sex differences Archives

"Evolution of Man. - Undoubtedly there once lived upon the earth races of men who were much lower in their mental organization than the present inhabitants.

Natural selection for racism and all pathology

November 5, 2017

by James Kohl with No Comment Adaptations Alternative Splicings base editing Cytosis Diseases & Disorders Ecology Nutrigenomics Physics RNA Directed RNA editing RNA-directed DNA methylation Variations

Why is natural selection hard to grasp? It is not what you think….

…human cognitive tendencies interfere more with deep understanding of how natural selection works.

Simply put, our intelligence and teleological reasoning interferes with the teaching of pseudoscientific nonsense. The nonsense does not place Darwin’s “conditions of life” before natural selection for reproductive fitness. Natural selection is food energy-dependent and pheromone-controlled in the context of biophysically constrained viral latency.
See for comparison: The vibrational theory of olfaction for the win

Darwin’s energy-dependent conditions of life link biophysically constrained viral latency to healthy longevity. Luca Turin’s works are among those that exposed the fraudulent claims of neo-Darwinian theorists.

See for example: Molecular recognition in olfaction

For physicists, maybe the single most important development that can be envisaged is the production of a high quality X-ray structure of a one or more olfactory receptors. This would open the door to large scale computer simulations that would help shed light on both the mechanical and electrical responses of olfactory receptors.

The X-ray structure of the virus that destroys olfactory receptors is more important. It can be viewed in the context of everything know to serious scientists who have linked quantum physics to quantum souls.
For example, see: Rosalind Franklin: The Hero Denied Her Due

Franklin was also a brilliant chemist and a master of X-ray crystallography, an imaging technique that reveals the molecular structure of matter based on the pattern of scattered X-ray beams. Her early research into the microstructures of carbon and graphite are still cited, but her work with DNA was the most significant — and it may have won three men a Nobel.
Franklin left King’s in 1953 in a long-planned move to join J.D. Bernal’s lab at Birkbeck College, where she discovered the structure of the tobacco mosaic virus. But in 1956, in the prime of her career, she developed ovarian cancer — perhaps due to her extensive X-ray work. Franklin continued working in the lab until her death in 1958 at age 37.
“As a scientist, Miss Franklin was distinguished by extreme clarity and perfection in everything she undertook,” Bernal wrote in her obituary, published in Nature. Though it’s her achievements that close colleagues admired, most remember Franklin for how she was forgotten. — C.E.

For comparison, these authors take the ball that Nesse and other theorists put into play, and these theorists run with it. They even pretend to be “biologically informed,” in response to my oft repeated claim that people like them are biologically uninformed science idiots.
The Future of Secularism: a Biologically Informed Theory Supplemented with Cross-Cultural Evidence

…earlier trends toward secularization (due to science education surrounding advancements in science) are currently being counter-balanced by genetic and reproductive forces. The authors also propose that the inverse association between intelligence and religiosity, and the inverse correlation between intelligence and fertility lead to predictions of a decline in secularism in the foreseeable future.

The agenda of at least two co-authors: Nyborg and Ellis, is clear. See: Race and Sex Differences in Intelligence and Personality: A Tribute to Richard Lynn at Eighty

Nyborg and Lee Ellis promote the works of J. Phillipe Rushton who was reported to be among the top racists of the 20th century.

See: Do pigmentation and the melanocortin system modulate aggression and sexuality in humans as they do in other animals?

Pigmentation of the hair, skin, cuticle, feather and eye is one of the most salient and variable attributes of vertebrates. In many species, melanin-based coloration is found to be pleiotropically linked to behavior. We review animal studies that have found darker pigmented individuals average higher amounts of aggression and sexual activity than lighter pigmented individuals. We hypothesize that similar relationships between pigmentation, aggression, and sexuality occur in humans. We first review the literature on non-human animals and then review some of the correlates of melanin in people, including aggression and sexual activity. Both within human populations (e.g., siblings), and between populations (e.g., races, nations, states), studies find that darker pigmented people average higher levels of aggression and sexual activity (and also lower IQ). We conceptualize skin color as a multigenerational adaptation to differences in climate over the last 70,000 years as a result of “cold winters theory” and the “Out-of-Africa” model of human origins. We propose life history theory to explain the covariation found between human (and non-human) pigmentation and variables such as birth rate, infant mortality, longevity, rate of HIV/AIDS, and violent crime.

Pigmentation is food energy-dependent and RNA-directed DNA methylation links food odors to pheromones and the physiology of reproduction in all living genera. It would be interesting to hear what Jay R. Feierman thinks about this since I met him at a 1995 conference that Lee Ellis organized and J. Phillipe Rushton also attended (by invitation only).

All (~90) attendees should be familiar with works that extended the social science theories to “hate-mongering.” I have tried to stop the hate-mongering, but history may repeat itself with Feierman’s help, of course.
See for comparison: Codon identity regulates mRNA stability and translation efficiency during the maternal-to-zygotic transition

The amino acid optimality code (Fig 6) provides an alternative perspective on sequence changes between paralogs in evolution and human disease.

Natural selection for energy-dependent codon optimality has been linked via olfaction from quantum physics to all biologically based RNA-mediated cell type differentiation via amino acid substitutions in organized genomes. But Nesse and others like him want to keep their teaching positions and that requires them to deny everything known to serious scientists about physics, chemistry, and molecular epigenetics.
See for comparison: A Civic Biology: Presented in Problems (New York, 1914): pp. 193-196, 253-254, 261-263.
Social scientists ignored Darwin’s “conditions of life.” Most of them don’t seem to understand why I claim that their ignorance has caused the deaths of millions.
See for comparison: The entire evolution of the microbial world and the virus world, and the interaction between microbes and viruses and other life forms have been left out of the Modern Synthesis…
Will history repeat itself? Will most of us return to the racism of Hunter (1914)?

In the review The Future of Secularism: a Biologically Informed Theory Supplemented with Cross-Cultural Evidence, they obfuscate the claim that Muslims are less intelligent and more fertile than Jews or Buddhists. What will happen when their claim is linked to this claim from Hunter: “A Civic Biology: Presented in Problems” pp. 195-196

Evolution of Man. – Undoubtedly there once lived upon the earth races of men who were much lower in their mental organization than the present inhabitants. If we follow the early history of man upon the earth, we find that at first he must have been little better than one of the lower animals.

Any and all links from intelligence to fertility are claims that attempt to support the pseudoscientific nonsense touted by neo-Darwinian theorists. Their ridiculous theories are the cause of all pathology.

The Root Cause Of Cancer and Why it Has Been Kept a Secret!

…the root cause of cancer is too much acidity in the body, meaning that the pH in the body is below the normal level of 7.365, which constitutes an “acidic” state. Warburg investigated the metabolism of tumors and the respiration of cells and discovered that cancer cells maintain and thrive in a lower pH, as low as 6.0, due to lactic acid production and elevated CO2. He firmly believed that there was a direct relationship between pH and oxygen.

Anyone who ever performed a blood gas analysis could have helped to establish the fact that the virus-driven degradation of messenger RNA is the cause of all pathology. See for instance: Dependence of RNA synthesis in isolated thymus nuclei on glycolysis, oxidative carbohydrate catabolism and a type of “oxidative phosphorylation”

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

That fact made it obvious to all serious scientists that energy-dependent RNA mediated DNA repair was required for healthy longevity. The anti-entropic virucidal energy of the sun was linked to the creation of ATP by Schrodinger (1944) in “What is Life?” The food energy-dependent pheromone-controlled physiology of reproduction in species from microbes to humans now links the creation of RNA to all biodiversity, and that links pheromones to biophysically constrained transgenerational epigenetic inheritance of healthy longevity via viral latency.

Nothing has been hidden. There was no reason to hide the facts after theorists made it possible to teach their pseudoscientific nonsense to students in high school via the Scopes Trial in Dayton, TN (1925). Sinclair Lewis published “Arrowsmith” in 1925 and since then, ATP-dependent biophysically constrained viral latency has been detailed in the context of the cell biology game “Cytosis” with its “Virus Expansion.”

Cytosis: A Cell Biology Board Game

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

Polycombic ecological adaptation as a science, not a theory (2)

November 1, 2016

by James Kohl with 3 Comments Adaptations Alternative Splicings Autophagy biophotonics Diseases & Disorders Ecology Human Brain Human Pheromones Light Energy Model Organisms Neuronal Plasticity Nutrigenomics Pharmacogenomics Physics RNA Directed RNA methylation RNA-directed DNA methylation RNA-mediated epigenetic regulation of gene expression RNA-mediated gene silencing RNA-mediated toxicity RNA–Mediated Epigenetic Heredity Variations

Evolutionary Constraints in the β-Globin Cluster: The Signature of Purifying Selection at the δ-Globin (HBD) Locus and Its Role in Developmental Gene Regulation

Conclusion:

… the results here presented indicate that purifying selection is driving not only HBD evolution but also its neighbor pseudogene, HBBP1. In the light of recent advances in the characterization of the β-globin cluster, we propose that the complex patterns of diversity observed in this genomic region arose from distinct functional constraints related with the intricate process of chromatin and protein interactions coordinating the differential expression of genes at the β-globin cluster during development.

My comment: No experimental evidence of biologically-based cause and effect suggests that any locus of genes or any pseudogene has ever evolved. Purifying selection cannot drive evolution. Only energy-dependent variations can can be linked to polycombic ecological adaptation, and only virus-driven energy theft has been linked to the creation of pseudogenes in the context of biophysical constraints on viral latency.

See for comparison: microRNA Function Is Limited to Cytokine Control in the Acute Response to Virus Infection

Excerpt:

miRNA function is generally limited to cytokine levels in response to RNA viruses

Reported as: Mount Sinai Researchers Use Cellular miRNA-Elimination Tool to Study Viral Infection Dynamics

Excerpt:

…while the loss of miRNAs had a negligible impact on the cell’s immediate reaction to a virus or the short-term biology of the cell, sustained depletion had dramatic results on gene expression that was coupled to a burst of cytokines. The researchers concluded in the paper that miRNA function is limited to modulating the biology of the cell over long periods of time.

My comment: In my model, energy-dependent changes in the microRNA/messenger RNA balance link nutrient energy-dependent changes to all healthy longevity and virus-driven energy theft is linked to all pathology. Over long periods of time, autophagy is the link to polycombic ecological adaptation or virus-driven hecatombic evolution of pathology via energy-dependent biophysically constrained RNA-mediated protein folding chemistry. For example, fixation of amino acid substitutions differentiates all cell types in all individuals of all living genera in the context of the physiology of reproduction. For comparison, virus-driven hecatombic pathology is linked from mutations to all pathology.

Simply put, in my model of polycombic ecological adaptation, differential gene expression is nutrient-dependent and controlled by the physiology of reproduction.

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

Conclusion:

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

My comment: Claims about RNA-mediated polycombic ecological adaptation were first placed into the context epigenetic imprinting in our 1996 review.

See: From Fertilization to Adult Sexual Behavior

Excerpt:

Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes (Saunders, Chue, Goebl, Craig, Clark, Powers, Eissenberg, Elgin, Rothfield, and Earnshaw, 1993; Singh, Miller, Pearce, Kothary, Burton, Paro, James, and Gaunt, 1991; Trofatter, Long, Murrell, Stotler, Gusella, and Buckler, 1995). 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: Polycombic ecological adaptation appears to link energy-dependent epigenetic effects on hormones (i.e., proteins) to chromatin structure in telomeric regions, which links the effect on transcription and silencing of various genes to hormone-organized and hormone-activated affects on behavior. The hormone-organized and hormone-activated behaviors link the epigenetic landscape of yeasts to the physical landscape of supercoiled DNA in species from bacteria to invertebrates and all vertebrates via the de novo creation of G protein-coupled receptors, which link chemotaxis and phototaxis to all biodiversity.

