic ecological adaptations are manifested in supercoiled DNA. Chromosomal inheritance links the adaptations from morphological phenotypes to healthy longevity via behavioral phenotypes.

For contrast, virus-driven energy theft is the link from messenger RNA degradation to negative supercoiling, constraint breaking mutations, and hecatombic evolution. The viral hecatomb links transgenerational epigenetic inheritance from archaea to Zika virus-damaged DNA, which typically is repaired by endogenous RNA interference and fixation of RNA-mediated amino acid substitutions in organized genomes.

Added support for the light-activated molecular epigenetics of autophagy:
Light-powering Escherichia coli with proteorhodopsin (2007)

…we quantify the coupling between light-driven and respiratory proton currents… and show that light-driven pumping by PR can fully replace respiration as a cellular energy source in some environmental conditions.

Structure of the Deactive State of Mammalian Respiratory Complex I (2018)

…the deactive state arises when critical structural elements that form the ubiquinone-binding site become disordered, and we propose reactivation is induced when substrate binding to the NADH-reduced enzyme templates their reordering. Our structure both rationalizes biochemical data on the deactive state and offers new insights into its physiological and cellular roles.

Global collective motions in the mammalian and bacterial respiratory complex I (2018)

…we identify here transitions between experimentally resolved structures of the mammalian complex I as low-frequency collective motions of the enzyme, highlighting similarities and differences between the bacterial and mammalian enzymes. Despite the reduced complexity of the smaller bacterial enzyme, our results suggest that the global dynamics of complex I is overall conserved.

The conservation of light-powered functional structures and energy-dependent proton gradients link the deactive state in critical structures to the active state via the creation of enzymes in species from bacteria to mammals. The energy-dependent creation of the enzymes links metabolism of the energy (e.g., food energy) from pheromones to biophysically constrained viral latency in the context of the physiology of reproduction.
The pheromone-controlled physiology of reproduction in species from microbes to humans links our visual perception of energy and mass in the context of how ecological variation must be linked to energy-dependent ecological adaptations in all living genera.
See: Olfaction Warps Visual Time Perception

Our perception of the world builds upon dynamic inputs from multiple senses with different temporal resolutions, and is threaded with the passing of subjective time. How time is extracted from multisensory inputs is scantly known. Utilizing psychophysical testing and electroencephalography, we show in healthy human adults that odors modulate object visibility around critical flicker-fusion frequency (CFF)-the limit at which chromatic flickers become perceived as a stable color-and effectively alter CFF in a congruency-based manner, despite that they afford no clear environmental temporal information. The behavioral gain produced by a congruent relative to an incongruent odor is accompanied by elevated neural oscillatory power around the object’s flicker frequency in the right temporal region ~150-300 ms after object onset, and is not mediated by visual awareness. In parallel, odors bias the subjective duration of visual objects without affecting one’s temporal sensitivity. These findings point to a neuronal network in the right temporal cortex that executes flexible temporal filtering of upstream visual inputs based on olfactory information. Moreover, they collectively indicate that the very process of sensory integration at the stage of object processing twists time perception, hence casting new insights into the neural timing of multisensory events.

See also: Odors Alter Subjective Time Experience Author: Dr. ZHOU Wen’s Research Group Update time: 2017/05/15

The brain is not a timepiece. Whereas it is equipped with senses like vision, audition, touch, smell, and taste, it has no direct access to or measure of the physical time (unless you read from a clock). Rather, it constructs the subjective “time” of an event from the dynamic multisensory inputs associated with that event. Yet different senses come with different temporal precisions. For instance, when standing near an apple tree, you can detect the falling of an apple much better with your eyes or ears than the nose. How does the brain coordinate multisensory signals entering different brain regions with different temporal resolutions, and come up with the subjective time?

