Amino acid modification FA_Epigenetics_Table1

Anti-entropy: an evolutionist's afterthought

Environmental inputs that affect longevity can also affect the chromatin landscape.

Enlarge the diagram to see that pheromones are linked to longevity via signaling and chromatin modifiers.

Epigenetic regulation of ageing: linking environmental inputs to genomic stability

Excerpt 1)

The longevity of worms and flies can be modulated by the opposite sex82,123,124 a process that can involve pheromone production and/or sensing82,124

Excerpt 2)

As secondary metabolites are evolutionarily conserved, the potential links between pheromonal signalling, chromatin and ageing deserve further exploration in other species.

My comment: The stability of organized genomes is nutrient-dependent and controlled by the physiology of reproduction. That fact has been placed into the context of evolution and longevity.
The link from metabolic network to genetic networks is easy to understand in the context of ecological variation that links pheromones to the physiology of reproduction and ecological adaptation via RNA-mediated events.
What does “evolve” mean outside the context of what is known about physics, chemistry, biology, and the RNA-mediated events that link epigenetically-effected gene duplication and amino acid substitutions to nutrient-dependent cell type differentiation and biodiversity via the physiology of reproduction in all living genera?
‘When I use a word,’ Humpty Dumpty said, in rather a scornful tone, ‘it means just what I choose it to mean — neither more nor less.’
My comment: Here’s what “evolution” means to Jerry Coyne. It means that all species evolve.
There are no “laws” in evolutionary biology comparable to those in physics, except perhaps that “all species evolve”…. — Jerry Coyne (Why Evolution is True)
My comment: Coyne claims that the laws of physics do not apply to evolutionary biology. His claims cannot be linked to anything serious scientists know about physics or about chemistry or about biology. You must simply accept his claim that “all species evolve.”
In Coyne’s world,  if you observe something that looks like what you can claim is evolution, you can remove everything else you observe about physical relativity in everyday life.
See for example: 4 Ways You Can Observe Relativity In Everyday Life

For an electron to jump to a higher energy level it needs to absorb a specific wavelength of light.

My comment: In the context of neo-Darwinian theory, a definition linked nutrient-dependent energy jumps to biodiversity via mutations. See: What is Life?
Excerpt 1)

…  in the offspring even of thoroughly pure-bred stocks, a very small number of individuals, say two or three in tens of thousands, turn up with small but ‘jump-like’ changes, the expression ‘jump-like’ not meaning that the change is so very considerable, but that there is a discontinuity inasmuch as there are no intermediate forms between the unchanged and the few changed. De Vries called that a mutation. The significant fact is the discontinuity. It reminds a physicist of quantum theory -no intermediate energies occurring between two neighbouring energy levels. He would be inclined to call de Vries’s mutation theory, figuratively, the quantum theory of biology.  We shall see later that this is much more than figurative. The mutations are actually due to quantum jumps in the gene molecule.

Excerpt 2)

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

My comment: De Vries quantum jumps should have been attributed to the sun’s biological energy. Please consider that fact before you accept the claim that “evolution is true” because evolutionary theorists defined “evolution” outside the context of the Laws of Physics. They will tell you evolution is true, so you must first realize that your acceptance of their theory means you need not accept anything known about physics since, I repeat, “There are no “laws” in evolutionary biology…” 
If neo-Darwinian evolutionary theory could be placed into the context of physics, the energy jumps linked to differences in the color of gold would be called mutations. The mutations that give the gold its color could be linked to the color of skin.
The claim that skin color arises in the context of beneficial mutations eliminates any need to explain how the sun’s biological energy is linked to the nutrient-dependent energy jumps that link RNA-mediated events from atoms to vitamin D and nutrient-dependent ecosystems in the context of everything known to serious scientists about biologically-based top-down causation.
Instead, evolutionary theorists start from the bottom up. That’s what a special issue of the journal “Cell” did. See the table of contents of the special issue (below) with links that allow you to read the abstracts.
These articles were supposedly written by experts in their disciplines. All the experts ignore the Laws of Physics and the chemistry of nutrient-dependent RNA-mediated protein folding. What’s worst is that the experts ignore everything known to serious scientists about biologically-based cause and effect, which requires some knowledge of how atoms are linked to ecosystems.
In what may have been intended as comic relief, the articles appear to include information on everything known about the origin of eukaryotes (organisms with a cell nucleus and mitochondria), the Cambrian explosion, the origin of terrestrial flora, and even the evolutionary history of birds.
After learning everything these experts know about the history of life on earth, The RNA World as a Model System to Study the Origin of Life reveals that they made it all up. They forced their claims to fit neo-Darwinian theory.
Only then are we told there must be a model that links the theory to facts. The model that is required links atoms to ecosystems via RNA-mediated events. We can ignore that model if we agree to believe in evolutionary theory. Watch how it explains the history of life outside the context of any model — before you are told that a model is required.
In the end, you will see that these experts “…care less about how our particular life arose and more about the possible ways life could arise under a variety of conditions.” Simply put, they care more about their ridiculous theories than facts.
They “…see the RNA World as a particularly tractable model system for studying the emergence of biological complexity during an origin of life.”
Serious scientists do not claim that biological complexity automagically emerged.