For comparison, see: Mutation-Driven Evolution

Excerpt:

Mutation… includes nucleotide substitution, insertion/deletion, segmental gene duplication, genomic duplication, changes in gene regulatory systems, transposition of genes, horizontal gene transfer, etc.

My comment: The definition above links mutations to any change in any genome.

See for comparison: Updates of the HbVar database of human hemoglobin variants and thalassemia mutations

Excerpt:

Single nucleotide substitutions or indels [insertions/deletions] can lead to several hemoglobin variants owing to amino acid replacements, while molecular defects [mutations] in either regulatory or coding regions of the human HBA2, HBA1, HBB or HBD genes can minimally or drastically reduce their expression, leading to α-, β- or δ-thalassemia, respectively.

My comment: The facts about nutrient energy-dependent amino acid substitutions link hemoglobin variants from ecological adaptation to healthy longevity and the facts also link molecular defects from mutations to the pathology of α-, β- or δ-thalassemia, respectively. It would be difficult to include facts about biophysically constrained energy dependent cell type differentiation in the context of any other model that links amino acid substitutions to healthy longevity and links mutations to all pathology in all living genera.

See for example: Criticisms of the nutrient-dependent pheromone-controlled evolutionary model

Excerpt:

…James Kohl presents an unsupported challenge to modern evolutionary theory and misrepresentations of established scientific terms and others’ research.

My comment: The claims of a biologically uninformed undergraduate student reviewer were placed into the context of modern evolutionary theory, which involves Masatoshi Nei’s simple-minded revision of neo-Darwinian pseudoscientific nonsense. Nei does not compare his theory of mutations to the facts about nutrient energy-dependent fixation of amino acid substitutions in supercoiled DNA. The problem appears to be the use of the term “mutation” in the textbook published on the same day as my 2013 review was published.

I linked the energy-dependent fixation of amino acid substitutions to all healthy longevity. Nei’s textbook misrepresentations did not link anything to healthy longevity, but linked mutations to what I claimed are nutrient-dependent pheromone-controlled polycombic ecological adaptations.

I failed to include what is known about energy-dependent codon optimality in the context of polycombic ecological adaptations because there was no experimental evidence of biologically-based cause and effect to support those claims at the time of our 1996 review or my 2013 review. For comparison, there has never been any experimental evidence of biologically-based cause and effect to support claims about mutation-driven evolution. Simply put, nothing known to serious scientists about cell type differentiation suggest that mutation-driven evolution can occur.

For comparison, see: New analysis of big data sheds light on cell functions
Excerpt:

With today’s technology, scientists are able to generate data about a cell’s or organism’s complete set of genes, proteins, RNA profiles, metabolites and much more—known as omic data. Using omic data, scientists can model complex biological interactions and gain a more holistic view of different cellular processes.

See also: Research Topic Multi-omic Data Integration

Excerpt:

Stable, predictive biomarkers and interpretable disease signatures are seen as a significant step towards personalized medicine. In this perspective, integration of multi-omic data coming from genomics, transcriptomics, glycomics, proteomics, metabolomics is a powerful strategy to reconstruct and analyse complex multi-dimensional interactions, enabling deeper mechanistic and medical insight.

My comment: Glycomics, transcriptomics, proteomics, metabolomics and genomics have established fact about the biological basis of complex multi-dimensional interactions that link the nutrient-dependent pheromone-controlled physiology of reproduction in bacteria from quorum sensing to the molecular mechanisms that enable deeper mechanistic and medical insight in the context of the National Microbiome Initiative and Precision Medicine Initiative.

See for example: ‘Oming in on RNA–protein interactions

Excerpt:

…the interactions between pre-mRNA and proteins fine-tune alternative splicing in a manner that can gradually create new protein functionalities without the need to create additional genes and without affecting existing proteins [4-6].

See for comparison: 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…. 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: Detailed examples of how the interactions between pre-mRNA and alternative splicings create new genes in the fine-tuned energy-dependent functional structure of supercoiled DNA explain how all cell types of all individuals of all living genera are protected from virus-driven energy theft. Energy-dependent RNA-mediated amino acid substitutions are fixed in organized genomes via the physiology of reproduction, which helps to prevent the transgenerational epigenetic inheritance of nearly all pathology by linking innate immune system to supercoiled DNA.

For comparison, viruses steal the energy that is required for cell type differentiation, which is how mutations are linked to all pathology. All differences between healthy longevity and virus-driven human pathology can be explained in the context of how nutrient energy-dependent microRNAs. The nutrient energy-dependent microRNAs are carried by erythrocytes in species with circulating blood.

See: Pitfalls of analysis of circulating miRNA: role of hematocrit

MicroRNAs are are delivered to the cell types on an as needed basis. When too few nutrient energy-dependent microRNAs are available, viruses use the existing energy they steal from cells to replicate. Eventually, the replication of the viruses causes the mutations, which are linked to all pathology. That’s why it is important to revisit the facts presented in the context of this article, which was published on 10/26/16

See: Multi-omic data integration enables discovery of hidden biological regularities
I reported this here as: Polycombic ecological adaptation as a science, not a theory for comparison to Biological evolution as a philosophy, not a science.
Despite several attempts to discuss the difference between science and philosophy, no progress was made.
See for example: Evolutionary assumptions (revisited)
See also the impasse that was reached in this attempt to discuss the anti-entropic virucidal energy of the sun.
It is worth joining The Battlefield FB group to see that others would rather hold on to their theories and opinions despite the overwhelming amount of experimental evidence that I have used to support my claims. For me, it is time to move forward and focus on the rediscovery of hidden biological regularities.
Finally, others have discovered that small intranuclear proteins generate alternative splicing techniques of pre-mRNA, which is how microRNAs link hydrogen-atom transfer in DNA base pairs in solution to the conserved molecular mechanisms of energy-dependent cell type differentiation, and to all cell type differences in all individuals of all living genera.
For comparison, this is an example of how virus-driven energy theft is linked viral replication and to virulence:
Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution

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

For an example of how nutrient energy-dependent RNA-mediated amino acid substitutions are linked to healthy longevity via the physiology of reproduction, see:

…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).”

My comment: The facts stated above have forced theorists to invent evolutionary cell biology.
See Evolutionary cell biology: Two origins, one objective
Reported as: Why some junk DNA is selfish, but selfish genes are junk
Excerpt:

“A commonly held but incorrect stance is that essentially all of evolution is a simple consequence of natural selection.” They point out, for example, that many pathways to greater complexity of both genomes and cells don’t confer any selective fitness.

My comment: Greater complexity requires a link from ecological variation to polycombic ecological adaptation, which links supercoiled DNA to protection from the virus-driven hecatombic evolution of all pathology.
My comment: New theories are worthless if they do not include information on the role of energy in cell type differentiation or the role of virus-driven energy theft in all pathology.
See for comparison the facts about: Detection of hemoglobinopathies and thalassemias using automated separation systems
See also: In vivo correction of anaemia in β-thalassemic mice by γPNA-mediated gene editing with nanoparticle delivery
Excerpt:

The combination of nanoparticle delivery, next generation γPNAs and SCF treatment may offer a minimally invasive treatment for genetic disorders of the blood that can be achieved safely and simply by intravenous administration.

My comment: That fact suggests all suffering and death caused by hemoglobin variants is caused by neo-Darwinian theorists who do not know how the variants link ecological variation to polycombic ecological adaptation.

Reported as: Scientists edit gene mutations in inherited form of anemia
Excerpt:

The researchers found that the technique corrected the mutation to such a degree that the mice no longer had symptoms of thalassemia. After 140 days, they tested hemoglobin levels in the animals and found them to be normal.
“The fundamental result here is that with nanoparticles containing PNAs, along with template DNA, and simple IV infusion of molecules, we achieved enough gene editing to effectively cure the anemia in mice that had thalassemia,” Glazer said.

My comment: The ability to correct the mutation requires a link from energy-dependent changes in hydrogen-atom transfer in DNA base pairs in solutions such as blood. That’s how their IV therapy works. It changes the microRNA/messenger RNA balance and that forces the innate immune system to repair the damaged DNA.
See also: Two novel loci, COBL and SLC10A2, for Alzheimer’s disease in African Americans
Excerpt:

Two SNPs at novel loci, rs112404845 (P = 3.8 × 10−8), upstream of COBL, and rs16961023 (P = 4.6 × 10−8), downstream of SLC10A2, obtained genome-wide significant evidence of association with the posterior liability.

Reported as: Study Identifies Two New Genes Responsible for Alzheimer’s in African Americans
Excerpt:

In 2013, a genome-wide association study of AD in more than 5,500 African Americans identified two genetic risk factors for AD. This study looked at genetic variants across subjects’ entire genome and compared their frequency in cases versus controls.
By doing so they were able to identify two new genes (COBL and SLC10A2) associated with risk of AD in African Americans.

My comment: The author’s study results link hydrogen-atom transfer in DNA base pairs in solution to energy-dependent changes in the microRNA/messenger RNA balance. The neuroscience news report claims they identified two new genes. The neuroscience news report then links the genes — instead of the energy-dependent changes — to the disease in a human population. Many African Americans are examples of how ecological variation has been linked to polycombic ecological adaptation via hemoglobin variants. The adaptations include amino acid substitutions linked to the stability of organized genomes in populations where malaria is endemic. Failed adaptations are included in examples of virus-driven energy theft linked to mutations and the pathology of Alzheimer’s disease.

My comment: The ability to edit out gene mutations clearly links RNA-mediated amino acid substitutions to supercoiled DNA and all biodiversity.
See also: Inventing neo-Darwinism
See also: Pioneering Geneticist Explains Ambitious Plan to “Write” the Human Genome

Many Edits, All at Once

Excerpt:

…he notes that with an editing tool like CRISPR, one base out of many can be altered, but with a synthesis approach, a hundred edits could be made. This sort of change, he tells JAMA, could make a cell resistant to multiple viruses.

My comments: All the changes in base pairs may already have been linked from natural selection for codon optimality and energy-dependent changes in RNA-mediated cell type differentiation to supercoiled DNA, which links the physiology of reproduction from the innate immune system to fixation of the amino acid substitutions that differentiate the cell types of all living genera. If so, what might happen to an organized genome when a hundred edits are made?

Will anyone be able to stop the hecatombic evolution of pathology via the polycombic ecological adaptation, which links autophagy to healthy longevity via protection of organized genomes from virus-driven entropy?

See also: Yale scientists edit gene mutations in inherited form of anemia Genetics & Genomics

A new gene therapy is being tested for its ability to treat thalassemia, a form of anemia caused by genetic mutations. So far, scientists have successfully corrected gene mutations causing the disease in mice, and now researchers are interested in seeing if the same approach will work effectively in humans.
“The fundamental result here is that with nanoparticles containing PNAs, along with template DNA, and simple IV infusion of molecules, we achieved enough gene editing to effectively cure the anemia in mice that had thalassemia. We demonstrated we have extremely low off-target effects.”

See for comparison:

Product Development Pipeline

Excerpt:

Each microRNA mimic in our pipeline is designed to replicate the activity of a single tumor suppressor miRNA and regulate the expression of key oncogenes across multiple oncogenic pathways which can prevent proliferation and induce apoptosis in cancer cells.