A team at the Institute of Psychology at Chinese Academy of Sciences tackled this issue using odors and images. Specifically, Dr. Bin Zhou, the study’s lead author, and his colleagues examined whether odors could modulate one’s temporal sampling and subjective duration of visual objects. In their study, participants viewed two series of flickering isoluminant images in red and green (Figure 1A). One of the series contained opposite images of an apple or bananas; the other contained only images of red and green fields. When the images alternated at a frequency beyond 20 Hz, the participants started to have difficulty reporting which series contained an object. Indeed, for most people, chromatic flicker fusion frequency (CFF), the limit at which alternating colors become perceived as a stable fused color, falls somewhere between 20 and 25 Hz. Interestingly, the participants’ object detection accuracies around CFF were improved under the exposure of a congruent, as opposed to an incongruent, odor. In other words, the participants detected a rapidly flickering apple better when they smelled an apple odor rather than a banana odor, and vice versa (Figure 1B, left panel). In effect, the presence of a congruent odor facilitated the brain’s temporal sampling of a visual object and elevated its CFF (Figure 1B, right panel). Based on electrical activities recorded from the participants’ scalp, the researchers found that the integration between smell and vision strengthened the signals of the corresponding object in a brain region heavily implicated in object representations called the right temporal cortex, about 150-300 ms after object onset. They further showed that such integration lengthened one’s subjective duration of the corresponding object in a duration comparison task. The researchers concluded that subjective time is warped by the neural energy involved in representing multisensory inputs at subsecond scales.

Until Philip C. Ball mentioned that Nick Lane believed proton gradients came before the energy-dependent creation of RNA, I did not realize how little they knew about this link from differences in the energy of photons to consciousness.
See: What Affective Neuroscience Means for Science Of Consciousness (2013)

The coupling of the two circuits promotes an endogenous feedback that supports conscious processes. Within this framework, we present the defence that detailed study of both affective and cognitive processes, their interactions, as well of their respective brain networks, is necessary for a science of consciousness.

The coupling of the two circuits links differences in the energy of photons from the proton motive force to the light-activated endogenous feedback loops and Feedback loops link odor and pheromone signaling with reproduction.
It is extremely difficult for intelligent people to not link this experimental evidence to biophysically constrained viral latency in the context of reports that claim “Creatures’ Adaptability Begins with Their Sensors.”
But, see for comparison: David Attenborough on creationsim May, 2015

My comment on his nonsense: First steps to neutralizing Zika: How highly potent antibody neutralizes Zika infection discovered

This is framed within the context of energy-dependent changes in pH, which facilitate receptor-mediated entry of nutrients or viruses into specific cell types of species-specific tissues via stress-linked changes in hydrogen-atom transfer in DNA base pairs.

Virus-driven energy theft has been linked to all pathology in all living genera via the conserved molecular mechanisms of RNA-mediated polycombic protein folding chemistry compared to the hecatombic evolution of pathology manifested first in the differences between archaea and bacteria. Admitting that Carl Woese was wrong about the different domains of life is the first step towards understanding the difference between healthy longevity and the evolution of all virus-driven pathology.

Carl Woese was wrong

God did not create the viruses. He created the anti-entropic virucidal energy of sunlight, which protects all organized genomes from virus-driven entropy. Only the choices of our ancestors could have led to the increasing amout of virus-driven pathology during the past ~6000 years that pseudoscientists place into the context of millions of years of evolution. Then, they blame God, like these two pseudoscientists do. Darwin knew they would do that, which is why he insisted that others put conditions of life before natural selection. But they bastardized his theory anyway and taught their revision to anyone who was foolish enough to believe in it. It’s called the “Modern Synthesis” and was based on de Vries 1902 definition of “mutation.”

Celebrate Your Inner Virus

It is important that we understand the design present in viruses because God made them.