History of life on Earth – Geoffrey North

Excerpt: As living things have evolved and diversified…

The tree view of life – Florian Maderspacher

Excerpt: Maybe it is enough to know that “we’re related to the grass”.

How life shaped Earth – Michael Gross

Excerpt (with my emphasis): …life has changed our planet and made it a more complex, diverse, and life-friendly place, but on the other hand it is no stranger to positive feedback loops that lead to mass extinctions and could in principle wipe out all life.

Archaea – Laura Eme, W. Ford Doolittle

Excerpt: Whether anything unites Archaea with Bacteria as ‘prokaryotes’, and whether or not any such shared features are primitive (present in the common ancestor of all extant life) or derived (arrived at convergently through streamlining, or by lateral gene transfer between the two domains) remain open questions.

Photosynthesis and early Earth – Patrick M. Shih

Introduction: Phototrophy has sustained life on Earth, possibly since the dawn of life.

Insect evolution – Michael S. Engel

Excerpt: When such a powerful combination of factors is permitted to run over hundreds of millions of years, the natural byproduct is unrivaled diversity.

Lobopodians – Javier Ortega-Hernández

Excerpt: Thus, onychophorans, tardigrades and euarthropods are all technically extant lobopodians, even though the latter have arthropodized rather than lobopodous limbs.

Phylogenomic Insights into Animal Evolution – Maximilian J. Telford, Graham E. Budd, Hervé Philippe

Conclusion: More sophisticated methods for mapping characters are necessary (Box 2) but the potential for convergent evolution on the one hand and for character loss or character state reversion on the other is not easily overcome (especially given that, as we have underlined, simplification is an evolutionary driving force). The next step of mapping homologous characters onto trees will require the collaboration between morphologists, developmental biologists, comparative genomicists, palaeontologists and phylogeneticists.

The Origin and Diversification of Birds – Stephen L. Brusatte, Jingmai K. O’Connor, Erich D. Jarvis

Conclusion: The flurry of recent work on avian evolution is a prime example of how fossil, morphological, genomic, phylogenetic, and statistical data can be combined to weave an evolutionary narrative, and explain how some of the modern world’s most familiar species became so successful.

The Evolutionary Origin of a Terrestrial Flora – Charles Francis Delwiche, Endymion Dante Cooper

Excerpt: …the charophyte green algae present great opportunities for model system development, and offer a wide range of structural features potentially of use, from simple filamentous and unicellular forms in the Zygnematophyceae; to disk-like branched filaments in the Coleochaetophyceae that show developmental complexity…

Endosymbiosis and Eukaryotic Cell Evolution – John M. Archibald

Excerpt: There is value in looking back at the history of cell evolution research. There is also a lot to be gained from attempting to divorce oneself from the past while looking forward at cell biological problems with modern data. And there is clearly much about the evolution of the eukaryotic cell that still needs to be worked out. In doing so, we should enjoy the view from both perspectives.