See also: VACRC Projects

Excerpt: Future Projects

The Influence of Carbon Dioxide Enhancement on Plant Growth

Thermoregulation in Honey Bees

Biochemistry and Taxonomy in Pine Trees

The Formation of Multiple Tree Rings in Bristlecone Pine Trees

The VACRC suddenly seems willing to take everything I have claimed about RNA-mediated cell type differentiation during the past twenty years and begin to investigate the claims. This would have been a desirable outcome 20 years ago, but now it might prevent progress via use of my model. The model links energy-dependent changes from angstroms to ecosystems in all living genera, it and links virus-driven energy theft to all pathology.

The Pacific Yew Tree and production of taxol is an example of how the physi0logy of reproduction in soil bacteria can be linked from plant growth to the honeybee model organism of thermoregulation and behavior, which must be linked to the biochemistry and taxonomy of all species. That becomes meaningful via the explanatory power of a model that links RNA-mediated amino acid substitutions to all energy-dependent biodiversity via the conserved molecular mechanisms of polycombic ecological adaptation we detailed in our 1996 review.

However, when others wait too long to accept a model that may already have led to a paradigm shift, they may also realize it. That fact was addressed by Kaveli Kull in the context of next week’s meeting of the Royal Society.

See: Kalevi Kull: Censorship & Royal Society Evo Event

Excerpt:

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.

My comment: Some work by young earth creationists has been at the cutting edge since 1996, as indicated here: Where do viruses come from?

Excerpt:

‘Viruses tend to keep nutrients away from the big stuff and keep them going around in the little stuff,’ says Fuhrman. If so, viruses have shaped the entire structure of the ecosystem.”9

My comment: 9 is Holmes, B. (1996) Who Rules the Waves? New Scientist 152(2054):8-9, supp I have not read it in its entirety but the claim fits into the context of everything else I have learned about physics, chemistry, and conserved molecular mechanisms of RNA-mediated cell type differentiation, which appears to be biophysically constrained in all living genera via their nutrient-dependent pheromone-controlled physiology of energy-dependent reproduction.

Chromatin: The structure of DNA (2)

September 21, 2016

by James Kohl with One Comment Adaptations Alternative Splicings Diseases & Disorders Ecology Light Energy Model Organisms Neuronal Plasticity Nutrigenomics Physics RNA Directed RNA methylation RNA-directed DNA methylation RNA-mediated epigenetic regulation of gene expression RNA-mediated gene silencing RNA-mediated toxicity RNA–Mediated Epigenetic Heredity Variations

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).

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?

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?

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.

Chromatin: The structure of DNA

September 19, 2016

by James Kohl with No Comment Adaptations Alternative Splicings Diseases & Disorders Ecology Human Brain Human Pheromones Light Energy Model Organisms Neuronal Plasticity Nutrigenomics Physics RNA Directed RNA methylation RNA-directed DNA methylation RNA-mediated epigenetic regulation of gene expression RNA-mediated gene silencing RNA-mediated toxicity RNA–Mediated Epigenetic Heredity Variations

Update on Inflammation and Degenerative Brain Disease

Excerpt:

While mapping connections of neurons has become the holy grail of current neuroscience, it is clear that communication of neurons with many other types cells is, also, vitally important to every aspect of brain function.

My comment:

Understanding dementia was placed into the context of understanding how virus-driven energy theft alters the de novo creation of olfactory receptor genes and causes the loss of function that is linked to all pathology via chromatin remodeling. The energy-dependent chromatin remodeling is linked from alternative RNA splicing to supercoiled DNA via the innate immune system and nutrient-dependent RNA-mediated amino acid substitutions.

An example of what is known about biologically-based cause and effect was placed into the context of two very different patent applications. One addresses prevention, the other is referred to as Church’s “billion dollar baby.”
For prevention see: Pheromones and the luteinizing hormone for inducing proliferation of neural stem cells and neurogenesis (2011)
For contrast, this is the billion dollar baby: RNA-Guided Human Genome Engineering (2015)
My comment: Nutrient-dependent pheromone-controlled codon optimality links natural selection for food to RNA-mediated cell type differentiation via amino acid substitutions in all cell types of all individuals of all living genera. Transgenerational epigenetic inheritance is the link to energy-dependent ecological adaptations.
Continuing to place the facts about cell type differentiation into the context of cellular intelligence and evolution, which is what Jon Lieff has done for several years, is a misrepresentation of what is known about biologically-based cause and effect. The facts about cell type differentiation place the experience-dependent energy-dependent de novo creation of olfactory receptor genes first.
The creation of new genes is the holy grail of biology. Misrepresentation of virus-driven energy theft, which causes all inflammation and pathology, is the link to replacing the holy grail of biology with the holy grail of neuroscience: mapping connections among neurons. Even when all the connections are mapped, most serious scientists agree that consciousness will not be found among the connections, and that only epigenetic effects on the connections will be linked to degenerative brain disease via chromatin structure and epigenetically-effected supercoiled DNA.
See: From Fertilization to Adult Sexual Behavior
Excerpt (with my emphasis):

Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes (Saunders, Chue, Goebl, Craig, Clark, Powers, Eissenberg, Elgin, Rothfield, and Earnshaw, 1993; Singh, Miller, Pearce, Kothary, Burton, Paro, James, and Gaunt, 1991; Trofatter, Long, Murrell, Stotler, Gusella, and Buckler, 1995). 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: In the context of our section on molecular epigenetics and sex differences that must be linked to alternative splicings of otherwise identical genes via chromosomal rearrangements in sex chromosomes, we included that fact that energy-dependent chromatin remodeling was the link from the alternative splicings to cell type differentiation via chromatin structure. Should we have specifically mentioned that what organisms eat determines the structure of chromatin?
What caused the 20 year-long delay between reporting what was known about role of epigenetically-effected chromatin in RNA-mediated cell type differentiation and what is being reported now in the context of mapping connections of neurons, which Jon Lieff refers to as the holy grail of current neuroscience? How did the holy grail of biology become the holy grail of neuroscience with the change from de novo gene creation to mapping the effects of new genes and the effects of gene losses in different cell types?
See:

Many researchers have reported the link from epigenetically-effected chromatin remodeling to gene regulation. Most have reported the link outside the context of energy-dependent chemical ecology and changes that must link angstroms to ecosystems in all living genera. The alternative is to dismiss everything known to physicists, chemists, and molecular biologists who have already done that.
See for example: Structural diversity of supercoiled DNA Can you dismiss supercoiled DNA?
See also: Excess of Deleterious Mutations around HLA Genes Reveals Evolutionary Cost of Balancing Selection Can you dismiss what is known about the innate immune system and codon optimality?
See also: Direct interrogation of the role of H3K9 in metazoan heterochromatin function Can you dismiss the role of H3K9?
Reported as: Tight DNA packaging protects against ‘jumping genes,’ potential cellular destruction
Excerpt:

Scientists discovered that the major developmental function of heterochromatin — a form of tight DNA packaging found in chromosomes — is likely the suppression of virus-like DNA elements known as transposons or ‘jumping genes,’ which can otherwise copy and paste themselves throughout the genome, potentially destroying important genes, and causing cancers and other diseases.

What will be the next think that pseudoscientists are forced to dismiss if they continue to try to support their ridiculous theories?
See also: Grand project to unify global efforts to understand the brain
Excerpt:

As brainy gatherings go, it takes some beating. Neuroscientists are meeting in New York today to agree on a global mission to understand the workings of the human brain and how to fix it when something goes wrong.
The lofty aim of the Coordinating Global Brain Projects meeting is to unify worldwide efforts to study the brain, in the same way that international collaborations have spurred on astronomy, physics and genetics.
“Neuroscience is coming of age, and it’s now ready for big science,” says Rafael Yuste at Columbia University in New York, who organised today’s meeting with Cori Bargmann at Rockefeller University, also in New York. “This is the first real meeting with all the players in the same room together,” says Yuste.

I mentioned the award that Cori Bargmann won in the narrative of this poster presentation, which was published to Youtube March 2, 2016.
See: RNA mediated molecular epigenetics and virus driven entropy

In two weeks, Cori Bargmann will receive an award that links a single neuron to all works on the lifespan and behavior of the nematode, C. elegans. That neuron integrates information from multiple chemical cues including food, oxygen and pheromones. The integration of the cues controls the expression of social behavior in the context of changes in pH. She is scheduled to present: “Genes, neurons, circuits and behavior: an integrated approach in a compact brain.

Perhaps she realizes there is no further need for her integrated approach, since energy-dependent RNA-mediated pheromone-controlled cell type differentiation has been linked from species of microbes to humans. Others do not seem to be aware of that fact.
See the discussion on the Neuroscience FB group
For example: Misha Zilberter is the first author of Dietary energy substrates reverse early neuronal hyperactivity in a mouse model of Alzheimer’s disease (2013). His work can be compared in the context of my model: Nutrient-dependent/pheromone-controlled adaptive evolution: a model and also this 2016 report on A Genetically Encoded Probe for Live-Cell Imaging of H4K20 Monomethylation
Excerpt:

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

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, but a potential solution has been found. As such, the researchers have overcome challenges to the performance of antibody fragments in live cells due to solubility issues.

For insight on what might prevent discussion of facts about RNA-mediated amino acid substitutions and cell type differentiation in all living genera, see:

Thanks to Anna Di Cosmo for calling attention to this. (Although he uses foul language to make his point, it is a point that needs to be made.)

Unfortunately, using Bill Nye to represent scientists may cause serious scientists to laugh along with anyone among the lay audience who does not believe what people like Bill Nye claim about evolution.

Like serious scientists, they may be waiting for Nye to present experimental evidence that links energy-dependent changes from angstroms to ecosystems in all living genera. Only then are they likely to believe that hydrogen-atom transfer in DNA base pairs in solution is contributing to the loss of species via climate warning.

If changes in the pH of the ocean are not considered, what experimental evidence that links ecological variation to ecological adaptation will be considered by those who think the “Science Guy” is biologically uninformed? Why, from his perspective on evolution, aren’t species simply acquiring more beneficial mutations to evolve — if that’s what theorists want you to believe in?

See also this discussion of As simple as random can be
See also this discussion of Four things you should know about brain research
What can anyone expect to come from any Grand project to unify global efforts to understand the brain. All past grand projects have failed to link what is known about biophysically constrained RNA-mediated protein folding chemistry to cell type differentiation in all living genera via what is known about chromatin, which links energy-dependent changes in the microRNA/messenger RNA balance to biophysically constrained cell type differentiation in all living genera, including those with the primitive brain of a nematode or the brain of a conscious human.
Most the grand projects seem designed to support the ridiculous theories of the project organizers.

Q and A: Energy-dependent cell type differentiation

August 8, 2016

by James Kohl with No Comment Adaptations Alternative Splicings biophotonics Diseases & Disorders Ecology Light Energy Model Organisms Physics RNA Directed RNA methylation RNA-directed DNA methylation RNA-mediated epigenetic regulation of gene expression RNA-mediated gene silencing RNA-mediated toxicity RNA–Mediated Epigenetic Heredity Variations What's in the News

Richard Lenski and other theorists will not discuss the amount of pseudoscientific nonsense they have included in their ridiculous claims. Rarely does anyone else attempt to unravel their claims in the context of the reports I will cite below, or in other reports that refute ridiculous neo-Darwinian theories. Recently, however, Greg Thurston made an honorable effort to learn about energy-dependent biophysically constrained cause and effect via a series of questions that could be answered with minimal jargon.
Q and A from correspondent: Greg Thurston Topic: Energy-dependent changes in the structure of supercoiled DNA
Q1) So this means that no changes would have occurred without energy being available?