It is no wonder that Sir David Attenborough and many others like Philip C. Ball and Nick Lane are confused about the energy-dependent creation of healthy longevity and consciousness. Even some young earth creationists have failed to link the creation of the sun’s anti-entropic virucidal energy from changes in electrons to ecosystems via the proton motive force. That leaves every aspect of creation to be placed back into the context of ridiculous theories. The theories start with the virus-driven theft of quantized energy as information. The energy theft links mutations to all virus-driven pathology. The theft of quantized energy as information cannot be linked by serious scientists from beneficial mutations to the evolution of one species from another.
For comparison, pseudoscientists have no problem touting this confusing nonsense:
Sign of selection on mutation rate modifiers depends on population size (
1)  Genetic variation—the raw material for evolution—is ultimately generated by mutation.
2). …beneficial alleles never become deleterious and deleterious alleles never become beneficial.

Whether these phenomena can be united in a single theoretical framework remains an open question that we are actively exploring. In any case, our results add to a growing appreciation of nonclassical population size dependence in evolution by natural selection (41, 42).

Funding for research that attempts to link natural selection to evolution via mutation-driven genetic variation should be used to link food odors and pheromones from the physiology of reproduction to biophysically constrained viral latency and ecological adaptations. It is time to stop creating more biologically uninformed theorists.


Light-activated feedback loops vs self-organization of ecosystems

John Lieff has been trying to update his ridiculous misrepresentations of biologically-based cause and effect to match the accurate representations we made in a section on molecular epigenetics in our 1996 Hormones and Behavior review.

From Fertilization to Adult Sexual Behavior

Nothing can stop him, but this will provide the next source for material that he must borrow as if he learned about it somewhere else.

Apoptosis analysis guide | Free ebook download

Virus-driven energy theft causes apoptosis, which releases cell contents for recycling in the context of autophagy, which helps to ensure food energy-dependent pheromone-controlled RNA-mediated DNA repair in species from microbes to humans.

Gene bivalency at Polycomb domains regulates cranial neural crest positional identity

Journal article abstract excerpt (figure: Epigenetic regulation of cranial NC cell identity.)

A Polycomb-dependent poised chromatin organization underlies the positional plasticity of cranial premigratory NC cell progenitors. This chromatin prepattern is maintained through migration. In response to local cues encountered by the NC cells during or after their migration, the regulatory elements (E) and promoters (P) of differentially expressed genes switch from a poised to an active chromatin state, establishing transcriptional identities specific to subpopulations of NC cells.

The use of the term “chromatin prepattern” must be linked from endogenous RNA interference to all all biodiversity via transgenerational epigenetic inheritance. Watch closely as all pseudoscientists, atheists and other biologically uninformed theorists finally realize there is no such thing as mutation-driven evolution except in the context of virus-driven energy theft, apoptosis, and the evolution of pathology. Virus-driven energy theft causes degradation of messenger RNA in the absence of nutrient energy-dependent pheromone-controlled RNA-mediated amino acid substitutions and DNA repair.

MicroRNAs Establish Uniform Traits during the Architecture of Vertebrate Embryos

Aberrant trait variance in miRNA mutant embryos uniquely sensitizes their vascular system to environmental perturbations. We discovered a previously unrecognized role for specific vertebrate miRNAs to protect tissue development against phenotypic variability.

Reported as: The role of tiny RNA in genetic diversity March 28, 2017

All species, from zebrafish to humans, possess a genetically diverse collection of traits that allow them to adapt to changing environments. Yet scientists do not fully understand how organisms reach a state of optimal diversity—just enough variability to respond to environmental risks but not too much to function properly.

Natural selection for energy-dependent codon optimality is the link to optimal diversity. Conserved molecular mechanisms of nutrient-dependent pheromone-controlled biodiversity have been linked from quorum sensing in bacteria to all cell type differentiation in all individuals of all species.
See: Feedback loops link odor and pheromone signaling with reproduction

These studies reveal a complex interplay between reproduction and other functions in which GnRH neurons appear to integrate information from multiple sources and modulate a variety of brain functions.