Morphological Phylogenetics in the Genomic Age – Michael S.Y. Lee, Alessandro Palci

Conclusion: …if morphological phylogenetics is to exploit the increasingly massive genetic datasets being gathered, the current generation of morphologists will need to work in a different way to their predecessors. In some ways, they need to emulate their molecular counterparts: they need to evaluate morphology at the level of individual species and organisms (instead of higher taxa), they need to analyse all aspects of the phenotype (rather than focus on parsimony-informative traits), and they need to be mathematically and computationally adept, in order to employ appropriate models to integrate increasingly vast morphological and genomic data arrays.

Novelty and Innovation in the History of Life – Douglas H. Erwin

Excerpt: Does evolutionary biology need a new research program in evolutionary novelty distinct from the existing work on adaptation and speciation [89]? Some evolutionary biologists view morphological novelty as built upon the variation existing within a species. Others, particularly many evolutionary developmental biologists, view novelty as based on evolutionary changes distinct from standing variation. Considerable experimental work will be required to test the hypothesis that evolutionary novelties are underpinned by the origin of particular gene regulatory network structures [89, 90, 91, 115]. I suspect that novel individuated morphological structures will be identified that are not associated with such gene network structures, which will draw attention to the developmental mechanisms that ensure their evolutionary stability. Turning from novelty to innovation, there is great opportunity for carefully documenting the environmental and ecological circumstances under which innovations arise, how closely they are linked to morphological novelty, and whether there are particular conditions that foster increased innovation.

Life in the Aftermath of Mass Extinctions – Pincelli Hull

Conclusion: …most species that have ever existed are now dead and those losses have shaped the history of life. An integrative understanding of the role of extinction and speciation in macroevolution has yet to be achieved but is central to understanding the evolution of life.

The RNA World as a Model System to Study the Origin of Life – Abe Pressman, Celia Blanco, Irene A. Chen

Excerpt: It has been proposed that the triplet codon sequences now in the genetic code may have originally functioned in amino acid binding [194]. Alternatively, the first codon triplets may have been small oligomers that bound to and stabilized early tRNAs, which were eventually ligated into small mRNAs that stabilized a series of tRNAs in turn (Figure 3B) [195]. Such early mRNAs may have evolved from random sequences that happened to coordinate the synthesis of favorable small peptides using primitive tRNAs [186, 196, 197, 198] (Figure 3C). At the same time, a simple peptide synthetase ribozyme might evolve into an increasingly large and complex system of molecular alignment, leading to the modern ribosome. Indeed, the ribosome can be thought of as essentially an entropy ‘trap’ for carefully aligned substrates [199], and the inferred oldest core of the ribosome consists of a few surprisingly simple sequences [200]. Perhaps ribozymes catalyzed nonspecific peptide formation initially [201] (Figure 3D,E), with ordering of amino acids emerging later. Alternatively, early peptides may have been aligned by aminoacyl-RNAs, but ribozyme catalysis was not initially part of the mechanism for peptide bond formation [197, 202]. Simple oligopeptides might help to stabilize folded RNAs, or even catalyze RNA replication or ligation, and therefore improved coding functions (e.g., higher fidelity, longer peptides) may have been selected. Recent work has also highlighted a dipeptide capable of stimulating vesicle growth, suggesting that some of the earliest peptides may have aided in vesicle growth and competition as well [203]. Eventually proto-mRNAs with their protein products presumably out-competed ribozymes of similar function, erasing many, but not all, traces of the RNA World [204]. The details of such a process are still not clear, however. A more radical hypothesis is that the earliest mRNAs may have served as templates for RNA synthesis by ligation, with the peptidyl transferase center of the ribosome having its origin as an RNA replicase ribozyme [200]. The mystery of this major evolutionary transition remains to be solved.