A1) The availability of energy is nutrient-dependent and altered by viruses. The lack of any differences in bacteria living in ocean sediments suggests that the absence of sunlight or presence of its biological energy determines all energy-dependent changes in morphological and behavioral phenotypes. Weekend evolution of the bacterial flagellum links virucidal UV light to florescence in P. fluorscens via nutrient-energy uptake and the physiology of pheromone controlled reproduction.

Q2) is there a difference between supercoiled DNA and regular DNA?

A2) Chromatin folding is energy-dependent. The difference in supercoiled DNA compared to any state that is not supercoiled is linked from nutritional epigenetics to the physiology of reproduction, or from virus-driven energy theft to all pathology.

Q3) When you say “from angstroms to ecosystems in all living genera” you mean to say from the smallest observable to the largest observable entities in biology? The whole nine yards, virtually everything?

A3) Yes. The differences in angstroms are not routinely observable, which is why they were not considered in the context of virus-driven pathology — until recently.

Q4) “innate immune system” is there any other type of immune system?

A4) Some people report there is an adaptive immune system, but I don’t know the difference between the innate immune system and an adaptive immune system. The innate immune system enables ecological adaptations, which are manifested in morphological and behavioral phentoypes.

Q5) Do all living genera have an innate immune system?

A5) I’m not sure that any individual or species can survive without one, but I cannot prove that “all living genera” have an innate immune system.

Q6) When you say “linked energy-dependent changes in the structure … via the innate immune system and the physiology of reproduction.” Do you mean changes in the structure were linked TO the innate immune system and the physiology of reproduction, or TO SOMETHING ELSE via these two things?

A6) Energy-dependent changes must be linked from the innate immune system to the physiology of reproduction for fixation of RNA-mediated amino acid substitutions to occur in the organized genomes of specific populations.

Q7) If the latter, what is the ‘something else’?

A7) No one has made claims that fixation occurs outside the context of the physiology of reproduction except those who put fixation of beneficial mutations into the context of population genetics. Pseudoscientists do that because otherwise neo-Darwinian theory has no explanatory power. The neo-Darwinists won’t tell you what was selected. And, they don’t mention virus-driven energy theft. Some are changing their claims about natural selection, but most still claim that mutations are selected. Without their ridiculous claims they have no theory, so they continue to claim that something must have been selected.

Q8)”Supercoiled DNA protects all organized genomes” — are there any genomes which are not organized?

A8) Incompletely organized genomes are found in behavioral morphs of some species that have not yet diverged (e.g., white throated sparrows)

Q9) “from virus-driven entropy.” what other kind of entropy is there, and what drives it?

A9) I use “entropy” in the context of thermodynamic cycles of protein biosynthesis and degradation. That helps to avoid debate about theories about open or closed systems.

Q10) Is there anything else which supercoiled DNA protects genomes from, or is it all virus-driven?

A10) I’m not willing to speculate. I’m providing facts linked to biologically-based cause and effect.

Q11) “The virucidal effect of ultraviolet light on RNA-mediated cell type differentiation is the source of all biodiversity. ” — Virucidal means UV light kills viruses?

A11) Yes.

Q12) Is there any other type besides RNA-mediated cell type differentiation?

A12) Not to my knowledge.

Q13) Are you saying that all biodiversity would not occur unless UV light was virucidal?

A13) I’m saying that mutation-driven evolution is not supported with experimental evidence of biologically-based cause and effect.

Q14) “the source of all biodiversity is biophysically constrained” — in other words there are rules in place which guide everything when it works properly?

A14) Yes. There are Laws of Biology. Biophysically constrained energy-dependent protein folding chemistry guides hydrogen-atom transfer in DNA base pairs in solution, and links microRNA flanking sequences to RNA-mediated amino acid substitutions and all biodiversity.

Q15) “they know that virus-driven energy theft breaks those constraints” — is ‘vdet’ the only thing which breaks those constraints?

A15) To my knowledge, no one else has made claims about how the constraints are broken.

Q16) This gets to the nub of the significance of this. That, I think is the pot of gold. What is the significance that they know, but are keeping mum on it? Is it because if they let the cat out of the bag, Darwinism is dead supposedly?

A16) Yes. But also, all theorists will look foolish for touting neo-Darwinian nonsense. George Church and others may only be protecting their biologically uninformed colleagues in academia.

Q17) Are they holding back science by not broadcasting this?

A17) Yes. The November, 2016 meeting of the Royal Society is scheduled in an attempt to save the theory of evolution via careful extraction of neo-Darwinian nonsense, albeit without claims about virus-driven entropy.

Q18. If they were to broadcast it, how would that change how science is done? (Apart from so many being crestfallen that their god is dead?)

A18) The change from gene-centric neo-Darwinian views to focus on energy-dependent changes in RNA methylation and RNA-mediated amino acid substitutions is required if science is to be done. It does little good to ridicule theorists, however, no matter how much fun it might be to show their god (of mutation-driven evolution) is dead. The ridicule simply encourages them to tell more lies.

Q19) I think I get your last paragraph. Except I’m not sure how methylation fits in there.
A19) RNA-methylation is the energy-dependent link to learning and memory in all living genera.
Thanks again. Your questions will help some others move forward despite the complexity. Ultimately, however, all serious scientists will learn why George Church et al., filed the patent for RNA-guided human genome engineering.
Perhaps they deserve to deliver their “billion dollar baby” without considering others who have placed their “baby” into the context of what was known about RNA-mediated links from fertilization to adult sexual behavior via cell type differentiation for more than 20 years.
But see: C2c2 is a single-component programmable RNA-guided RNA-targeting CRISPR effector
Abstract conclusion:

C2c2 could protect bacteria from virus spread via programmed cell death and dormancy induction. A single-effector RNA targeting system has the potential to serve as a general chassis for molecular tools for visualizing, degrading, or binding RNA in a programmable, multiplexed fashion.

Article excerpt:

…there is a possibility that C2c2 functions solely as an RNA-guided RNA-targeting CRISPR effector.

From their Conclusions:

C2c2 cleaves RNA through conserved basic residues within its two HEPN domains, in contrast to the catalytic mechanisms of other known RNases found in CRISPR-Cas systems (25, 48). Alanine substitution of any of the four predicted HEPN domain catalytic residues converted C2c2 into an inactive programmable RNA-binding protein (dC2c2, analogous to dCas9).

Conclusion:

The CRISPR-C2c2 system represent a distinct evolutionary path among class 2 CRISPR-Cas systems. It is likely that other, broadly analogous class 2 RNA-targeting immune systems exist, and further characterization of the diverse members of class 2 systems will provide a deeper understanding of bacterial immunity and provide a rich starting point for the development of programmable molecular tools for in vivo RNA manipulation.

My comment: They link the nutrient energy-dependent pheromone-controlled physiology of reproduction to fixation of the alanine substitution and stability of all organized genomes in the context of other RNA-mediated amino acid substitutions such as Val66Met in mice and Val158Met in humans during life history transitions in morphological and behavioral phenotypes.
See for other examples: Nutrient-dependent/pheromone-controlled adaptive evolution: a model

Two additional recent reports link substitution of the amino acid alanine for the amino acid valine (Grossman et al., 2013) to nutrient-dependent pheromone-controlled adaptive evolution. The alanine substitution for valine does not appear to be under any selection pressure in mice. The cause-and-effect relationship was established in mice by comparing the effects of the alanine, which is under selection pressure in humans, via its substitution for valine in mice (Kamberov et al., 2013).

These two reports (Grossman et al., 2013; Kamberov et al., 2013) tell a new short story of adaptive evolution. The story begins with what was probably a nutrient-dependent variant allele that arose in central China approximately 30,000 years ago. The effect of the allele is adaptive and it is manifested in the context of an effect on sweat, skin, hair, and teeth. In other mammals, like the mouse, the effect on sweat, skin, hair, and teeth is due to an epigenetic effect of nutrients on hormones responsible for the tweaking of immense gene networks that metabolize nutrients to pheromones. The pheromones control the nutrient-dependent hormone-dependent organization and activation of reproductive sexual behavior in mammals such as mice and humans, but also in invertebrates as previously indicated. That means the adaptive evolution of the human population, which is detailed in these two reports, is also likely to be nutrient-dependent and pheromone-controlled, since there is no other model for that.

Conclusion:

This study suggests that there are specific genetic variants and physiological mechanism(s) that differ among West African and European populations, which when in the context of male sex, result in lower central adiposity. Further research, likely requiring larger sample sizes, is needed to identify these putative specific genetic factors and their corresponding physiological mechanisms. The identification and understanding of these mechanisms could lead to improved prevention and treatment approaches. It will also be important to also consider and examine non-genetic factors that may underlie the greater racial disparity among women.

My comment: Their conclusion ignores everything known to serious scientists about energy-dependent RNA-mediated cell type differentiation which links all sex differences in cell types to all other RNA-mediated differences via the nutrient-dependent pheromone-controlled physiology of reproduction in yeasts and fixation of amino acid substitutions in organized genomes. See: From Fertilization to Adult Sexual Behavior for details on the molecular epigenetics of energy-dependent cell type differention, which have since been linked from one-carbon metabolism to genetic networks in all living genera.

Abstract introduction:

Rising atmospheric CO2 concentrations are likely to affect many ecosystems worldwide.

Article conclusion:

In conclusion, our study shows that changes in Ci availability act as an important selective factor in cyanobacterial communities. Some strains perform better at low Ci concentrations, whereas other strains are better competitors at high Ci levels, causing a succession of different Ci uptake genotypes during bloom development. Models and laboratory experiments predict that rising atmospheric CO2 levels will lead to higher CO2(aq) and bicarbonate concentrations, and a later onset and shorter duration of CO2-depleted conditions during dense summer blooms (14, 15). Our results suggest that this increased Ci availability will favor low-affinity but high-flux bicarbonate uptake genotypes. Hence, future harmful cyanobacterial blooms will most likely have a genotype composition that differs from contemporary blooms and will be adapted to the new conditions in a high-CO2 world.

My comment: The harmful blooms link virus-driven energy theft from the proliferation of strains that reproduce faster (‘perform better’) at high Carbon ion concentrations, which link virus-caused changes in hydrogen-atom transfer in DNA base pairs in solution to all pathology in all living genera.

See for comparison: Tempo and mode of genome evolution in a 50,000-generation experiment

Excerpt (with my emphasis):

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 it is generally thought that such selection is extremely weak, affects only a small fraction of sites at risk for synonymous mutations, or both 36,37.

My comment: They admit that their lie about synonymous substitutions, which they call point mutations, does not hold up to scrutiny in the context of biophysically constrained nutrient energy-dependent RNA-mediated protein folding chemistry. They, they continue to make vague claims about how selection for synonymous mutations occurs. The fact that selection for amino acid substitutions is controlled by the physiology of reproduction in all genera is not given any consideration whatsoever. It is dismissed with claims about synonymous mutations that were first called synonymous substitutions. They use wordplay to obfuscate the fact that energy-dependent amino acid substitutions are not mutations. Without the wordplay, they would be forces to admit that their experiment is designed to link ecological variation to ecological adaptation via the energy-dependent physiology of pheromone-controlled reproduction in species from microbes to humans.
See for instance two of the works they cited:

Different Trajectories of Parallel Evolution During Viral Adaptation (1999)
Whole genome, whole population sequencing reveals that loss of signaling networks is the major adaptive strategy in a constant environment (2013)
My comment: Lenski’s group clearly knows his experiment links ecological variation to ecological adaptation in a constant evironment. But Lenski has been reporting it as if it linked mutations to evolution. See: The Man Who Bottled Evolution
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:

…adaptation may not just be in response to direct selective forces; it may also be influenced circuitously by conditions like temperature and acidity that may select for changes in stability.

