Alternative splicing of pre-mRNA

Cracking the Olfactory Code?

What a smell looks like

Excerpt: 

This experiment was created so scientists could study how animals and humans use smells to navigate their surroundings. That question forms the heart of a new $6.4 million project, sponsored by the National Science Foundation and the White House Brain Initiative, called Cracking the Olfactory Code.

My comment to the PBS site:
Re: “Smell was part of very ancient evolution…. Bacteria use olfaction, single-celled organisms use olfaction, worms use olfaction.”
The de novo creation of G protein-coupled receptors links everything known to physicists, chemists, and molecular biologists from quantized energy-dependent changes in angstroms to the interactive health of all ecosystems in all living genera. Virus-driven energy theft is linked to all pathology.
Any attempt to put that fact back into the context of evolutionary theory should be viewed as an attempt to stop the progress that has already been made via the Precision Medicine Initiative and the National Microbiome Initiative. Taken together, those initiatives have helped to link metabolic networks to genetic networks without claims about beneficial mutations, natural selection, or evolution.
One month ago, Paul M. Lieberman included a concise statement of everything known about biologically-based cause and effect in the context of this review: “Epigenetics and Genetics of Viral Latency.”
He wrote: “…viral latency is responsible for life-long pathogenesis and mortality risk…” Simply put, all pathology can be linked to virus-driven energy theft, and all healthy longevity can be linked from nutrient energy-dependent biologically-based cause and effect to supercoiled DNA, which protects all organized genomes from virus-driven entropy.
In 1980, Lewis Thomas wrote: “I should think we might fairly gauge the future of biological science, centuries ahead by estimating the time it will take to reach a complete comprehensive understanding of odor. It may not seem a profound enough problem to dominate all the life sciences, but it contains, piece by piece, all the mysteries” (p. 732). — as cited in The Scent of Eros: Mysteries of Odor in Human Sexuality (1995/2002).
The biggest mystery of all time involves questions about why the future of biological science was put on hold by neo-Darwinian theorists who used de Vries 1902 definition of “mutation” as the foundation for their assumptions and theories about evolution.
See also: Cracking the Olfactory Code (Olfactory) An Ideas Lab Activity Program Solicitation NSF 15-547
Excerpt 1)

The conceptual foundation of neuroscience rests on the idea that behavior derives from the emergent properties of a distributed collection of neural circuits.

My comment: Energy as information is linked to behavior via RNA methylation and the biophysically constrained chemistry of protein folding that links hydrogen-atom transfer in DNA base pairs in solution from amino acid substitutions to the stability of all organized genome in all living genera. Supercoiled DNA exemplifies how top-down causation must link quantized energy to what is currently known to serious scientists about biologically-based cause and effect. Supercoiled DNA protects organized genomes from virus-driven energy theft and genomic entropy.
The ridiculous claim about the conceptual foundation of neuroscience exemplifies how much collective ignorance has been taught to generations of biologically uninformed students by their biologically uninformed professors. Most were taught to believe in emergence and evolution that somehow occurred outside the context of energy-dependent changes that serious scientists have linked from angstroms to ecosystems.
Excerpt 2)

The National Science Foundation strives to invest in a robust and diverse portfolio of projects that creates new knowledge and enables breakthroughs in understanding across all areas of science and engineering research and education.

My comment: New knowledge is never created. Understanding why some people make breakthroughs and why others do not is simple. Neo-Darwinian theorists do not make scientific breakthroughs because they do not learn how to link energy-dependent changes in all living genera from angstroms to ecosystems. If you tell someone that mutations link what is known to serious scientists about the links from angstroms to ecosystems and they believe you, that person is a theorist. Theorists will continue to submit proposals for NSF funding until the NSF stops funding research on the emergence of behavior or the evolution of behavior.
I repeat: Energy as information is linked to behavior via RNA methylation…
See also:

Cracking the Olfactory Code (2/22/05)

Cracking the olfactory code of a butterfly: the scent of ageing (March 6, 2012)

Cracking the Olfactory Code (June 1, 2016)

“cracking the olfactory code” in On the Scent: A journey through the science of smell by Paolo Pelosi (May 24, 2016)

Description:

In humans, the perception of odours adds a fourth dimension to life, from the scent of flowers, the aroma of foods, and all the subtle smells in the environment. But how many types of odours can we distinguish? Why do we like the food we like? Which are the most powerful odorants, and how well does the human sense of smell perform compared with that of a dog or a butterfly?
The sense of smell is highly complex, and such complexity discouraged scientists for a long time, leaving the world of smell in an atmosphere of mystery. Only recently, thanks to the new tools furnished by molecular biology and neuroscience, are we beginning to answer these questions, uncovering the hidden secrets of our sense of smell, and decoding the language used by most animals to communicate. In this book, Paolo Pelosi, one of the leading figures in the development of the science of olfaction, recounts how the chemical alphabet behind smell has been pieced together over the past three decades. Drawing on anecdotes from his own scientific career, and celebrating the rich variety of smells from herbs to flowers to roast coffee and freshly baked bread, he weaves together an engaging and remarkable account of the science behind the most elusive of our senses.