Escherichia coli and the peppered moth typically are typically used by biologically uninformed theorists as examples of mutation-driven evolution.
See: The Man Who Bottled Evolution
See the refutation: Evolutionary resurrection of flagellar motility via rewiring of the nitrogen regulation system

…this system enables us to understand the adaptive process in detail at the genetic and phenotypic level [over the weekend]. We identified a tractable model for gene network evolution and observed, in real time, the rewiring of gene networks to enable the incorporation of a modified component (NtrC′) creating a novel regulatory function by a highly repeatable two-step evolutionary pathway with the same point mutations often recurring in independent lineages.

They failed to differentiate between the term mutation and what occurs in the context of energy-dependent pheromone-controlled changes in the microRNA/messenger RNA balance via fixation of RNA-mediated amino acid substitutions in supercoiled DNA.
See: Structural diversity of supercoiled DNA

Six decades after the elucidation of its double helical structure, DNA continues to surprise us by revealing new information. Our cryo-ET, biochemical, and computational studies show the astounding versatility and dynamism of DNA depending on the degree of supercoiling. DNA simultaneously exists in a largely inactive B-form with bases tucked in and protected and an active, highly varied structure with exposed bases. Our data provide relative comparisons of supercoiling-dependent twisted, writhed, curved, and kinked conformations and associated base exposure. Each of these structural features may be differentially recognized by the proteins, nucleic acids, and small molecules that modulate DNA metabolic processes.

See for comparison: Helicoverpa armigera images

Identification and Evaluation of Suitable Reference Genes for Normalization of MicroRNA Expression in Helicoverpa armigera (Lepidoptera: Noctuidae) Using Quantitative Real-Time PCR

…10 candidate genes of H. armigera were selected and analyzed for their expression stability under different biotic and abiotic conditions….  miR-9 and U6 snRNA for developmental stages, miR-100 and U6 snRNA for larval tissues, miR-100 and miR-305 for adult tissues, miR-9 and miR-279 for parasitic treatment, miR-998 and U6 snRNA for nuclear polyhedrosis virus infection, miR-9 and U6 snRNA for insecticide treatment, miR-92a, miR-100, and miR-279 for temperature treatment, miR-92a, miR-305, and miR-998 for starvation treatment, miR-9 and miR-279 for light treatment, miR-305 and miR-998 for hormone treatment, and there was not one reference gene suitable for all samples.

Nutrient-dependent pheromone-controlled reproduction in this moth species links the works of Karlson and Luscher (1959) Pheromones: a new term for a class of biologically active substances to the Bruce McEwen’s works on stress via Effects of Carnitine on Fatty-Acid Oxidation by Muscle (1959) and Dependence of RNA synthesis in isolated thymus nuclei on glycolysis, oxidative carbohydrate catabolism and a type of “oxidative phosphorylation” (1964)

The synthesis of RNA in isolated thymus nuclei is ATP dependent.

Taken together, these works are linked to energy-dependent Normalization of MicroRNA Expression. The anti-entropic virucidal energy of sunlight is the obvious link from the de novo creation of microRNAs to the ATP-dependent biosynthesis of messenger RNA and healthy longevity.  Virus-driven energy theft clearly links the degradation of messenger RNA, which would otherwise link the creation of microRNAs from sunlight to the nutrient energy-dependent pheromone-controlled biosynthesis of ATP and all cell type differentiation in all living genera.

For example see: Genetic 3’UTR variation is associated with human pigmentation characteristics and sensitivity to sunlight

To our knowledge, this is the first time that these two 3’UTR SNPs have been associated with sun-sensitivity traits. We state the potential implication of these SNPs in human pigmentation and sensitivity to sunlight, possibly as a result of changes in the level of gene expression through the disruption of putative miRNA-binding sites.

See also:: Race-dependent association of sulfidogenic bacteria with colorectal cancer

reported as: Study links sulfide-producing bacteria and colon cancer in African-Americans

“These bacteria are using nutrients associated with an animal-based diet,” Gaskins said.