My comment: The selective forces link biophysically constrained energy-dependent changes in cell type differentiation to healthy longevity or they link virus-driven energy theft to all pathology. Nothing links the selective forces to the evolution of one species from another. The Man Who Bottled Evolution is the man who bottled long term ecological adaptation in an experiment he referred to as the Long Term Evolution Experiment (LTEE). Now that Lenski admits he has been caught in a lie, he refuses to move forward by linking codon usage to biophysically constrained RNA-mediated protein folding chemistry, which links the innate immune system to supercoiled DNA without any neo-Darwinian nonsense.
See also: New Perspectives on Ebola Virus Evolution (2016) with my emphasis

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: Positive selection for nutrient energy-dependent RNA-mediated amino acid substitutions again replaces the vague claims about ‘natural’ selection made by neo-Darwinian theorists. The energy-dependent physiology of pheromone-controlled reproduction in mosquitoes must be linked to virus-driven energy theft and DNA damage in humans, or all claims about ‘natural’ selection and evolution must be ignored.
What’s worse is that this admission must also be ignored.

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

My comment: Anyone who claims that any species evolved from another via natural selection in the context of mutation-driven evolution is propagating Lenski’s lie. They must ignore the fact that the physiology of reproduction is energy-dependent and controlled by pheromones in species from microbes to humans.
See for comparison: Epigenetics and Genetics of Viral Latency
Excerpt:

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

1) Ignoring the fact that healthy longevity is nutrient energy-dependent;

2) Ignoring the facts about viral latency, which is linked to all pathology; and

3) Ignoring the fact that a single amino acid substitution in the influenza virus is linked to seasonal differences in its virulence/pathology;

sums up the amount of ignorance that is taught when neo-Darwian theory is taught to unsuspecting students.

Energy dependent RNA-mediated immunity (2)

March 4, 2016

by James Kohl with 2 Comments Adaptations biophotonics Ecology Light Energy Model Organisms Neuronal Plasticity Nutrigenomics Pharmacogenomics Physics RNA Directed RNA-directed DNA methylation RNA-mediated epigenetic regulation of gene expression RNA-mediated gene silencing RNA-mediated toxicity RNA–Mediated Epigenetic Heredity Variations

Neuroscience of Early-Life Learning in C. elegans

“We have long been recording behavior in worms, but we and others have concluded that, if you want to get physiologically relevant neural activity patterns, you have to look at neurons inside a behaving animal,” Samuel explained. “Only in that context are all feedback loops intact, where behavioral output modulates neural activity which, in turn, shapes behavior.”

As all serious scientists continue to link ecological variation to ecological speciation via nutrient-dependent pheromone-controlled reproduction in species from microbes to humans, my antagonists have all but disappeared.
Clearly, it is time to finally begin discussion of how virus-driven energy theft links hydrogen-atom transfer in DNA base pairs in solution from mutations to pathology instead of from nutrient-dependent RNA-mediated DNA repair via amino acid substitutions to supercoiled DNA, which protects organized genomes from virus-driven entropy.
The text and the narrative from this poster session will be available on March 16th. I am posting it here in advance because the news about early-life learning and regulatory evolution has been placed into the context of innate immunity by theorists who do not understand how biophysically-constrained energy-dependent cell type differentiation occurs in species from microbes to humans. Evolution does not regulate itself. The innate immune system links nutrient-dependent immune system function to supercoiled DNA, which protects all organized genomes from virus-driven entropy. Ecological speciation in nematodes clearly links what they eat to biodiversity via the innate immune system and the physiology of reproduction, which is how ecological adaptations occur in all living genera.
See for example: Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution. My comment on this article was removed and replaced with a “response” by the authors. I forced them to admit that “The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.”
See also the comment by Roy Niles on Neuroscience of Early-Life Learning in C. elegans.
An editor at The Scientist warned me not to respond with any more off topic claims. It has since become perfectly clear that he knew my claims were about to expose the nonsense that has since been touted about sensory input, the immune system, learning and ecological adaptation via nutrient-dependent RNA-mediated amino acid substitutions in all living genera.

RNA-mediated molecular epigenetics and virus-driven entropy

Abstract: Energy-dependent molecular epigenetics support Einstein’s complete molecular mechanical theory via established links from microRNA flanking sequences to DNA base pair substitutions and amino acid substitutions in adhesion proteins. The adhesion proteins include heat shock proteins that link the epigenetic landscape to biophysically constrained nutrient-dependent RNA-mediated protein folding chemistry and cell type differentiation via the structure and function of supercoiled DNA. Einstein’s theory fits into the context of Darwin’s “conditions of life” via the de novo creation of nucleic acids; the nutrient-dependent function of the ribosome; and the de novo creation of olfactory receptor genes. De novo gene creation is the “holy grail” of biophysically constrained chemistry and biologically-based cause and effect. The discoveries reviewed here link the nutrient-dependent microRNA/messenger RNA balance from metabolic networks to genetic networks and to healthy longevity or virus-driven pathology in the context of what is known about all model organisms.

Summary:

The Zika virus and other viruses steal energy that links odors and the nutrient-dependent prenatal migration of GnRH neurosecretory neurons to pheromones that also alter the HPG and HPA axes. GnRH pulsatility modulates energy-dependent hydrogen-atom transfer in DNA base pairs in blood that links ingestive behavior to metabolic networks and genetic networks during the concurrent maturation of the neuroendocrine, reproductive, and central nervous systems via the physiology of reproduction, sex differences in behavior, and other behavioral differences, which are linked by RNA-mediated amino acid substitutions to morphological phenotypes and behavioral phenotypes.

Physics
Indeed, in the case of higher animals we know the kind of orderliness they feed upon well enough, viz. the extremely well-ordered state of matter in more or less complicated organic compounds, which serve them as foodstuffs. After utilizing it they return it in a very much degraded form -not entirely degraded, however, for plants can still make use of it. (These, of course, have their most power supply of ‘negative entropy’ the sunlight) — Erwin Schrödinger (1944)

Chemistry
The quantised nature of light and energy is central to all of chemistry. It explains how matter and light interact – why grass is green and the sky is blue – as well as providing the basis of all the spectroscopic methods that enable us to decode the structures of molecules. — Philip Ball (2005)

Molecular Epigenetics

The authors note that on page 17184, right column, first paragraph, line 4, “effect” should instead appear as “affect.” — Bruce McEwen (2013)

Nutritional epigenetics. Energy-dependent molecular mechanisms link Einstein’s complete molecular mechanical theory from microRNA flanking sequences to base pair substitutions in DNA and to RNA-mediated amino acid substitutions in adhesion proteins via the ribosome. The adhesion proteins include heat shock proteins that link biophysically constrained nutrient-dependent RNA-mediated protein folding chemistry to cell type differentiation and supercoiled DNA. [1-2]

Metabolic energy-dependent alternative splicing (AS) catalyzes the removal of intronic sequences and the joining of selected exons. Biophysically constrained nutrient-dependent combinatorial differences in joined sequences link thermodynamic cycles of protein biosynthesis and degradation to the pH-dependent creation of multiple splice-variants.The splice variants link hydrogen-atom transfer in DNA base pairs in solution from the energy-dependent origin of nucleic acids, the “RNA-world,” and the genetic code to the creation of different proteins from a single gene via pH and the biophysically constrained chemistry of RNA-mediated protein folding. [3-4]For example, metabolic energy links guanine nucleotide binding proteins (G proteins) to the experience-dependent de novo creation of monoallelic G protein-coupled receptors (GPCRs). Ligand-receptor binding links the de novo creation of olfactory receptor genes, which are GPCRs, to the creation of other receptors such as photoreceptors. [5]Nutrient-dependent de novo gene creation and chemotaxis coordinate phototaxis and responses to other sensory input throughout life history transitions in all living genera. [6] Sensory input links the epigenetic landscape to the physical landscape of supercoiled DNA, which appears to protects all organized genomes from virus-driven entropy.

Viruses-driven pathology. Retroviral integrase catalyses the integration of viral DNA into host target DNA. [7] Viruses enter cells and they steal metabolic energy to replicate. [8] The stolen energy is required to link AS to the de novo creation of receptors that allow different nutrients to enter different cell types. Theoretically, this is how the an accumulation of viruses prevents nutrient-dependent cell type differentiation. The viruses link perturbed protein folding to pathology via metabolic networks and genetic networks in the context of the Precision Medicine Initiative.[9]

Neo-Darwinian theorists ignore biophysically constrained RNA-mediated protein folding chemistry. They use statistical inferences and assumptions to link definitions of mutation to definitions of evolution. They link evolution to biodiversity in different species. [10]

Neo-Darwinists typically do not include the role of virus-driven pathology for comparison to the role of nutritional epigenetics in the context of healthy longevity. They typically fail to link transgenerational epigenetic inheritance from the physiology of nutrient-dependent pheromone-controlled reproduction in soil bacteria to the bull sperm microRNAome via nutrient-dependent microRNAs and biophysically constrained protein folding chemistry in all living genera.[11]

More than 47,000 published works link nutrient energy-dependent microRNAs to biophysically constrained RNA-mediated DNA repair and cell type differentiation. The most recent addition linked a specific microRNA DNA repair.[12]

Many recent news reports continue to claim the conserved molecular mechanisms and pathways of cell type differentiation via DNA repair may not link unicellular life to multicellular life.[13] Theorists and science news journalists who fail to link unicellular life to multicellular life via changes in the nutrient-dependent microRNA/messenger RNA balance and/or virus-driven pathology exemplify a failure that is addressed in the context of the integrated facts about microRNAs, which are displayed here

For example, the quality of foraging in crustaceans and insects links microRNA flanking sequences from sunlight to energy metabolism and genetic networks via amino acids and transgenerational epigenetic inheritance of sex differences in morphological and behavioral phenotypes in bulls and cows.[14] Conserved molecular mechanisms link nutrient energy-dependent changes in microRNAs to cell type differentiation and morphological and behavioral phenotypes of humans. [15]

In the context of what is currently known about the links from atoms to ecosystems in all invertebrates and all vertebrates, it has become obvious that viruses steal the nutrient dependent-energy that links hydrogen-atom transfer in DNA base pairs in solution to cell type differentiation in all living genera.Biophysically constrained RNA-mediated protein folding chemistry links UV light to chemotaxis, phototaxis, learning, memory and supercoiled DNA in the honeybee model organism. Nutrient-dependent metabolic networks and genetic networks link RNA-mediated DNA repair and supercoiled DNA to protection against virus-driven entropy in all organized genomes. [16-18]A drug that is commonly used to prevent the model organism C. elegans from laying eggs appears to alter nutrient energy-dependent RNA-mediated DNA repair via microRNAS that link pH, temperature, and oxygen levels from the absence of stress to healthy longevity. [19] The nematode may be the first model organism used to link virus-driven energy theft to pathology in the context of what is known about the nutrient-dependent innate immune system of all cell types in all living genera; the physiology of reproduction; and how ecological variation is linked to ecological adaptation in the context of speciation. (P. pacificus is an adapted C. elegans.)