Richard Doty’s book about pheromones is cited. Trystam Wyatt’s book about pheromones is cited.  For comparison, Einstein’s works, Schrodinger’s works, and Dobzhansky’s works appear to have not been of interest to this author. The book I co-authored with Robert Francoeur is not mentioned.
The Scent of Eros: Mysteries of Odor in Human Sexuality (1995/2002)
Description:

Scientists have long known that chemical communication via pheromones is a powerful influence on how animals develop, mate, bond, and nurture their offspring. Human animals are no exception. Pheromones, explain the authors, alter hormone levels, can accelerate puberty, control women’s menstrual cycles, influence our choice in a mate, and even influence our sexual orientation. They help us tell lovers and family members from strangers and are essential to the mother-infant bond. Pheromones influence how often we have sex, and with whom. They influence how the brain develops, what we remember, and how we learn.
Grounded in solid scientific research, yet maintaining an easy-to-read style, The Scent of Eros is an engrossing read about a whole new world under our noses!
Kohl and Francoeur show the pathway from social-environmental sensory input to the hormones that influence our behavior, especially our sexual behavior. The authors suggest and show that pheromones are the primary link between the nature and the nurture of human sexuality.

Biological anthropologist, Helen Fisher said this about The scent of eros: mysteries of odor in human sexuality (by Kohl and Francoeur 1995):

“This is science at its best, with adventure, ideas, and lots of facts”.

review by Mark Sergeant  Senior Lecturer in Psychology at Nottingham Trent University
review by Ralph Underwager, Institute for Psychological Therapies
review by Jan Peregrine
For an example of what NSF funding has done to answer the questions that have been answered by serious scientists who have linked energy-dependent changes from angstroms to ecosystems in all living genera, see: Viewpoint: The First Sounds of Merging Black Holes
Excerpt:

Does gravity really behave as predicted by Einstein in the vicinity of black holes, where the fields are very strong? Can dark energy and the acceleration of the Universe be explained if we modify Einstein’s gravity? We are only just beginning to answer these questions [11, 12].

rp_levels-of-organization.jpg

Energy-dependent RNA methylation (9)

Epigenetics and How Our Decisions Affect Our DNA

Excerpt (with my emphasis):
With the Genetics and Genomics 2016 virtual conference now on demand, we are extending the genetics conversation into this month with a new infographic. Epigenetics has been in the news quite a bit lately as researchers have been able to learn more about its process and influences. It turns out that epigenetics is an ever-changing process within our cells, causing more rapid modification within a generation. Unlike standard evolution, where small mutations can span generations before any actual variation takes place, an epigenetic change can affect a person within their lifetime.
Here are a few interesting facts about epigenetics and one cool infographic:
Epigenetics decides which genes are expressed and how much of that gene is expressed. Since every cell in a person has the same DNA, epigenetics control what cells become and how they behave. It is these non-direct changes in DNA sequence that influence a person’s physical traits and propensity for certain diseases.

The first human disease to be linked to epigenetics was cancer…

My comment: “RNA-mediated physics, chemistry, and molecular epigenetics” is available in the “Genome Technology Innovations” of the poster hall, and also available with a narrative from the Labroots Youtube page.

Published on 3 May 2016

Olfaction and the innate immune system link energy as information from the epigenetic landscape to the physical landscape of supercoiled DNA. The sun’s biological energy is the source of the information that links angstroms to ecosystems via physics, chemistry, and molecular epigenetics.
RNA-mediated protein folding chemistry and amino acid substitutions link the anti-entropic quantized energy of sunlight from the virucidal effects of ultraviolet (UV) light to healthy longevity via biophysically-constrained energy-dependent hydrogen-atom transfer in DNA base pairs in solution and cell type differentiation.
Biomarkers link energy-dependent differences in base pairs and amino acid substitutions to biosignatures across the healthy life span. RNA-mediated amino acid substitutions also reveal the increasing complexity of interactions among cell types as pathology progresses. For comparison, successful reproduction links energy from supercoiled DNA to protection of all organized genomes from virus-driven energy theft and pathology.
This model links the sun’s biological energy from top-down causation in microbes to the most recent model of bottom-up gene activation and cell type differentiation in vertebrates. Citations to extant literature provide examples of what is currently known about how ecological variation leads to biophysically constrained cell type differentiation in the context of nutritional epigenetics and Precision Medicine, which clearly link metabolic networks and genetic networks to pharmacogenomics.
See also: Epigenetics and Genetics of Viral Latency

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

As more researchers learn that The first human disease to be linked to epigenetics was cancer… and that “…viral latency is responsible for life-long pathogenesis and mortality risk…” they will be forced to accept the facts about nutritional epigenetics and healthy longevity in the context of the alternative, which is virus-driven energy theft and all pathology.

rp_levels-of-organization.jpg

Energy-dependent RNA methylation (7)

“…viral latency is responsible for life-long pathogenesis and mortality risk…” – Lieberman (2016)

My comment: Energy-dependent RNA-mediated amino acid substitutions are responsible for life-long healthy longevity and decreased mortality risk.