For information on the biophysically constrained energy-dependent origins of race-dependent associations see:

Common origins of RNA, protein and lipid precursors in a cyanosulfidic protometabolism

…precursors of amino acids glycine, serine, alanine and threonine, are inevitable by-products of this RNA assembly chemistry…

Like all chemistry, this can be placed into the context of how quantum physics must be linked from quantum chemistry to quantum biology via food as energy.

The link from food enery to the nutrient-dependent pheromone-controlled physiology of reproduction and racial differences in colon cancer was predicted based on difference in diet and links from the National Microbiome Initiative to the Precision Medicine Initiative.

See for comparison: Sonny Williams

Re: … much ado about nothing — Jay R. Feierman.

SONNY [NEW]: As we’ve discussed many times, I reject your criteria for judging the merits of a scientific observation.  Arguing that something is “much ado about nothing,” if “the results can’t be predicted by common sense or by simple observation and deductive reasoning,” is exceptionally poor reasoning.  Frankly, I’m bewildered that someone like you would cling to it.  I’ll repeat:  any judgment that includes an evaluation based on “common sense” is DOA.  It’s useless.  Whose “common sense” do you intend to use?

More importantly, the authors DID establish a pre-observation “prediction.”

They predicted that young children will show the same variation in temperament as adults, and which is associated with the various BDNFval/66met polymorphisms.  They wrote, “To the best of our knowledge, there are no studies investigating the role of BDNFval66met with regard to individual differences in temperament during infancy, a period in which genetically-based behavioral traits are hypothesized to be more easily observed (Posner & Rothbart, 2009; Rothbart et al., 2000). Hence, the purpose of the current study was to explore the association between the BDNFval66met polymorphism and individual differences in temperament in a sample of healthy 4-month-old full-term infants.”

Moreover, the authors did a far better job than you did in discussing limitations.

They wrote as follows: “The current study had some limitations. First of all, due to sample size findings cannot be generalized and future studies with larger samples are needed in order to differentiate the impact of met-homozygous and heterozygous profiles of BDNFval66met genotype. Second, infants’ temperament was measured through a parent-reported measure. A more direct account of the effects of BDNF met allele on observed temperament and regulatory behavior is warranted to be investigated in future research. Finally, single polymorphism studies are at risk of underrepresenting the role of environmental conditions, including maternal caregiving behavior. As the quality of early caregiving has been found to regulate BDNF transcriptional functioning (Unternaehrer et al., 2015), we suggest that upcoming studies should target gene x environment interactions using genetic and epigenetic approaches.

To the best of our knowledge, this study is unique in providing evidence of an association between the BDNFval66met polymorphism and infants’ temperament at 4 months of life. The present study adds to previous genetic association research on temperament in infants looking at other polymorphisms (Auerbach et al., 2001; Ivorra et al., 2011), preliminarily suggesting a further genetic factor involved in temperament. Future research is warranted to investigate the BDNF-temperament association in greater populations of infants at low- and high-risk (e.g., preterm infants) and assuming a gene-x-gene and gene-x-environment approach (Papageorgiou & Ronald, 2013).”

Sonny Williams and Jay R. Feierman are antagonists who ignore the facts that link our predictions to all energy-dependent biophysically constrained biodiversity from our 1996 Hormones and Behavior. Our predictions were based on Bruce McEwen’s advice to start with the activation of genes. That is why we included a section on molecular epigenetics.

From Fertilization to Adult Sexual Behavior

All predictions have since been linked from the anti-entropic virucidal energy of sunlight to biophysically constrained RNA-mediated biodiversity by changes in base pairs linked from amino acid substitutions to differences in morphological and behavioral phenotypes during the development of moths and humans. The epigenetic effects of sunlight were predicted in the context of the nutrient energy-dependent de novo creation of microRNAs.
Anything ever linked to the gene-centric theories of neo-Darwinists has been replaced by what is known about energy-dependent endogenous RNA interference and all biophysically constrained biologically-based biodiversity on Earth. For example, pheromones biophysically constrain the physiology of reproduction in all living genera. They protect against virus-driven entropy by linking what organisms eat to the species-specific pheromone-controlled transgenerational epigenetic inheritance of species from microbes to humans.
See also: Epigenetic regulation of face formation
See also: Explaining the accelerating expansion of the universe without dark energy