The obfuscation of the idea above that “the ribosome can be thought of as essentially an entropy ‘trap’ can be placed into the context of biophysically constrained protein folding chemistry that is nutrient-dependent and controlled by the fixation of RNA-mediated amino acid substitutions, which are linked to biodiversity manifested in all morphological and behavioral phenotypes that can only arise in the context of sucessful organism-level thermoregulation and DNA repair that protects them from virus-driven entropic elasticity that links genomic entropy to extinction.
These articles linked above will all disappear behind a paywall in two weeks.  After that, anyone who intends to claim that they provide evidence that “evolution is true” will need to pay to try and access supporting documentation that shows neo-Darwinian theory is, after all, nothing more than pseudoscientific nonsense. If you do not start with experimental evidence of an anti-entropic force, you cannot invent one later — when you realize it is required to make you appear to be more than just another pseudoscientist.
See for comparison: 72318Re: Transgenerational non genetic inheritance of acquired behaviors
Michael Ragland: Jay: The Bohacek article “Transgenerational non genetic inheritance of acquired behavior is too above me to really understand. However, the author(s) are very open to the idea that transgenerational non genetic inheritance of acquired behaviors is evident in mammals. You stated (as I recall) that such evidence in very weak in mammals. Have I misread/misinterpreted you (as I have sometimes done)? Or am I misinterpreting what Bohacek has stated?
Jay R. Feierman [NEW]: The evidence is strong in invertebrates, like worms. The evidence is weak in vertebrates, weaker in mammals and even weaker in humans. It does not mean it does not occur, just that the evidence is not strong especially in humans.
Michael Ragland: Do you think epigenetics (as it is construed today) is largely a political fad that will go extinct like the mental modules of evolutionary psychology . . .
Jay R. Feierman [NEW]: No, I don’t think epigenetics is a political fad. It is one of the hottest topics in neuroscience today. It is also very important. It was what was missing when I first studied genetics in the 1960s. We didn’t know what turned genes on and off. We now know how the same genes can make an arm, a leg, a kidney and a brain.
Michael Ragland: . . . or do you think it will increase in scientific discoveries/evidence but perhaps not be so politicized i.e Native Americans, Holocaust survivors, African Americans, etc.

Jay R. Feierman [NEW]: Yes. There will be an exponential increase in knowledge of what regulates genes in the next few decades. The idea that social problems present in current populations whose ancestors suffered various abuses many generations ago are due to epigenetic mechanisms is what I believe is the current fad that will fade into oblivion over the next decade or two.

For a historical perspective on what the moderator of the International Society for Human Ethology thinks, see:

7/26/13 Re: [human-ethology] Interjecting where I find others failing, at as much, even here…
James Kohl: It is now perfectly clear that this statement and any statement or inference like it is WRONG: Random mutations are the substrates upon which directional natural selection acts.
Jay R. Feierman: I am absolutely certain that if you showed this statement to any professor of biology or genetics in any accredited university anywhere in the world that 100% of them would say that “Random mutations are the substrate upon which directional natural selection acts” is a correct and true statement. Produce one such person. You can try to recruit such a person however you like. Don’t give links to articles and abstracts that don’t address that exact sentence. Your arrogance amazes me. It would be like me saying that gravity does not cause items with mass to fall to earth at 32 feet/sec/sec in a vacuum as that is how fundamental the statement that random mutations are the substrate upon which directional natural selection acts is to biology and genetics. You really want us to believe that you are the expert on this topic when 100% of university level biology textbooks for Biology 101 and all biology and genetics professors will say the exact same sentence or something almost identical.
My summary: The arrogance of biologically uninformed theorists continues to amaze me. They do not know how evolution occurs, but claim that “evolution is true” or that Random mutations are the substrates upon which directional natural selection acts, while ignoring that fact that the anti-entropic effect of the sun’s biological energy must be linked to the creation of all differences in all cell types of all individuals of all living genera via the biophysically constrained chemistry of nutrient-dependent RNA-mediated protein folding and the physiology of reproduction that enables the fixation of RNA-mediated amino acid substitutions in the organized genomes via protection against virus-driven genomic entropy.


Foundamentals of theory

There are foundations of epigenetics and fundamentals of molecular mechanisms. They have been detailed in this atoms to ecosystems model of RNA-mediated cell type differentiation. Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems.

I have never seen anyone mention the “foundamentals” of epigenetics. It appears the word has been invented. Similarly, the word “mutation” was invented in 1904 by de Vries.

Inventing words and defining them to fit ridiculous theories about neo-Darwinian evolution is required to continue convincing theorists that they are something more than biologically uninformed science idiots.