See for comparison: How cancer was created by evolution

Excerpt 1)

But even though it is evolutionary processes that have made cancer such a problem, it is also evolutionary thinking that is now leading to pioneering treatments that could stack the odds against cancer and in favour of our health.

Excerpt 2)

Genetic diversity is “the spice of life, it’s the substrate upon which natural selection acts”, says Swanton. By this he means evolution by natural selection, first proposed by Charles Darwin in 1859.

See for comparison:

Evolution by natural selection cannot be the outcome if something is not first selected. Selection is always for nutrients. It is as simple as that.” — James V. Kohl (7/24/13)

My comment: Thinking about evolutionary processes in the context of cancer pathology, which is obviously a problem that arises in the context of virus-driven energy theft, is like not thinking at all.

See for comparison:  Engaging epigenetics experts

The comments represent the only success I have had with attempts to explain what is currently known about RNA-mediated cell type differentiation in any FB group.

Excerpt:

I don’t see a lot of research on the role of ‪#‎epigenetics‬ in suppressing endogenous retroviruses, so I was intrigued by this one. The investigators in this article in Development turn off the gene Setdb1, a histone methylator, and let slip the dogs of MLV. I’m certain one of our regular visitors will find this interesting.
Working on mouse cells, the team of researchers from Germany’s Ludwig Maximilians University and elsewhere discovered that releasing Setdb1’s hold on endogenous retroviruses definitely allows murine leukemia virus (MLV) to ramp up protein production, ultimately killing the host cells. Of course.

See for comparison:  Creationism and Creationism

My comment: Many people seem more interested in arguing about the religious beliefs of others compared to learning about energy-dependent cell type differentiation for comparison to virus-driven energy theft and pathology.

See also: Impairment of DNA Methylation Maintenance Is the Main Cause of Global Demethylation in Naive Embryonic Stem Cells

Excerpt:

…global demethylation is, contrary to previous assumptions, a consequence of neither loss of de novo methylation nor active Tet-dependent demethylation but caused by impaired maintenance methylation.

My comment: Maintenance methylation is energy-dependent and it is RNA-directed.

See: RNA directed DNA methylation and cell types or Google rna-directed dna methylation or search PubMed rna directed dna methylation

RNA-directed DNA methylation is a conserved molecular mechanism that typically prevents transgenerational epigenetic inheritance of damage due to virus-driven energy theft. It is like a reset button on your router, or initiating “restart” on your computer after the problem with virus-driven energy theft of programming information has been corrected. In all living genera, “restart” works wll until the efficiency of energy transfer to the information in programming has been corrupted by the accumulation of viruses and mutations in your ancestors.

The only way to prevent the damage your ancestors knew about was to follow the laws of biology that link virus-driven energy theft to pathology across generations of people who failed to follow those laws. Now, some offspring are susceptible to Zika virus energy theft, which causes craniofacial abnormalities and brain damage in infants — but not always.

There are clear links from nutritional epigenetics that predict when damage is most likely to be transgenerationally (epigenetically) inherited. Anatagonist Sean Ovis (Sirius Cyantis),  put them into God’s plan to kill us all via the creation of viruses, which means he linked the viruses to craniofacial abnormalities and brain damage in infants via the same model — as if God’s intent was to start killing his Creation from the time of birth.

See also: Creationism

My comment: That’s the clearest example of hate-mongering I have seen in this group, so far. And he twisted my model of virus-driven energy theft to do it. Group members wanted a definition of virus-driven energy theft. They refused to accept the fact that it has been linked to all pathology in my model and in the accurate representations of biologically-based cause and effect by all other serious scientists. However, some of the scientists who failed to make the obvious connection are trying to link what is known from a loss of function mutation to the creation of new oncohistones.

Neo-Darwinin theories about mutations, natural selection, and evolution have lost nearly all their appeal among serious scientists. Facts replaced theories about human brain development and the National Microbiome Initiative predictably will undoubtedly continue to be linked to the Precision Medicine Initiative in all publications — except those published by theorists.