See also: A distinct role for Lgr5+ stem cells in primary and metastatic colon cancer
Reported by Genentech as: Cancer stem cells have long been thought to influence tumor growth, but a clear link has been difficult to show. Now, in a new study in Nature, our scientists show for the first time that removing cancer stem cells in a model of colorectal cancer can indeed reduce tumor growth. See how these findings could help guide new therapies aimed at targeting cancer stem cells.
What took them so long to link virus-driven energy theft from messenger RNA degradation to the negative supercoiling of DNA via G protein-coupled receptors?
Feedback loops link odor and pheromone signaling with reproduction

At least 10,000 neurons in 26 different brain areas appear to transmit signals directly to GnRH neurons.  GnRH neurons 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. 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.


Virulence and your UTI

Nobody wants to belong to the party of losers. One of the best strategies in such a case is evidently an interpretation of the change as a gradual accumulation of knowledge while their work has always been at the cutting edge. — Kalevi Kull


Take on the role of a virus competing to infect a host cell and replicate your viral components!

If you have played this game, you probably know more about virulence than the researchers and journalists who report on it.

Bacterial virulence phenotypes of Escherichia coli and host susceptibility determine risk for urinary tract infections

…our findings suggest that UTI risk and outcome may be determined by complex interactions between host susceptibility and the urovirulence potential of diverse bacterial strains.

Reported as: Urinary tract infections reveal the importance of interactions between host susceptibility and bacterial gene expression

…infection depends on both the host environment and gene expression levels in the bacteria.

The epigenetically-effected host environment biophysically constrains viral latency in all living genera. Viral latency exemplifies how ecological variation must be linked to nutrient energy-dependent pheromone-controlled ecological adaptations and gene expression in E. coli, which prevent virus-driven genomic entropy in all living genera.

They reveal the importance of energy-dependent pheromone-controlled quorum sensing, which links virus-driven energy theft to messenger RNA degradation and all pathology via what is known about bacteria in the light organ of the bobtail squid and the microRNAome of all mammals. 

  …sperm have been reported to carry both RNA and microRNA to the fertilized zygote [17], [18]. MicroRNA (miRNA) are important regulators in translation, and their altered expression often leads to disease or cancer.

Telling us about UTIs does nothing to reveal the importance of biophysically constrained energy-dependent viral latency to the understanding of all pathology.

For example, if you were taught that antibiotic resistance is due to mutations in bacteria such as E.coli, which causes most UTIs, you may never learn that bacteriophages drive the nutrient-dependent pheromone-controlled ecological adaptations in the bacteria and viral latency is the key to healthy longevity in all living genera. UTI risk is predicted by differences in the microRNA/messenger RNA balance that link amino acid substitutions in the host to protection from amino acid substitutions in viruses that cause virulence.

Ask yourself where the terms virus and virulence came from — if not from what was suspected or what is known about virus-driven energy theft.


RNA methylation, RNA-directed DNA methylation, learning and memory

sink testing

Lab medicine The illegal practice of providing false test results on clinical specimens–eg, vials of blood, urine specimens, that were deliberately discarded–ie, down the sink, without actually testing them

Pylori Story #1: Acid Attack

Pylori Story #2: Journey to the Center of the Stomach

The “Modern Synthesis” is analogous to sink testing in the medical laboratory.

See for example: 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.

The assumptions that were taught as fact led to this revelation: “It was really surprising,” Dr. Bernstein said. “Why would a metabolism gene cause cancer?”