See for comparison:

Absence of canonical marks of active chromatin in developmentally regulated genes


…strong chromatin marking is related to transcriptional and post-transcriptional stability, an association that we also observe in mammals. Our results support a model in which chromatin marking is associated with the stable production of RNA…

Reported as:

Shaking up the foundamentals of epigenetics


The results of this study contrast sharply with the generally accepted view of the key roles that these epigenetic marks play in regulating gene expression.

My comment: If true, this should have been reported before the top three 2015 Nobel Prizes for science were awarded to researchers who linked physics, chemistry, and conserved molecular mechanisms of epigenetically effected RNA-mediated cell type differentiation in species from microbes to man via DNA repair in the context of the physiology of reproduction. See: DNA Repair Pioneers Win Nobel
Pretending there is any contrast to the accurate representations of what experimental evidence has clearly detailed in the context of an atoms to ecosystems model is like returning to the 20th century definition of “mutation” and trying to link it to evolution while all serious scientists are linking nutrient-dependent RNA-mediated amino acid substitutions from ecological variation to ecological adaptation via DNA repair.
See also: A Nutrient-Driven tRNA Modification Alters Translational Fidelity and Genome-wide Protein Coding across an Animal Genus

These results reveal a strikingly direct mechanism by which recoding of entire genomes results from changes in utilization of a nutrient.

Reported as: 

Nutrient availability can cause whole-genome recoding


“When queuine is abundant, organisms naturally recode its codons to favor the use of ones that are more efficiently translated by Q-modification,” Drummond said. “In this way, a single nutrient causes a snowballing effect that leads to wide-spread changes in how proteins are encoded

The “snowballing effect” was manifested as “re-evolution” of the bacterial flagellum over-the-weekend. See: Evolutionary Rewiring
The epigenetic effect of nutrient stress can also be placed into the context of the anti-entropic epigenetic effects that link heat shock proteins to nutrient-dependent ecological adaptations or compared to virus-driven genomic entropy during thermodynamic cycles of protein biosynthesis and degradation.
In the model organisms that reportedly are Shaking up the foundamentals of epigenetics, ecological variation is linked to ecological adaptation via the anti-entropic effects of food and the pheromone-controlled physiology of reproduction that link the biodiversity of all species from atoms to ecosystems as shown in the collective works of this year’s Nobel Laureates in Physics, Chemistryand Physiology and/or Medicine.
See also: Reversible, Specific, Active Aggregates of Endogenous Proteins Assemble upon Heat Stress

Proteins synthesized in response to heat shock, such as the chaperone Hsp104, show an increase in both pre- and post-shock ratios, indicating new synthesis; increased signal in both channels reflects incorporation of imported post-shock amino acids and residual or recycled pre-shock amino acids (Figure 6B).

My comment: The synthesis of proteins links nutrient-dependent thermodynamioc cycles of protein biosynthesis and degradation to RNA-mediated cell type differentiation in the context of feedback loops.  See: Feedback loops link odor and pheromone signaling with reproduction
See also: Mechanisms of stress in the brain
Abstract excerpt:

…continually changing pattern of gene expression mediated by epigenetic mechanisms involving histone modifications and CpG methylation and hydroxymethylation as well as … the activity of retrotransposons … may alter genomic stability.

The continually changing patterns of epigenetically effected gene expression linked to genomic stability are perturbed by viruses, which steal the nutrient energy that is required for proper RNA-mediated protein folding chemistry that is mediated by amino acid substitutions.
Journal article excerpt:

Glucocorticoids are not the sole mediators of these effects, in which excitatory amino acids and many other cellular mediators also play important parts (Box 1). These mediators span influences from extracellular adhesion molecules to cytoskeletal elements and at least one nuclear pore complex protein.

My comment: The role of RNA-mediated events that link amino acid substitutions to cell type differentiation in all cells of all tissues of all organs and all organ systems attests to the amount of pseudoscientific nonsense touted by evolutionary theorists who still can’t seem to stop making claims that are unsupported by any experimental evidence of biologically-based cause and effect.