Within the next year or two, we should see the mutation-driven evolution approach that theorists have linked to the development of the human brain and behavior become recognized as the theory that is the source of all preventable pathology. Serious scientists continue to make progress, and they will enlist others who are “Combating Evolution to Fight Disease.”
The only researchers left fighting against scientific progress will be the neo-Darwinian theorists, and they may be subjected to something akin to the Spanish Inquisition, or the Salem Witch Trials. “What caused you to keep thinking your magical thoughts about cell type differentiation, you witch?”
See for comparison: Regulation of prefrontal cortex myelination by the microbiota

Excerpt 1)

“… we believe we demonstrate for the first time that the microbiome is necessary for appropriate and dynamic regulation of myelin-related genes with clear implications for cortical myelination at an ultrastructural level. The microbiota is therefore a potential therapeutic target for psychiatric disorders involving dynamic myelination in the PFC.”

My comment: I believe everything that is reported in the context of the belief that it has been demonstrated for the first time should be placed into the context of a model of biologically-based cause and effect. If the model links what is known about RNA-mediated amino acid substitutions and cell type differentiation in all living genera, it could be used to predict what would be demonstrated next for the first time and demonstrated next for the first time after that, ad infinitum.

Eventually, everyone who has ever demonstrated for the first time that the microbiome is the key component of what they have demonstrated for the last time may link the microbiome from metabolic networks to genetic networks via the physiology of energy-dependent reproduction in all living genera and demonstrate for the last time that all other demonstrations linked from virus-driven energy theft to pathology have shown the same thing.

No one has ever shown anything else besides that fact that cell type differentiation is energy-dependent and that RNA-mediated fixation of amino acid substitutions occurs in the context of the physiology of reproduction linked to supercoiled DNA by the innate immune system.

Excerpt 2)

Studies utilizing approaches such as monocolonization in either GF or microbiota-depleted animals using antibiotics would allow deciphering whether specific bacterial strains have the capacity to normalize the observed altered myelination patterns in these animals.

My comment: Those studies could be linked from pattern recognition in other species to demonstrate for the last time that all pathology is caused by virus-driven energy theft, which alters everything known about how metabolic networks are linked to genetic networks by biophysically constrained RNA-mediated protein folding chemistry. Physics and chemistry link quantized energy from angstroms to ecosystems via the physiology of reproduction and biologically-based cause and effect in all living genera.

Summary: Unique microRNAs (miRNAs) appear to link the nutrient-dependent pheromone-controlled life history transitions of bees to RNA-mediated metabolic networks and genetic networks in all genera via base pair substitutions and amino acid substitutions that differentiate all cell types in all living genera. Jon Lieff continues to present what is known about cell type differentiation in articles that an educated audience can understand. I’ve added more technical representations from the most recently reported sources of information.

See also: Microbes Effect on the Brain in my blog post from May 25, 2015: Pattern recognition: biogeochemical structure and function

See also: Counting viruses and bacteria in photosynthetic microbial mats

My comment: Photosynthesis in the ecological regions at the lowest level of a body of water such as the ocean appears to link the minimum amount of quantized virucidal energy from ultraviolet (UV) light and the maximum amount of water molecules found on Earth. The speed of biologically-based symbiotic interactions has now been measured in the context of femtosecond blasts of UV light, which links RNA-mediated DNA repair to amino acid substitutions and cell type differentiation at every subsequent level of examination. All levels of examination have always required a link from an anti-entropic source of energy. All serious scientists have linked atoms to ecosystems in all living genera, via the physiology of reproduction and supercoiled DNA, which protects all organized genomes from virus-driven entropy.  Only recently have serious scientists linked angstroms to ecosystems in the context of the physiology of reproduction and supercoiled DNA.

The serious scientists that did that appear to be having great fun demonstrating “…for the first time that the microbiome is necessary for appropriate and dynamic regulation of myelin-related genes with clear implications for cortical myelination at an ultrastructural level.”

See for example:


C. David Allis’s group seems to want others to believe cell type differentiation is not all about the base. He may want them to believe it’s all about histones. Others have also suggested that approach.
See: Epigenetic (re)programming of caste-specific behavior in the ant Camponotus floridanus reported as: Social behavior in carpenter ants reprogrammed using epigenetic drugs
Excerpt:

It’s All About the Histone The almost decade-long collaboration between the Berger, Liebig, and Reinberg labs, supported by the Howard Hughes Medical Institute, blends molecular biology with observations of animal behavior to understand how caste-based differences arise in ants.

Allis’s group is now reporting the existence of oncohistones (cancer causing histones). They invented the term.
See: An oncohistone deranges inhibitory chromatin

Missense mutations (that change one amino acid for another) in histone H3 can produce a so-called oncohistone and are found in a number of pediatric cancers. For example, the lysine-36–to-methionine (K36M) mutation is seen in almost all chondroblastomas. Lu et al. show that K36M mutant histones are oncogenic, and they inhibit the normal methylation of this same residue in wild-type H3 histones. The mutant histones also interfere with the normal development of bone-related cells and the deposition of inhibitory chromatin marks.