The facts about biologically-based nutrient-dependent RNA-mediated cell type differentiation, which is perturbed by viruses, led to this revelation:

See for example: Breath Test for Stomach Cancer
My comment: The test for H. pylori is one of the simplest tests to perform in the lab. The breath test for stomach cancer will link gut bacteria from metabolic networks to genetic networks in all invertebrates and vertebrates via what is currently known about RNA-mediated cell type differentiation and the stability of all organized genomes in all living genera.
DNA methylation changes in plasticity genes accompany the formation and maintenance of memory

The ability to form memories is a prerequisite for an organism’s behavioral adaptation to environmental changes. At the molecular level, the acquisition and maintenance of memory requires changes in chromatin modifications. In an effort to unravel the epigenetic network underlying both short- and long-term memory, we examined chromatin modification changes in two distinct mouse brain regions, two cell types and three time points before and after contextual learning. We found that histone modifications predominantly changed during memory acquisition and correlated surprisingly little with changes in gene expression. Although long-lasting changes were almost exclusive to neurons, learning-related histone modification and DNA methylation changes also occurred in non-neuronal cell types, suggesting a functional role for non-neuronal cells in epigenetic learning. Finally, our data provide evidence for a molecular framework of memory acquisition and maintenance, wherein DNA methylation could alter the expression and splicing of genes involved in functional plasticity and synaptic wiring.

See also: Search Results for ‘RNA-directed DNA methylation’

I don’t think this will become clearer.

  1. Base pair changes are nutrient energy-dependent
  2. RNA-directed DNA methylation is nutrient-dependent
  3. RNA-mediated amino acid substitutions are nutrient-dependent
  4. Alternative splicings of microRNAs are nutrient-dependent
  5. Chromatin modification is nutrient-dependent
  6. Histone modifications are nutrient-dependent
  7. Plasticity is nutrient-dependent
  8. DNA repair is nutrient-dependent
  9. Ecological adaptation is nutrient-dependent


  1. Nutrient-dependent epigenetically-effected learning and memory links RNA-directed DNA methylation from microRNAs to cell adhesion proteins and supercoiled DNA in the organized genomes of all living genera.
  2. Alternative splicings of microRNAs are linked from the microRNA/messenger RNA balance to learning and memory via amino acid substitutions in the histones of supercoiled DNA .
  3. Viruses steal the nutrient energy that links the perturbed microRNA/messenger RNA balance to mutation-driven pathology.

See also: Elucidating MicroRNA Regulatory Networks Using Transcriptional, Post-transcriptional, and Histone Modification Measurements

This study demonstrates that decoupling transcriptional changes from post-transcriptional changes and integrating them with epigenetic alterations in a computational framework can elucidate the transcriptional network that tunes and amplifies the effect of miRNA loss. The computational framework introduced here may benefit studies of miRNAs by shifting emphasis to the rewired transcriptional networks that cause the majority of the transcript-level changes.

Re: “…the rewired transcriptional networks that cause the majority of the transcript-level changes.” They link the nutrient-dependent pheromone-controlled physiology of reproduction to weekend evolution of the bactrerial flagellum.
See: Evolutionary Rewiring

The results highlight the importance of gene duplication in evolution, said Hughes, and the ability of the resulting diverged proteins to “moonlight” in roles aside from their main function. Indeed, said Jeff Barrick of the University of Texas in Austin who was not involved in the work, such cross-talk gives organisms “greater robustness,” allowing them “to restore a function even though they are missing a genetic part.”

My comment: Indeed, Barrick makes no mention of his own work with Richard Lenski, like this one:
Large Chromosomal Rearrangements during a Long-Term Evolution Experiment with Escherichia coli

IMPORTANCE Bacterial chromosomes are dynamic structures shaped by long histories of evolution.