See also: Archaeal ancestors of eukaryotes: not so elusive any more

The challenge lies in the investigation of the biology of these organisms. Although we can never know what precisely happened more than a billion years ago, to me, demonstration of the archaeal–bacterial endosymbiosis in the laboratory would mean the completion of the bridge. This is an extremely tall order but then again, who would have predicted 25 years ago that complete genome sequencing of microbes that do not grow in culture would become a near routine exercise?

My comment: Who would have predicted that Koonin would continue making unsupported claims about the origin of endosymbiosis after he admitted “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…
Why hasn’t he searched for information about RNA-mediated epigenetic regulation of gene expression or RNA-mediated gene silencing. What is know about cell type differentiation in species from microbes to man should be considered in the context of how viruses perturb protein folding before any more unsubstantiated claims are made by Koonin or anyone else.


Nutrient-dependent RNA-directed DNA methylation

Pattern recognition
Establishing, maintaining and modifying DNA methylation patterns in plants and animals
FIGURE 2 | Model for RNA-directed DNA methylation.

Gene duplication pathway

Single-stranded RNA transcripts corresponding to transposons and repeat elements are thought to be generated by RNA polymerase IV (Pol IV). CLASSY 1 (CLSY1, also known as CHR38), a putative chromatin-remodelling factor, is likely to function early in RNA-directed DNA methylation (RdDM), possibly recruiting Pol IV to chromatin or aiding in ssRNA transcript processing. RNA-DEPENDENT RNA POLYMERASE 2 (RDR2) is proposed to generate dsRNA from the ssRNA transcripts. DICER-LIKE 3 (DCL3) is thought to process the dsRNAs into 24-nucleotide (nt) small interfering RNAs (siRNAs), which are bound by an Argonaute protein, AGO4. AGO4 localizes to Cajal bodies, and although the function of this association remains unknown, it seems to be necessary for wild-type levels of RdDM33. AGO4 also colocalizes with two Pol V subunits — NUCLEAR RNA POLYMERASE E1 (NRPE1) and NRPE2 — and DOMAINS REARRANGED METHYLTRANSFERASE 2 (DRM2) at a distinct nuclear focus, the AGO4–NRPE1 body (not depicted), which may represent a site of active RdDM33. Pol V is thought to transcribe intergenic non-coding (IGN) regions throughout the genome. NRPE1 association with chromatin requires another putative chromatin-remodelling factor, DEFECTIVE IN RNA-DIRECTED DNA METHYLATION 1 (DRD1), and a structural maintenance of chromosome (SMC) domain protein, DEFECTIVE IN MERISTEM SILENCING 3 (DMS3). IGN transcripts may serve as a scaffold for recruiting AGO4, which interacts with the GW/WG motifs of NRPE1 and SUPPRESSOR OF TY INSERTION 5-LIKE (SPT5L, also known as KTF1), possibly through interactions between AGO4-bound siRNAs and the nascent transcript. An RNA-binding protein, INVOLVED IN DE NOVO 2 (IDN2), is proposed to recognize the siRNA–nascent transcript duplex. These associations may aid in targeting DRM2 to genomic loci that produce both 24-nt siRNAs and IGN transcripts. Recruitment or retention of DRM2 at such loci may be aided by SUPPRESSOR OF VARIEGATION 3-9 HOMOLOGUE 9 (SUVH9) and SUVH2, two proteins that bind methylated DNA and are likely to act late in RdDM. ‘?’ indicates a putative function. The red circles represent DNA methylation.

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Where did this pattern come from? It is clearly a consideration in the context of Sensory feedback shapes individuality to provide equal space for behavioral excellence and in Feedback loops link odor and pheromone signaling with reproduction. The pattern went missing in this report:
Algal ancestor of land plants was preadapted for symbiosis

The innovations that allowed the algal ancestor of land plants to succeed in such a transition remain unknown. Beneficial interaction with symbiotic fungi has been proposed as one of these innovations. Here we show that the genes required for this interaction appeared in a stepwise manner:

The article was reported on October 5, 2015 as: Ancient alga knew how to survive on land before it left water and evolved into the first plant
Excerpt: [they]

…analysed DNA and RNA of some of the earliest known land plants and green algae and found evidence that their shared algal ancestor living in the Earth’s waters already possessed the set of genes, or symbiotic pathways, it needed to detect and interact with the beneficial AM fungi.