My comment: By placing the change in the base pair that precedes the energy-dependent change in the amino acid substitution, biologically uninformed researchers will focus on the oncohistones, not the virus-driven energy theft that links all mutations to all pathology. The focus of drug development on histones is on damage control or repair.
Allis’s group can develope treatments for disorders of cell type differentiation that link virus-driven energy theft from base pairs to detrimental amino acid substitutions without mentioning the role of energy-dependent amino acid substitutions in cell type stability in all living genera. Cell type stability is controlled by the physiology of reproduction, which links the amino acid substitution to the histones and supercoiled DNA , which protects all organized genomes from virus-driven energy theft and genomic entropy.
See also: Censorship & Upcoming Royal Society Evo Meeting discussion on the Creationism FB group

Filtering light through a prism to identify tissue type

Energy-dependent RNA methylation (6)

After I published Nutrient-dependent/pheromone-controlled adaptive evolution: a model, Lynnette Ferguson and Justin O’Sullivan invited me to submit this review of nutritional epigenetics for inclusion in a special issue of the journal “Nutrients.”
Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems (April 10, 2014)
Abstract:

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

My comment: My invited review was promptly returned without review. That’s why I published my review to the figshare.com site. I realized that the guest editors had “baited” me so that I would supply the latest information to them. Here are some examples of how the information was used by Lynnette Ferguson.
The Interaction between Epigenetics, Nutrition and the Development of Cancer (2015) Received 28 July 2014. This article belongs to the Special Issue Nutritional Epigenetics
Abstract excerpt:

The epigenetic modifications investigated include DNA methylation, histone modifications and the influence of microRNAs.

Conclusion:

…it is imperative to understand the implications of diet on epigenetic modifications, and the effect of those modifications on the development of cancer today and in future generations. Such an understanding and an appropriate resultant response would help decrease the level of risk in future generations.

My comment: Claiming that interactions occur does nothing to explain cause and effect. Ferguson co-authored an article that took my explanations out of their context and put them back into the context of theories about interactions that have no explanatory power.
For comparison, see: Role of olfaction in Octopus vulgaris reproduction (18 October 2014)
Excerpt:

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

My comment: The authors linked the claims from my 2013 review to their experimental evidence of biologically-based cause and effect. It took only one citation to my published 2013 review by ethical researchers (Polese, Bertapelle & Di Cosmo) to defeat the attempts of people who attempted to steal the information and use it without attribution — as if it supported their ridiculous theories.
However, in this case, Eleckonich and Robinson (2000) had also cited our 1996 Hormones and Behavior review of RNA-mediated cell type differentiation: From Fertilization to Adult Sexual Behavior. We included a section on molecular epigenetics that linked microRNAs, which at the time were called pre-mRNAs, to the physiology of reproduction in yeasts, all invertebrates, and all vertebrates. When they cited my 2013 review and Elekonich and Robinson (2000),  Polese, Bertapelle & Di Cosmo (2015) established a context-based history of advances in understanding molecular epigenetics.
For contrast, Lynnette Ferguson has repeatedly attempted to sneak though the back door of serious scientists with this article: Genomic instability in human cancer: Molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition and this comment from Are We Eating Our Way to Prostate Cancer—A Hypothesis Based on the Evolution, Bioaccumulation, and Interspecific Transfer of miR-150
Excerpt:

The discovery of miRNA in sperm effectively overshadowed the previous experimental findings that worms and plants used miRNA in a transgenerational inheritance pattern [58], as it indicated that mammalian miRNAs evolved from other mammals, mimicking their divergent inheritance pattern. There is another seemingly neglected mechanism of miRNA inheritance—which is of paramount importance in the context of miR-150 and oncogenesis—can plant miRNA be recognized and allowed to play epigenetic roles by the mammalian immune system upon oral ingestion? [59]. The discovery that miRNA evolution is linked to complex food web interactions is crucial to our current knowledge, as it involves miRNA in the nutrigenomics of oncogenesis (Figure 2).

See for comparison: The Bull Sperm MicroRNAome and the Effect of Fescue Toxicosis on Sperm MicroRNA Expression (Dec 2, 2014).
In the context of my 2013 review, the authors  helped to establish facts about RNA-mediated cell type differentiation that we presented in our 1996 review. They linked Einstein’s claims from Schrodinger’s claims (1944) to Dobzhansky’s claims (1973) about amino acid substitutions.
The claims about energy-dependent RNA-mediated amino acid substitutions are still being ignored by most theorists. After it became clear that biologically uninformed pseudoscientists would  continue stealing information from me and begin linking the information on microRNAs to amino acids and cancer, I decided to forgo further attempts to publish in journals.
In February 2015, I founded this domain: RNA-mediated.com and the FB discussion group: RNAmediated. I’ve continued to disseminate facts about energy-dependent cell type differentiation that you are not likely to see represented anywhere else, until after I have detailed them.
I also prepared and presented several poster sessions with recorded narratives that are available from Labroots conferences with the following themes.
Neuroscience: From hydrogen atom transfer in DNA base pairs to ecosystems (March 2, 2016)
Excerpt: 

This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on DNA base pairs in solution and RNA-mediated amino acid substitutions to chromosomal rearrangements via pheromone-controlled changes in the microRNA / messenger RNA balance.