My comment: The long histories were just reduced to the history of weekend evolution of the bacterial flagellum via nutrient-dependent pheromone controlled chromosomal rearrangements.

amino acid homeostasis

Cell types, SNVs, CNVs, and chromosomes

See also: A “new” code enables ecological adaptation

For comparison, see:

Genome-Wide Detection of Single-Nucleotide and Copy-Number Variations of a Single Human Cell

Single-molecule and single-cell studies reveal behaviors that are hidden in bulk measurements (1, 2). In a human cell, the genetic information is encoded in 46 chromosomes. The variations occurring in these chromosomes, such as single-nucleotide variations (SNVs) and copy-number variations (CNVs) (3), are the driving forces in biological processes such as evolution and cancer. Such dynamic variations are reflected in the genomic heterogeneity among a population of cells, which demands characterization of genomes at the single-cell level (4–6).

My comment: Many evolutionary theorists seem to think the same biological processes are linked to cancer and evolution. They based their thoughts and theories on assumptions that incorporated de Vries turn of the 20th century definition of “mutation.” Population geneticists assumed that accumulated mutations, which lead to cancer, also lead to evolution. Their assumptions have not changed in more than 100 years.
See for contrast:
Rare event of histone demethylation can initiate singular gene expression of olfactory receptors
Reported as: Singular Expression of Olfactory Receptors

…activation and feedback can indeed generate OR singularity a striking example of enzyme kinetics, in which the nervous system utilizes the relative timescales of slow epigenetic changes (histone demethylation) and fast transcriptional regulations (depletion of the demethylase) to generate a dramatic outcome in neurogenesis. Our conclusions are generally applicable to other systems where singularity is desired, such as V(D)J recombination in the immune system and the expression of protocadherins.

My comment: V(D)J recombination in the immune system and the expression of protocadherins were placed into the context of an epigenetic trap that stabilizes organized genomes.
See: An Epigenetic Trap Stabilizes Singular Olfactory Receptor Expression

Singular olfactory receptor (OR) gene expression is stabilized by an  epigenetic trap  in which the LSD1 demethylase desilences an OR gene but is then downregulated as a consequence of OR protein expression, preventing the activation of additional OR alleles.

My comment: Nutrient-dependent microRNAs and the biophysically constrained chemistry of RNA-mediated gene duplication link the fixation of RNA-mediated amino acid substitutions in the context of reproduction to protein folding and cell type differentiation in all cell types of all individuals of all genera. That fact is not quite clear in:
Distinct E-cadherin-based complexes regulate cell behaviour through miRNA processing or Src and p120 catenin activity

However, no experimental evidence of biologically-based cause and effect has supported the assumptions of evolutionary theorists who have not changed their ridiculous opinions about mutations and evolution.All experimental evidence of cause and effect links physics to chemistry and the conserved molecular mechanisms of epigenetically-effected cell type differentiation in all cells of all individuals of all living genera via epigenetic traps that link the epigenetic landscape to the physical landscape of DNA via RNA-mediated DNA repair mechanism.See:   Reprogramming Cancer Cells Back to Normal CellsExcerpt:

The investigators discovered that PLEKHA7 maintains the normal state of the cells, via a set of miRNAs, by tethering the microprocessor to E-cadherin and p120. In this state, E-cadherin and p120 exert their good tumor suppressor sides.

My comment: The fact that miRNAs and E-cadherin and p120 suppress tumors suggests that something that causes the tumors must be suppressed. In my model of atoms to ecosystems, the proliferation of viruses that links viral microRNAs from entropic elasticity to genomic entropy is suppressed by nutrient-dependent microRNAs.
Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems

My comment: No experimental evidence of biologically-based cause and effect has supported the assumptions of evolutionary theorists.
See for comparison to everything known about cell type differentiation, which has been accurately represented during the past 100 years:
Evidence for Retromutagenesis as a Mechanism for Adaptive Mutation in Escherichia coli 

Retromutagenesis is apt to be a universal method of evolutionary adaptation, which enables the emergence of new mutants from mutations acquired during counterselection rather than beforehand, and it may have roles in processes as diverse as the development of antibiotic resistance and neoplasia.

My comment: This claim could be predicted based on the collective ignorance of all evolutionary theorists who refuse to accept the fact that ecological adaptations are nutrient-dependent and controlled by the physiology of reproduction.