My comment: As always, their pseudoscientific nonsense starts with genes and symbiotic pathways that had already somehow evolved.
Also reported on October 5, 2015
Youyou Tu is the 12th women awarded the Nobel Prize in Physiology or Medicine (2015) for her discoveries concerning a novel therapy against Malaria.
Historical perspective: Lasker~DeBakey Clinical Medical Research Award

Tu discovered a passage in the Handbook of Prescriptions for Emergencies (340 CE) by Ge Hong that referenced Qinghao’s malaria-healing capacity. It said “Take a handful of Qinghao, soak in two liters of water, strain the liquid, and drink.” She realized that the standard procedure of boiling and high-temperature extraction could destroy the active ingredient.

My comment: She did not start with the ridiculous assumption that genes and symbiotic pathways had automagically evolved. She started from a textbook written 1675 years ago that appears to have included several thousand years of traditional medicine, which she linked to “modern” medicine via what is known about the biophysically constrained chemistry of RNA-mediated protein folding.
See: Non-mainstream scientist shares Nobel prize in Medicine

Thank God, she recognized the importance of thermodynamic cycles of protein biosynthesis and degradation, or her work might have remained obscure.

I am reminded of a similar problem with the growth of bacteria on media that was heated, which destroyed one of the nutrients required for the microbe’s growth.
A Better Way to Grow Cells: A 120-year-old mystery that’s stumped microbiologists has been solved.
My comment: Do not forget this  if you intend to address the interactions among viruses and microbes.

It turns out the agar is the problem, says microbiologist Yoichi Kamagata at Hokkaido University in Japan.
The standard recipes require mixing agar and phosphate solution before sterilizing them via intense heat. But Kamagata and his team realized this sequence creates hydrogen peroxide, which destroys most of the cells. Sterilize the ingredients separately, and voila, a roughly tenfold increase in cell survival rates.

My comment: A solution of hydrogen peroxide is used to help identify difference in bacterial species because it destroys the cell wall. Staphylococci are catalase positive whereas Streptococci are Catalase negative. Catalase is an enzyme used by bacteria to induce the reaction of reduction of hydrogen peroxide into water and oxygen. A positive catalase text is one in which “bubbles” of oxygen are observed.

If the media used to grow the different types of bacteria contained hydrogen peroxide, identification of Staphylococcus species would be perturbed because the protein folding required to form the cell wall could not link any RNA-mediated events to cell type differentiation.
The human race is doomed. Only a Nobel Laureate whose works in the 60’s led from 5000 year-old wisdom to an effective treatment for malaria would find recognition decades later for reports that linked thermodynamic cycles of protein biosynthesis and degradation from the nutrient-dependent pheromone-controlled physiology of reproduction to a treatment for a virus-containing pathogen.
For an example of doom and gloom that can be attributed to theorists, see: Four laws of evolutionary biology

There are no “laws” in evolutionary biology comparable to those in physics, except perhaps that “all species evolve”. But that’s not very exciting. What we have in my field are not unbreakable “laws,” but patterns or generalizations.

My comment: The first pattern that attests to the validity of the first of “Kohl’s Laws of Biology” is that all living genera must eat to reproduce. Thermodynamic cycles of protein biosynthesis and degradation link the epigenetic landscape to the physical landscape of DNA in all living genera.
No organism that has ever contributed to the earth’s biomass appears to have automagically evolved, which makes all the claims of evolutionary theorists appear to be absurd. However, keep in mind that the works of this year’s Nobel Laureates in Medicine will continue to force all theorists to reassert their ridiculous claims or abandon them before the evolution industry and big bang cosmology industries
Until then, here are links to more articles that I can keep track of. Each links one or more aspects of what is known about RNA-mediated cell type differentiation in species from microbes to man. Each must be considered in the context of the others.