1] The phylogenetic utility and functional constraint of microRNA flanking sequences

[2] Structural diversity of supercoiled DNA

[3] UV-Induced Charge Transfer States in DNA Promote Sequence Selective Self-Repair

[4] Phosphorylation -Mediated Regulation of Alternative Splicing in Cancer

[5] An Epigenetic Signature for Monoallelic Olfactory Receptor Expression

[6] Cyanobacteria use micro-optics to sense light direction

[7] Cryo-EM reveals a novel octameric integrase structure for betaretroviral intasome function

[8] Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution

[9] RNA-Mediated Regulation of HMGA1 Function

[10] An expanded sequence context model broadly explains variability in polymorphism levels across the human genome

[11] The Bull Sperm MicroRNAome and the Effect of Fescue Toxicosis on Sperm MicroRNA Expression

[12] miR-30e controls DNA damage-induced stress responses by modulating expression of the CDK inhibitor p21WAF1/CIP1 and caspase-3

[13] Redefining part of 300 year-old classification system for grouping members of the animal kingdom

[14] Systematic microRNAome profiling reveals the roles of microRNAs in milk protein metabolism and quality: insights on low-quality forage utilization

[15] Human milk miRNAs primarily originate from the mammary gland resulting in unique miRNA profiles of fractionated milk

[16] Neuroscience of Early-Life Learning in C. elegans

[17] Differential Odour Coding of Isotopomers in the Honeybee Brain

[18] Breast Milk Sugars Support Infant Gut Health

[19] C. elegans lifespan extension by osmotic stress requires FUdR , base excision repair, FOXO, and sirtuins

Narrative:

My name is James Kohl. I’m a medical laboratory scientist. I don’t know anyone who has ever performed patient testing and reported their results in the context of a series of mutations and the biodiversity of human tissue types. Other medical laboratory scientists us experimental evidence of biologically-based cause and effect to link what is known about the difference between nutrient-dependent healthy longevity and pathology.

For example, after I submitted the abstract for this poster presentation, an article linked everything known about quantum physics to induction of gonadotropin releasing hormone messenger RNA expression. Gonadotropin releasing hormone (or GnRH) links all cell type differentiation in vertebrates to all the microRNAs in the bull sperm that is linked to fertility.
I don’t think that the authors realized they had linked docosahexaenoic acid and another fatty acid from microRNA-9 and microRNA-200 to nutrient-dependent transcription factors and human fertility. The transcription factors link the development of the olfactory systems and the immune systems of all vertebrates to GnRH synthesis in hormone-secreting neurons. Neurons that secrete GnRH are linked to every aspect of nutrient-dependent vertebrate morphological and behavioral diversity.
If you only look at the works cited in this poster session, you could link everything known about nutrient-dependent cell type differentiation to healthy longevity. You could also link everything known about viruses to all pathology. For example, the nematode model of learning and memory links amino acid sensing to RNA-mediated amino acid substitutions that protect our organized genomes from virus-driven changes in nerve cells that alter olfactory acuity and specificity in Alzheimer’s disease.
In two weeks, Cori Bargmann will receive an award that links a single neuron to all works on the lifespan and behavior of the nematode, C. elegans. That neuron integrates information from multiple chemical cues including food, oxygen and pheromones. The integration of the cues controls the expression of social behavior in the context of changes in pH. She is scheduled to present: “Genes, neurons, circuits and behavior: an integrated approach in a compact brain.
Her work links cell type differentiation in a compact neuronal system to everything known to scientists inside and outside the hospital laboratory. Many scientists know how ecological variation and ecological adaptation link atoms to ecosystems in all living genera. For example, food, oxygen, pH, and temperature link the nutrient-dependent pheromone-controlled physiology of reproduction from C. elegans to the GnRH neuronal system of all vertebrates. All behavior is linked to supercoiled DNA in species from microbes to humans.Supercoiled DNA is the link from RNA-mediated DNA repair to examples of ecological adaptation. In this model, nutrient-dependent microRNAs link energy-dependent changes from hydrogen-atom transfer in DNA base pairs in solution to the molecular mechanisms that link morphological and behavioral phenotypes to survival of the species via their physiology of reproduction.
In the first part of this poster session, six citations link everything known about nutritional epigenetics from microRNAs to RNA-mediated amino acid substitutions. The substitutions differentiate all cell types in all living genera. Fixation of beneficial amino acid substitutions in organized genomes is the key to ecological adaptation. Fixation occurs in the context of the energy-dependent physiology of reproduction.
In the second part of this poster, 4 more citations link virus-driven energy theft to all pathology.
Part 3 links 9 more citations and examples of biologically-based cause and effect from the Zika virus to differences in human craniofacial and behavioral phenotypes.
The key to the model of nutrient-dependent transgenerational epigenetic inheritance of healthy longevity compared to virus-driven pathology is the energy that is required for RNA-mediated cell type differentiation.The Zika virus and other viruses steal energy that links odors and the immune system to the GnRH neuronal system in all vertebrates from a single neuron in C. elegans. Nutrient energy-dependent prenatal migration of GnRH-secreting neurons links the epigenetic effects of food odors and pheromones to changes in the HPG and HPA axes that link hormones to behavior.The energy-dependent GnRH pulse modulates energy-dependent hydrogen-atom transfer in DNA base pairs in blood. Our blood links what nematodes eat from their metabolic networks and genetic networks to the stability of all organized genomes when the networks lead to supercoiled DNA.In all vertebrates, the neurons that secrete GnRH link metabolic networks to genetic networks during the concurrent maturation of the neuroendocrine, reproductive, and central nervous systems. The GnRH neuronal system can be compared to a single neuron in C. elegans because GnRH links the physiology of reproduction, sex differences in behavior, and other behavioral differences that link RNA-mediated amino acid substitutions to morphological phenotypes and behavioral phenotypes. For example, what nematodes eat links the behavior of C. elegans to the behavior of P. pacificus, a predatory nematode with teeth.I’ve added quotations from Schrödinger, Philip Ball, and Bruce McEwen. I hope their works will encourage others to learn more about the anti-entropic energy of the sun and how it links light and energy to the biophysically constrained chemistry of protein folding. Protein folding starts with epigenetic Effects on genes that are linked to Affects on behavior in the context of the systems biology represented in this model.In the early 1990s I learned to differentiate between the effects on hormones and the affects of hormones on behavior. That led me to link the sun’s virucidal energy from UV light to supercoiled DNA, which protects organized genomes from virus-driven entropy.
From the perspective of physics, higher animals metabolize food and they return the degraded forms of food which are the power supply that link soil bacteria to the growth of plants. But, sunlight is the source of anti-entropic energy in plants.
The quantised nature of light and energy links all of Einstein’s theories to chemistry. Quantum physics explains how matter and light interact, which most people can link to the reasons why grass is green and the sky is blue. Medical laboratory scientists know that the nature of light and energy is measured in the spectroscopic methods that enable us to decode the structures of molecules, which link hydrogen-atom transfer in DNA base pairs to the visible spectrum of light, but also to UV light and infrared light.
In the context of light, chemistry and molecular epigenetics, medical laboratory scientists learn the difference between an “effect” on their test results and an affect on their behavior.
The epigenetic effects of the sun’s biological energy are linked to affects on behavior in all living genera by supercoiled DNA that protects organized genomes from virus-driven entropy.

Bringing RNA back to epigenetics (20 years later)

February 19, 2016

by James Kohl with No Comment Adaptations Diseases & Disorders Ecology Model Organisms Nutrigenomics Pharmacogenomics Physics RNA Directed RNA-directed DNA methylation RNA-mediated epigenetic regulation of gene expression RNA-mediated gene silencing RNA-mediated toxicity Variations

Has Contemporary Academia Outgrown the Carl Sagan Effect? [Subscription required]
Excerpt (with my emphasis):

[Sean Carroll] offered 13 pieces of advice…: “Do good research; Make an impact in the field; Bring in grant money… Don’t be too well known outside the field; Don’t write a book; Choose your hobbies wisely.” Carroll argued that academics look askance at colleagues that have too high of a public profile. Not out of envy—but because they worry that public scientists care more about their media presence than about discovery.

Excerpt:

…institutions must find new incentives for dissemination, and the Royal Society has recommended the implementation of “a more effective support system” and “the introduction of significant departmental rewards” (Royal Society, 2006) for those who communicate. These are worthwhile goals, but more pressing perhaps is the need to overcome lingering ambivalence toward engagement in public discourse.

My comment: The book I wrote and published in 1995 with co-author Robert T. Francoeur is available here in an updated paperback from 2002. See: The Scent of Eros: Mysteries of Odor in Human Sexuality. With other co-authors, I subsequently linked the nutrient-dependent physiology and behavior of species from microbes to humans via RNA-mediated events.
Metabolic networks and genetic networks are RNA-mediated. The networks link atoms to ecosystems in all living genera via the physiology of reproduction. Supercoiled DNA in organized genomes protects all genera against virus-driven pathology. Examples that link virus-driven pathology from bacteria to plants and animals have since repeatedly confirmed the links from atoms to ecosytems in the context of energy-dependent hydrogen-atom transfer in DNA base pairs in solution that link nutrient energy-dependent reproduction to RNA-mediated amino acid substitutions and all biomass and all biodiversity.
For comparison, see:
RNA Epigenetics January 1, 2016

MicroRNA-mediated RNA epigenetics January 4, 2016

New RNA letter regulates gene expression: Discovery brings RNA to the fore of epigenetics February 16, 2016
My comment: RNA has been at the fore of epigenetics since our 1996 Hormones and Behavior review. In our section on molecular epigenetics, we wrote:

Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes (Saunders, Chue, Goebl, Craig, Clark, Powers, Eissenberg, Elgin, Rothfield, and Earnshaw, 1993; Singh, Miller, Pearce, Kothary, Burton, Paro, James, and Gaunt, 1991; Trofatter, Long, Murrell, Stotler, Gusella, and Buckler, 1995). 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.

Among other published works, we cited:

Adler, B. K., and Hajduk, S.L. (1994). Mechanisms and origins of RNA editing. Curr. Opin. Genet. Dev. 4, 316-322.

Clemson, C. M., and Lawrence, J. B. (1996). Multifunctional compartments in the nucleus: Insights from DNA and RNA localization. J. Cell. Biochem. 62, 181-190.

Green, M. R. (1991). Biochemical mechanisms of constitutive and regulated pre-mRNA splicing. Annu. Rev. Cell Biol. 7, 559-599.

Guthrie, K. M., Anderson, A. J., Leon, M., and Gall, C. (1993). Odor-induced increases in c-fos mRNA expression reveal an anatomical “unit” for odor processing in the olfactory bulb. Proc. Natl. Acad. Sci. USA 90, 3329-3333.

Schneider-Gadicke, A., Beer-Romero, P., Brown, L. C., Mardon, C., Luoh, S. W., and Page, D. C. (1989). Putative transcription activator with alternative isoforms encoded by human ZFX gene. Nature 342, 708 -711.

Our focus was on sex differences in cell types. Others have since linked RNA-mediated events from the epigenetic landscape to the physical landscape of DNA in all living genera via the physiology of reproduction.
See for example:

See also: The Bull Sperm MicroRNAome and the Effect of Fescue Toxicosis on Sperm MicroRNA Expression
My comment: Science news outlets appear to be following my series of more that 600 blog posts and my FB group posts at RNA-mediated. If I were following reports from other news services I would not already have linked: Watson–Crick Base Pairing Controls Excited–State Decay in Natural DNA, which was reported as: Base-pairing protects DNA from UV damage, from microbes to mammals.
See for example: Applying humanized mouse models to immune therapy research
Excerpt:

Mouse models have been a mainstay in biomedical research for decades. As these models have become more sophisticated, their application has grown and now includes a wide variety of immunodeficient strains that can be used to examine the in vivo growth of human tumors and to test new cancer treatments.