Neuroscience: RNA mediated molecular epigenetics and virus driven entropy (March 2, 2016)
Excerpt:

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.

Molecular Diagnostics What is life when it is not protected from virus driven entropy (March 30, 2016)
Excerpt:

The anti-entropic force of virucidal ultraviolet light links guanine–cytosine (G⋅C) Watson–Crick base pairing from hydrogen-atom transfer in DNA base pairs in solution to supercoiled DNA, which protects the organized genomes of all living genera from virus-driven entropy.

Genetics and Genomics RNA-mediated physics, chemistry, and molecular epigenetics (May 3, 2016)
Excerpt:

Olfaction and the innate immune system link energy as information from the epigenetic landscape to the physical landscape of supercoiled DNA.

See also: Endogenous retroviruses function as species-specific enhancer elements in the placenta (February 10, 2013)
Excerpt:

We speculate that ERV variation, exposed by the permissive epigenetic state within the placenta, allows the fetus increased evolvability against maternal defenses. Specifically, by relaxing epigenetic repression of ERV activity, the placenta gains access to a highly polymorphic source of enhancer elements that may dramatically influence its developmental phenotype (Fig. S5). As the placenta is a transient organ, the long-term advantage conferred by increased developmental evolvability would outweigh the potentially mutagenic effects of ERV activity. We propose this model as a plausible explanation for the persistence of placenta-specific ERV activity, which has been observed in all major mammalian taxa31.

My comment: Developmental phenotypes are energy-dependent in all living genera. After I was alerted to more recent claims about virus-driven pathology, my focus changed from energy-dependent RNA-mediated cell type differentiation to nutrient energy-dependent protection of complex functional structures like the bacterial flagellum and teeth. When I realized that virus-driven energy theft was the cause of all pathology, I paid more attention to reports that attested to the claims I had already included in my published works and publications on RNA-mediated cause and effect.
For example see: Water-Mediated Collagen and Mineral Nanoparticle Interactions Guide Functional Deformation of Human Tooth Dentin
The authors link what is known to physicists and chemists to the conserved molecular mechanisms of energy-dependent RNA-mediated cell type differentiation via differences in the diet of C. elegans and P. pacificus, a predatory nematode with teeth. Unfortunately, the “…optimization of tooth dentin to reliably resist…” that requires experience-dependent exposure to loads was placed into the context of “evolutionary optimization.”
Attempts have failed to explain to others why “evolutionary optimization” is not possible in the context of what is known to serious scientists about biophysically constrained RNA-methylation and energy-dependent protein folding chemistry, which must be linked to species-specific behavior via the physiology of reproduction.
No matter how much more information or raw insight is added to what is already known, theorists will not look at the experimental evidence, or perhaps they will simply continue to ignore it. People like Lynnette Ferguson, will continue to do what they have always done. They will steal the energy that serious scientists use in attempts to accurately portray what is currently known about biophysically constrained energy-dependent biologically-based cause and effect.
See for instance: Philosopher earns 14th retraction for plagiarism
My comment: As the experimental evidence continues to become an overwhelming threat to the pseudoscientific nonsense touted by theorists, we will see more claims like this:
Conclusion:

This review is far from comprehensive or complete and yet hopefully shows the enormous complexity of viral latency and its regulation at the genetic and epigenetic levels. This information provides great opportunity for the development of innovative and highly selective therapeutic intervention. As viral latency is responsible for life-long pathogenesis and mortality risk, the tasks ahead are in sight, but challenges remain. — Epigenetics and Genetics of Viral Latency (May 11, 2016)

My comment: My reviews were conclusive and I established the fact that virus-driven energy theft must be biophysically constrained by the availability of nutrients and lack of social stress that predicts the changes in pH that lead to viral replication. The need to model cause and effect in the context of energy-dependent changes that link angstroms to ecosystems has become increasingly clear.
See also: Viral Reprogramming of the Daxx Histone H3.3 Chaperone during Early Epstein-Barr Virus Infection
Conclusion:

These findings also demonstrate that host chromatin assembly is an important form of host cell intrinsic resistance to viral infection.