My comment: I linked the mouse model organism to humans via one base pair change and one amino acid substitution in my 2013 review: Nutrient-dependent/pheromone-controlled adaptive evolution: a model
Excerpt:

The recently detailed mouse model (Li et al., 2013) builds on what is known about olfactory/pheromonal communication in species from microbes to man and incorporates works from mammals that elucidate the molecular mechanisms that are clearly involved. Sex-dependent production of a mouse ‘chemosignal’ with incentive salience appears to have arisen de novo via coincident adaptive evolution that involves an obvious two-step synergy between commensal bacteria and a sex-dependent liver enzyme that metabolizes the nutrient chemical choline.

Excerpt:

They identified a link between VTE and three variants in a chromosome — rs2144940, rs2567617, and rs1998081 — associated with decreased expression of thrombomodulin, a protein that regulates clotting. Approximately 36 percent of American Americans have at least one of these variants, however, these variants were found in much lower frequency in other ethnicities from previous studies.
“This study not only brings us closer to understanding the cause of VTE in African Americans,” Perera said in a statement, “it demonstrates the importance of conducting populations-specific research in precision medicine.

My comment: Do neo-Darwinian theorists think that these variants are mutations? Are they claiming that 36 percent of African Americans are mutants? If so, what are they claiming about the other 64 percent of African Americans who do not have these three variants in a chromosome?
See also: Transposons, and why you should love them

Although TEs can have deleterious effects, in higher animals they have become essential contributors to evolution, and have been described as the “motors of evolution”. By carrying out processes such as gene rearrangement, mutation of gene and regulatory sequences, genomic recombination, gene duplication, and other types of rearrangements, TEs have provided the adaptive benefit of increased genetic diversity and plasticity for their host species. TEs and their hosts have been forced to coevolve, and have achieved a fine balance between the potentially damaging and potentially beneficial effects of TEs.

My comment: They seem to be claiming that mutants co-evolved with organisms that ecologically adapted in the context of their nutrient-dependent physiology of reproduction, which is linked to the supercoiled DNA that protects all organisms from virus-driven entropy. Others have yet to link the virucidal effects of sunlight from hydrogen-atom transfer in DNA base pairs in solution to the physiology of nutrient-dependent pheromone-controlled RNA-mediated cell type differentiation in soil microbes to the cancer treatment “taxol.” When someone else finally does that, their report will be a follow-up to this one: Discovery brings RNA to the fore of epigenetics.
Until then, see: Delving into dark matter
Excerpt:

Bhardwaj added, “The ncRNAs in cancers where odd RNAs were being activated and transcribed had unusual patterns that were similar to some pathogens, and this causes them to stimulate an innate immune response.”
“All in all, we believe these ncRNAs may play a significant role in mediating immune responses against cancer, but much work remains to describe their precise interactions,” said Greenbaum. “If we could characterize the ncRNA and link it with specific pathways, we could understand its role in the tumor environment and determine how it can be utilized for patient therapy.”

My comment: They fail to recognize the difference between nutrient-dependent microRNAs and viral microRNAs, which is why they cannot categorize the difference in pathways that lead to nutrient-dependent healthy longevity, which could be compared to virus-driven pathology. Instead, most researchers are still trying to determine how what they once called “Junk DNA” and now call “dark matter” links metabolic networks from genetic networks to supercoiled DNA that typically protects all organized genome from virus-driven entropy.
A new kind of periodic table
Conclusion:

According to Marsh, researchers are still very interested in trying to understand the evolutionary pathways of protein complexes, in particular heteromeric complexes. “We are currently doing some work on how the assembly pathways of heteromers are related to their evolution. Now that I’ve started my own research group in Edinburgh, one of my main focuses is on understanding how pathogenic mutations can disrupt the assembly of protein complexes, and how protein complex assembly and quaternary structure can influence the phenotypic impacts of mutations.”

See also: How to Build Life in a Pre-Darwinian World Perhaps chemistry played a more instrumental role in the origin of life than scientists thought.

Conclusion: Hud and his collaborators propose that RNA and proteins evolved in tandem, and those that figured out how to work together survived best. This idea lacks the simplicity of the RNA world, which posits a single molecule capable of both encoding information and catalyzing chemical reactions. But Hud suggests that facility might trump elegance in the emergence of life. “I think there’s been an overemphasis on what we call simplicity, that one polymer is simpler than two,” he said. “Maybe it’s easier to get certain reactions going if two polymers work together. Maybe it’s simpler for polymers to work together from the start.”

My comment: They fail to link sunlight and gravitational waves from hydrogen-atom transfer in DNA base pairs in solution and claim emergence and evolution. Since our 1996 review brought RNA to the fore of epigenetics, please return to this blog site to find information that others may still be missing during the next 20 years, or if I gave up trying to tell them anything more about about the obvious links from angstroms to ecosystems.

Excerpt:

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.

See for comparison: Evolution silences harmful mutations
Excerpt:

…researchers looked more closely at four synonymous but costly mutations in the gene for a ribosomal protein. They observed that the main problem with these mutations was that they caused a decrease in production of the mutated ribosomal protein. The cells entered into a vicious circle in which low protein levels resulted in defective ribosomes that in turn caused further problems with protein synthesis. By allowing these low fitness bacteria to grow for many generations it was possible to see that evolution solved the problem of synonymous mutations by creating compensatory mutations that restored the level of ribosomal protein to normal. In this way, the researchers have gained a greater understanding of why silent mutations might reduce fitness was and how bacteria could compensate for them.

My comment: Organisms that have enough food can reproduce. Successful reproduction links nutrient-dependent pheromone-controlled ecological adaptations to supercoiled DNA in species that control the replication of viruses and virus-driven genomic entropy.

Excerpt:

They identified a link between VTE and three variants in a chromosome — rs2144940, rs2567617, and rs1998081 — associated with decreased expression of thrombomodulin, a protein that regulates clotting. Approximately 36 percent of American Americans have at least one of these variants, however, these variants were found in much lower frequency in other ethnicities from previous studies.
“This study not only brings us closer to understanding the cause of VTE in African Americans,” Perera said in a statement, “it demonstrates the importance of conducting populations-specific research in precision medicine.

Embryos in a particular phylum of the animal kingdom tend to most resemble one another at a stage in the middle of embryogenesis known as the phylotypic period; a transcriptional analysis of embryogenesis from single embryos of ten different phyla reveals that the transcripts expressed at the phylotypic stage (or mid-developmental transition) differ greatly between phyla, and a ‘phylum’ may be defined as a set of species sharing the same signals and transcription factor networks during the mid-developmental transition.

My comment: All development transitions are nutrient-dependent and RNA-mediated. Other variants in chromosomes are reported in terms that link energy-dependent hydrogen-atom transfer in DNA base pairs to phenotypic changes in the mouse model that clearly are linked from amino acid substitutions to morphological and behavioral phenotypes via the physiology of nutrient-dependent phermone-controlled reproduction.
Again, see: Nutrient-dependent/pheromone-controlled adaptive evolution: a model

Two additional recent reports link substitution of the amino acid alanine for the amino acid valine (Grossman et al., 2013) to nutrient-dependent pheromone-controlled adaptive evolution. The alanine substitution for valine does not appear to be under any selection pressure in mice. The cause-and-effect relationship was established in mice by comparing the effects of the alanine, which is under selection pressure in humans, via its substitution for valine in mice (Kamberov et al., 2013).

These two reports (Grossman et al., 2013; Kamberov et al., 2013) tell a new short story of adaptive evolution. The story begins with what was probably a nutrient-dependent variant allele that arose in central China approximately 30,000 years ago. The effect of the allele is adaptive and it is manifested in the context of an effect on sweat, skin, hair, and teeth. In other mammals, like the mouse, the effect on sweat, skin, hair, and teeth is due to an epigenetic effect of nutrients on hormones responsible for the tweaking of immense gene networks that metabolize nutrients to pheromones. The pheromones control the nutrient-dependent hormone-dependent organization and activation of reproductive sexual behavior in mammals such as mice and humans, but also in invertebrates as previously indicated. That means the adaptive evolution of the human population, which is detailed in these two reports, is also likely to be nutrient-dependent and pheromone-controlled, since there is no other model for that.

Multiple Instances of Ancient Balancing Selection Shared Between Humans and Chimpanzees
Functional characterisation of a SNP in the ABCC11 allele—Effects on axillary skin metabolism, odour generation and associated behaviours
Odor perception between heterosexual partners: its association with depression, anxiety, and genetic variation in odorant receptor OR7D4
Excerpt:

Genetic variants in OR7D4 receptor can modify the detection of the steroids androstenone and androstadienone, two pheromones that have the potential to evoke behavioral changes in many mammals, including humans, including mood changes (Kohl et al., 2001) and inter-sex communication (Kohl et al., 2001).

Excerpt:

…it was observed that the rating of partner odor was significantly associated with rs8109935 genotypes suggesting that genetic variability in the OR7D4 might have a role in the odor perception between partners. In fact, the data of this study replicate, for the first time, the results of Keller et al. (2007) about the influence of genotype variations in OR7D4 on odor perception.

The difference in pollinator communities between regions may indicate that different pollinators select for differences in floral scent chemicals, but further experiments would be required to test this theory. Nonetheless, the authors state their study is the first to find consistent regional differences in selection on floral scent, showing that this could be one mechanism behind geographical floral chemical scent divergence.
Karin Gross notes: “The observed regional differences in selection are an important evolutionary force contributing to divergence in floral fragrances. Other traits such as plant height were also affected by selection, but in a more uniform way.”

My comment: The changes in the orchid’s scent link ecological variation in the soil bacteria to the nutrient-dependent pheromone-controlled physiology of reproduction in mammals.
Epistasis Among Adaptive Mutations in Deer Mouse Hemoglobin
Repeated elevational transitions in hemoglobin function during the evolution of Andean hummingbirds
Evidence from cyclostomes for complex regionalization of the ancestral vertebrate brain
Reported as: Reported as: Jawless fish brains more similar to ours than previously thought
See also: Distinct Circuits for the Formation and Retrieval of an Imprinted Olfactory Memory
Reported as: Neuroscience of Early-Life Learning in C. elegans
See also: The Bull Sperm MicroRNAome and the Effect of Fescue Toxicosis on Sperm MicroRNA Expression
The information that connects all of the above from ecological variation to ecological adaptation in all living genera via hydrogen-atom transfer in DNA base pairs in solution arrives so quickly that biologists must look at conference abstracts to stay current and they must also pay attention to advice like this:
Biologists urged to hug a preprint
Excerpt:

Both Vale and Vosshall think that preprints will become widely accepted only if the life-sciences community develops a consensus that preprint publication establishes a priority for any discovery.

See my invited review of nutritional epigenetics, which was published as a preprint when it was returned without review. Note, however, that Vosshall has referred to all my works as pseudoscience that she will not address. Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems. I would value her opinion if I thought she was a serious scientist. Instead, she is trying to genetically engineer mosquitoes to prevent the transmission of pathogens. Obviously, she doesn’t know enough about RNA-mediated cell type differentiation to predict that the pathogens will adapt faster than the organisms she genetically engineers.