My comment: I have placed that claim into my model and repeatedly stated clearly that energy-dependent RNA-mediated amino acid substitutions are linked to supercoiled DNA, which protect the organized genomes of all living genera from virus-driven energy theft and genomic entropy. The virus-driven energy theft links mutations to all pathology. I reiterate:

“…viral latency is responsible for life-long pathogenesis and mortality risk…” – Lieberman (2016)

My comment: Energy-dependent RNA-mediated amino acid substitutions are responsible for life-long healthy longevity and decreased mortality risk.
See also: Retrotransposon derepression leads to activation of the unfolded protein response and apoptosis in pro-B cells
Reported on 6/7/16 (with my emphasis) as:

“I don’t see a lot of research on the role of ‪#‎epigenetics‬ in suppressing endogenous retroviruses, so I was intrigued by this one. The investigators in this article in Development turn off the gene Setdb1, a histone methylator, and let slip the dogs of MLV. I’m certain one of our regular visitors will find this interesting.

Working on mouse cells, the team of researchers from Germany’s Ludwig Maximilians University and elsewhere discovered that releasing Setdb1’s hold on endogenous retroviruses definitely allows murine leukemia virus (MLV) to ramp up protein production, ultimately killing the host cells. Of course.
Previously, it hadn’t quite been clear whether cells lacking Setdb1 died due to viral protein production or some other reason, and this work is a solid step toward the former explanation.
Check out the article here in Development.
http://dev.biologists.org/content/143/10/1788
-CW New England Biolabs”
My comment: I am a regular visitor at the New England Biolabs FB page and a regular contributor of comments on the information they disseminate. But, given the return without review of my invited review by the guest editors who requested it, I have become increasingly suspicious of what may be subtle attempts to “bait” me, again.
Fortunately, others are moving forward. See for example: The Quantum Nature of Drug-Receptor Interactions: Deuteration Changes Binding Affinities for Histamine Receptor Ligands (May 9, 2016) reported by John Hewitt on June 7, 2016 as: Using the ‘deuterium switch’ to understand how receptors work
Excerpt: 

…olfaction is probably the space where these deuterium switches and chiral switches most informatively converge to elucidate how receptors might operate. In fact, the authors explicitly highlight the fact that their histamine receptor model may have something to say about olfactory receptors. Importantly, both of these receptor classes belong to the so-called GPCR (G-protein coupled receptor) family that vertebrates use to detect odorants; half of our own 800 GPCRs are provisioned almost exclusively to olfaction.
The author’s main comments, here, center on the aromatic groups of molecules, features that are typically associated with delocalized electrons. For example, the imidazole ring of histidine (histamine’s the amino acid precursor) is aromatic at all pH values; four of its pi electrons form two double bonds and two from a nitrogen lone pair. The authors propose that a major fallout of deuteration is that the aromatic moiety shrinks the effective C–D distance relative to its C–H value. Aromatic C–H bonds act as proton donors and form weak hydrogen bonds with water molecules and proton acceptors at the receptor binding site.

My comment: Thanks for trying to help others to understand the overwhelming complexity, John Hewitt. I noticed that they cited “Molecular vibration-sensing component in Drosophila melanogaster olfaction,” which was co-authored by Luca Turin, but these authors failed to link cell type differentiation from all invertebrates to all vertebrates via what is known about nutritional epigenetics, microRNA flanking sequences, RNA methylation, the innate immune system, supercoiled DNA, behavior, and consciousness.

Others may want to see “Dose-Dependent Effects of the Clinical Anesthetic Isoflurane on Octopus vulgaris: A Contribution to Cephalopod Welfare” and other works by Anna Di Cosmo’s group. Michael Crawford’s group has also made progress by ignoring claims about “quantum Darwinism” and focusing on the energy-dependent de novo creation of GPCRs, like olfactory receptor genes. See for example: A quantum theory for the irreplaceable role of docosahexaenoic acid in neural cell signalling throughout evolution

For comparison, see: Periodic Scarred States in Open Quantum Dots as Evidence of Quantum Darwinism

Reported as: Bridge to the quantum world: Darwinian concept of natural selection figures into theory about core of physical reality

Excerpt:

It describes the transition from quantum to classical world as a “decoherence” process that involves a kind of evolutionary progression somewhat analogous to Charles Darwin’s concept of natural selection.

My comment: I’ve mentioned repeatedly that serious scientists have always had the choice to stop investigating claims that Feedback loops link odor and pheromone signaling with reproduction in species from microbes to humans.

SARCASM ALERT: Why should pseudoscientists be the only people who accept the claim that mutations and natural selection replaced the sun’s biological energy as the anti-entropic source that links ultraviolet light to prevention of virus-driven energy theft in all living genera via decoherence in the context of “…a kind of evolutionary progression”? The pseudoscientists need only continue to ignore that fact that Darwin insisted that they ensure “conditions of life” were considered before natural selection.