Virus-perturbed alternative splicings

January 22, 2016

by James Kohl with No Comment Adaptations Alternative Splicings biophotonics Diseases & Disorders Ecology Light Energy Model Organisms Neuronal Plasticity Nutrigenomics Pharmacogenomics Physics RNA Directed RNA-mediated epigenetic regulation of gene expression RNA-mediated gene silencing RNA-mediated toxicity RNA–Mediated Epigenetic Heredity Variations

Computing in mammalian cells with nucleic acid strand exchange
Abstract excerpt:

…we established that functional siRNA could be activated through strand exchange, and used native mRNA as programmable scaffolds for co-localizing gates and visualizing their operation with subcellular resolution.

Reported as:

Scientists Demonstrate Basics of Nucleic Acid Computing Inside Cells

Excerpt:

Cells, of course, already know how to sense toxic molecules and the development malignant tendencies, and to then take action. But those safeguards can be turned off by viruses or cancer cells that know how to circumvent natural cellular processes.

My comment: They seem unwilling to tell others how the proliferation of viruses links nutrient energy theft from viral microRNAs in cancer cells to all RNA-mediated cell type pathology. Perhaps it is just the reporting of their research that leaves out the most important aspect of top-down causation. The anti-entropic epigenetic effect of UV light links hydrogen-atom transfer in DNA base pairs to healthy longevity or virus-driven genomic entropy in all living genera.
Other works from this group attest to that fact.
2013 Conditionally fluorescent molecular probes for detecting single base changes in double-stranded DNA
2014 MicroRNA-Based Single-Gene Circuits Buffer Protein Synthesis Rates against Perturbations
2015 Learning the Sequence Determinants of Alternative Splicing from Millions of Random Sequences
See also: 1996 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…. That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.
A potential ramification of epigenetic imprinting and alternative splicing may be occurring in Xq28, a chromosomal region implicated in homosexual orientation… Xq28, therefore, is a chromosomal region that has many of the heterochromatic and telomeric characteristics that participate in sexual determination and behavior in other species.

My comment: Epigenetically-effected RNA-mediated cell type differentiation has since been linked from soil bacteria and grasses to the reproductive physiology and behavior of mammals via nutrient-dependent microRNAs.
See: The Bull Sperm MicroRNAome and the Effect of Fescue Toxicosis on Sperm MicroRNA Expression
See also: Soma-to-Germline Transmission of RNA in Mice Xenografted with Human Tumour Cells: Possible Transport by Exosomes
See also the comment on this article by Abhay Sharma

Cossetti et al. provide experimental evidence supporting a role of exosomal RNA mediated soma to germline information transfer in transgenerational epigenetic inheritance. Notably, it is consistent with the previous bioinformatic evidence and theoretical prediction. First, analysis of genome level expression profiling data recently suggested that circulating and exosomal miRNAs may potentially mediate this transfer (1). Next, similar evidence for exosomal mRNAs and proteins was also provided (2). Later on, inheritance of behavioral effects of traumatic stress in mouse was found to accompany upregulation of an miRNA, miRNA-375, in hippocampus, serum and sperm of the exposed animals (3). Experimental designs to test a hypothetical role of exosome borne miRNAs in intercellular communication in epigenetic inheritance have also been proposed recently (4). In conclusion, prior evidence supports Cossetti et al.’s findings.
1. Sharma A. Novel transcriptome data analysis implicates circulating microRNAs in epigenetic inheritance in mammals. Gene 538:366-372 (2014).
2. Sharma A. Bioinformatic analysis revealing association of exosomal mRNAs and proteins in epigenetic inheritance. J. Theor. Biol. 357:143-149 (2014).
3. Gapp K, Jawaid A, Sarkies P, Bohacek J, Pelczar P, Prados J, Farinelli L, Miska E, Mansuy IM. Implication of sperm RNAs in transgenerational inheritance of the effects of early trauma in mice. Nat. Neurosci. 17:667-669 (2014).
4. Smythies J, Edelstein L, Ramachandran V. Molecular mechanisms for the inheritance of acquired characteristics-exosomes, microRNA shuttling, fear and stress: Lamarck resurrected? Front. Genet. 5:133 (2014).

Xist-ing on planet Earth

October 20, 2015

by James Kohl with No Comment Adaptations Alternative Splicings Ecology Model Organisms Nutrigenomics Pharmacogenomics RNA Directed RNA-mediated epigenetic regulation of gene expression RNA-mediated gene silencing Variations What's in the News

Sex Differences in the Brain

(revisited) A comment that was complementary led me to add this:
Ideas about evolutionary processes that automagically led to sex differences in cell types can be dissmissed in the light of experimental evidence of biologically-based cause and effect.
Since 1996, for example, serious scientists have known about the role of Xist in chromosome inactivation. See also, from 2015:An Xist-activating antisense RNA required for X-chromosome inactivation
In our Hormones and Behavior review we (TB) wrote:
“Genomic-imprinting is also manifest in specific parts of the X-inactivation region’s related XIST gene. Here male- and female-specific methyl-group patterns participate in X-inactivation in females and also in the preferential inactivation of the paternal X in human placentae of female concepti (Harrison, 1989; Monk, 1995). This process indicates that tissues of the early conceptus can sense and react differentially to epigenetic sexual dimorphisms on the female conceptus’ own two X chromosomes. Furthermore, variations of X-inactivation patterns often account for traits discordance in monozygotic twin females. In other words, they are often found to have nonidentical patterns of X-inactivation, yielding differing expression of noticeable X-linked traits (Machin, 1996).”
The methyl-group patterns, which lead to increasing organismal complexity, are RNA-directed and they link nutrient-dependent fixation of RNA-mediated amino acid substitutions to the differentiation of all cell types in all individuals of all living species via the physiology of reproduction. (It’s not just about sex differences, Peg.)
Evolutionary theorists seem to think that cell type diferentiation automagically occurs outside the context of the biophysically constrained physiology of reproduction. That leads some of them to conclude that the differences between asexual reproduction and sexual reproduction arise in the context of their definition of “mutation” and assumptions about how long it would take a new species to emerge.
In the context of sex differences in cell types, there is no such thing as the automagical emergence of males and females, which suggests it is unlikely that any new species that reproduces sexually has ever emerged. For comparison, see this example of what happens when ecological variation appears to be on the verge of leading to ecological adaptations manifested in differences in morphological and behavioral phenotypes that are directly attributed to ecological speciation without the pseudoscientific nonsense of evolution.
Estrogen receptor α polymorphism in a species with alternative behavioral phenotypes
SARCASM ALERT (1)
Once everyone has realized that sex difference in cell types do not automagically emerge, someone can address the “re-evolution” of the bacterial flagellum, which “emerged” over-the-weekend. See: Evolutionary Rewiring.
If the molecular mechanisms of biophysically constrained nutrient-depenendent cell type differentiation are conserved in all living genera, microbes are linked to humans via the physiology of reproduction and ecological speciation. If others think the molecular mechanisms are not conserved, they may be from another planet.
SARCASM ALERT (2) Alternatively, they may be emergently-evolved mutants who automagically arose to conquer the Earth in an epic of Biblical proportions.

Multi-omic analysis features (SNPs, miRNA)

September 8, 2015

by James Kohl with No Comment Adaptations Alternative Splicings Diseases & Disorders Ecology Model Organisms Nutrigenomics Pharmacogenomics Physics RNA Directed Variations

Central to life is the faithful replication, inheritance, and maintenance of genomic DNA. The MRE11/RAD50/NBS1 (MRN) complex andATMplay a critical role in this biological mandate (Ciccia and Elledge, 2010). Cellular double-strand breaks (DSBs) are sensed by MRN and trigger the assembly of DNA damage response (DDR) foci that amplify global ATM signaling to induce cell-cycle arrest and DNA repair (Polo and Jackson, 2011). DNA viruses are an ancient and persistent threat to both cellular genome integrity and viability.

You can lean more about RNA-mediated correction factors here.

Excerpt:

Innovative multi-omic analysis features (SNPs, miRNA).

My comment: Typically, RNA-mediated events control virus-driven DNA damage. How could any serious scientist not consider the effects of viral microRNAs on cell type differentiation? All effects must be compared to the epigenetic effects of nutrient-dependent microRNAs on DNA repair, which links ecological variation to ecological adaptation via the biophysically constrained chemistry of nutrient-dependent RNA-mediated protein biosynthesis and degradation.
See also: RNA Pol IV and V in gene silencing: Rebel polymerases evolving away from Pol II’s rules
Abstract excerpt:

Noncoding RNAs regulate gene expression at both the transcriptional and post-transcriptional levels, and play critical roles in development, imprinting and the maintenance of genome integrity in eukaryotic organisms [1,2,3]. Therefore, it is important to understand how the production of such RNAs are controlled.

My comment: Biologically uninformed researchers cannot understand how the production of potentially beneficial noncoding RNAs is controlled by nutrient energy and how cell type differentiation is perturbed by viruses that steal the nutrient energy that is required for fixation of RNA-mediated amino acid substitutions in the organized genomes of all living genera.
See also: Combating Evolution to Fight Disease
Excerpt:

An alternative theory proposes environmentally induced change in an organism’s behavior as the starting point (1), and “phenotypic plasticity” that is inherited across generations through an unspecified process of “genetic assimilation” (2).
This is now more than merely an alternative theory of genetic assimilation. It links transgenerational epigenetic effects from nutrient uptake and RNA-mediated events to amino acid substitutions that differentiate the cell types of all cells in all individuals of all organisms. See, for example: Starvation-Induced Transgenerational Inheritance of Small RNAs in C. elegans.
The nutrient stress-induced RNA-mediated events, which link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man, also link morphological and behavioral diversity via conserved molecular mechanisms exemplified in the context of biologically plausible ecological speciation in nematodes.
See: System-wide Rewiring Underlies Behavioral Differences in Predatory and Bacterial-Feeding Nematodes
A difference in their feeding behavior and in the anatomy of their mouth parts is linked from nutrient-dependent pheromone-controlled feedback loops to ecological, social, and neurogenic niche construction. The change in focus from mutations, natural selection, and the evolution of biodiversity via unknown evolutionary events to nutrient-dependent pheromone-controlled RNA-mediated events that differentiate cell types may be required for others to realize the difference between evolutionary theories and biologically-based facts about RNA-mediated events.
RNA-mediated events are biophysically constrained, which means they are a biologically plausible way to link the physics and chemistry of protein folding to increasing organismal complexity via molecular biology. RNA-mediated events can also be compared to any unknown evolutionary events that might arise in the context of an alternative theory about constraint-breaking mutations, or other theories that include no mention of RNA-mediated events.

My comment: Any article that mentions the evolution of anything without consideration of Darwin’s ‘conditions of life’ is an article that bastardized his theory. Darwin clearly linked ecological variation to ecological adaptation before cause and effect was linked via nutrient-dependent RNA-mediated chromosomal rearrangements in white-throated sparrows and all other living genera.
See: Estrogen receptor α polymorphism in a species with alternative behavioral phenotypes
Excerpt:

Estrogen receptor-mediated differences in parental feeding behavior appear to contribute to sex differences and species differences in morphology and in overt social behavior.

My comment: “…the evidence mentioned above indicates that viruses likely arose from their hosts and not the other way around. As molecular biologist and biochemist Peter Borger notes, “The most parsimonious answer is: the RNA viruses got their genes from their hosts.”6
See also: Armed Forces in the Cell Keep DNA Healthy
Excerpt:

We aren’t surprised to notice that these articles say nothing about evolution.

See also: Ready to Return and Nutrient-dependent / Pheromone-controlled thermodynamics and thermoregulation.
For comparison of what is known to serious scientists about ecological variation and ecological adaptation in the context of an atoms to ecosystems model, see this video representation of my invited review of nutritional epigenetics: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems
See also: Scientists map genes at work in human embryos’ earliest days