Darwin’s “conditions of life” are energy-dependent and controlled by the physiology of reproduction. There is no experimental evidence of biologically-based cause and effect that links the energy-dependent physiology of reproduction from mutations to the diversity of morphological phenotypes and all  experimental evidence of biologically-based cause and effect links energy-dependent RNA methylation from the innate immune system to supercoiled DNA.

 
 
 
 
 
 

rp_levels-of-organization.jpg

Energy-dependent RNA methylation (5)

Deadly fungus uses unexpected system to control its virulence

Excerpt:

The QSP1 gene codes for a peptide, a short string of amino acids. In an intriguing sidelight, the researchers showed that C. neoformans secretes a precursor to this peptide that matures outside the cell. The fully formed peptide is then imported back into the cell to regulate virulence via its actions on a receptor that is yet to be identified.

My comment: Top down causation links virulence from nutrient energy-dependent quorum sensing in a fungus to nutrient energy-dependent quorum sensing in bacteria and all other living genera via the physiology of reproduction and supercoiled DNA. Virulence is determined by amino acid substitutions.
Energy-dependent RNA methylation and amino acid substitutions can be linked to healthy longevity. Virus-driven energy theft can be linked from energy-dependent replication of viruses to the mutations that cause all pathology.
The molecular mechanisms of RNA methylation that link RNA-directed DNA methylation from the innate immune system to to the species-specific behaviors of mammals via what is currently known about sensing, secreting, and signaling in all cell types of all living genera are now well known to all serious scientists. Apparently, however, the mechanisms are not known to neo-Darwinian theorists and/or skeptics who believe in their pseudoscientific nonsense.
There is probably a need for someone to link RNA methylation from energy-dependent learning and memory to mammalian behavior to show theorists that they have nothing to fall back on.
See for example:  Epigenetics and Genetics of Viral Latency

Excerpt:

Epigenetics and Viral Chromatin
DNA in the nucleus must be assembled into some form of nucleoprotein structure to avoid DNA damage signaling and nucleolytic attack.

Conclusion (with my emphasis):

This review is far from comprehensive or complete and yet hopefully shows the enormous complexity of viral latency and its regulation at the genetic and epigenetic levels. This information provides great opportunity for the development of innovative and highly selective therapeutic intervention. As viral latency is responsible for life-long pathogenesis and mortality risk, the tasks ahead are in sight, but challenges remain.

See also: Structural diversity of supercoiled DNA
Conclusion:

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

See also: GAM: a web-service for integrated transcriptional and metabolic network analysis
My comment: This allows you to link ecological variation to energy dependent metabolic networks and genetic networks to ecological adaptation.

See also: MutaBind estimates and interprets the effects of sequence variants on protein-protein interactions
Excerpt:

MutaBind evaluates the effects of variations and disease mutations on protein-protein interactions. It predicts if a mutation disrupts an interaction and calculates the change in binding affinity. The structure of a protein-protein complex is required for this method.

My comment: This allows you to link energy dependent from mutations to all pathology.
See also: HbVar: A Database of Human Hemoglobin Variants and Thalassemias
My comment: This will help you differentiate between the definition of “mutation” and facts about RNA methylation and amino acid substitutions that differentiate more than 1180 hemoglobin variants.
Compare what is currently known to all serious scientists to the inferences of theorists who have failed to link what is known about biophysically constrained RNA-mediated cell type differentiation to behavior.

See: Protein Contacts, Maximum Entropy in Biology, and Why Behavioural Mechanisms Matter: the PLOS Comp Biol May Issue

Inferring Contacting Residues within and between Proteins: What Do the Probabilities Mean?

It has recently been argued that there is no reason to assume that protein sequences should follow maximum entropy distributions, and that it is therefore puzzling that the max-ent formalism is successful for predicting interacting residues in proteins. Erik van Nimwegen argues that such apparent puzzles result from a misconception of the meaning of the max-ent formalism and, more generally, of the meaning of probabilities.
The Maximum Entropy Fallacy Redux?
Maximum entropy has a long and contested history in statistical physics, the field in which it was first introduced. In contrast to the positive evaluation of maximum entropy in science presented by Erik van Nimwegen (above), Erik Aurell contributes to the ongoing discussion about the use of maximum-entropy models in the modeling of biological data by arguing that max-ent provides no grounds to believe in direct coupling analysis (DCA).
To Cooperate or Not to Cooperate: Why Behavioural Mechanisms Matter
Mutualistic cooperation often requires multiple individuals to behave in a coordinated fashion. Hence, while the evolutionary stability of mutualistic cooperation poses no particular theoretical difficulty, its evolutionary emergence faces a chicken-and-egg problem: an individual cannot benefit from cooperating unless other individuals already do so. Arthur Bernard and colleagues use simulations in evolutionary robotics to study the consequences of this problem.