See also: DNA methylation dynamics, metabolic fluxes, gene splicing, and alternative phenotypes in honey bees
Mechanisms of stress in the brain

Protein aggregation after heat shock is an organized, reversible cellular response

Morphological characterization of the action potential initiation segment in GnRH neuron dendrites and axons of male mice
Plasticity-driven individualization of olfactory coding in mushroom body output neurons


Microbes to humans 2015 Nobel Prize

3 Scientists Win Nobel Prize in Medicine for Parasite-Fighting Therapies

Excerpt 1)

Success in antimalarial therapy depends on how clever scientists are in using combinations of drugs.

Excerpt 2)

Dr. Omura played down his accomplishments, saying, “I merely borrowed the power of microbes.”

My comment: These two excerpts appear within the context of three paragraphs that clearly link RNA-mediated cell type differentiation in species from microbes to humans. The context attests to what at first may appear to be a political agenda inserted into Western medical practice.
The first appearance of that Westernized political agenda was never removed during my career as a medical laboratory scientist.
Excerpt 3)

“…malaria parasites have developed resistance against Artemisinin in Asia — but not Africa…”

My comment: In species from microbes to humans, RNA-mediated cell type differentiation links nutrient-dependent base pair changes to biodiversity via single amino acid substitutions in the context of the physiology of reproduction, which leads to fixation of beneficial substitutions that stabilize organized genomes.
For example, Dobzhansky (1973) claimed that “…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.”
Recent reports in “Science Magazine” linked this RNA-mediated event from the nutrient-dependent physiology of reproduction in bacteria to humans via what is known about thermodynamic cycles of protein biosynthesis and degradation.
The cycles of cold and heat prevent viral replication which ultimately occurs when viruses try to ecologically adapt to a new cell type via a single amino acid substitution. See: 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.

Moving forward: These Nobel Laureates have helped to remove any further consideration of mutations and evolution in all living genera by focusing individually and collectively on the conserved molecular mechanisms that link physics, chemistry, and molecular epigenetics to disease prevention and treatment.

Clearly, they are among others who are “Combating Evolution to Fight Disease” But, in this case, they have been doing that since the 60’s and 70’s.

See also: Three share Nobel medicine prize for new tools to kill parasites (Update)

Working in the 1970s, Omura isolated new strains of Streptomyces bacteria and cultured them so that they could be analyzed for their impact against harmful microorganisms, the Nobel committee said.

See also: The Man Who Bottled Evolution and Mutation-Driven Evolution
See for comparison: Antiparasite Drug Developers Win Nobel
My comment: Reports or books that link theories about mutations and evolution to antibiotic resistance and/or all biodiversity should already have been corrected. Two generations of researchers need not have been taught to believe in pseudoscientific nonsense. They might have learned the difference between a mutation and a nutrient-dependent RNA-mediated amino acid substitution.
Instead, de Vries 1904 definition of mutation is still used by neo-Darwinian theorists who don’t know that viruses steal energy that cells require to ensure proper protein folding.
Viruses do not cause de Vries “energy jumps.” The energy jumps are nutrient-dependent. They enable the innate immune system to “jump” to a higher level of control in the context of the physiology of reproduction that transgenerationally protects organized genomes from virus-driven genomic entropy. Simply put, the energy jumps link RNA-mediated events to DNA repair and healthy longevity via protection against virus-driven entropic elasticity that would otherwise lead to genomic entropy much faster than it ultimately does.


Non-mainstream scientist shares Nobel prize in Medicine

Youyou Tu is the 12th women awarded the Nobel Prize in Physiology or Medicine (2015) for her discoveries concerning a novel therapy against Malaria.

Historical perspective: Lasker~DeBakey Clinical Medical Research Award


Tu discovered a passage in the Handbook of Prescriptions for Emergencies (340 CE) by Ge Hong that referenced Qinghao’s malaria-healing capacity. It said “Take a handful of Qinghao, soak in two liters of water, strain the liquid, and drink.” She realized that the standard procedure of boiling and high-temperature extraction could destroy the active ingredient.

My comment: Recent learning about the thermodynamic stability of the active ingredient suggests that traditional Chinese medicine integrated what is now known about the biophysically constrained  chemistry of protein folding during thermodynamic cycles of protein biosynthesis and degradation in bacteria and plants.
The cycles link ecological variation to ecological adaptations via nutrient-dependent RNA-mediated amino acid substitutions in all living genera. The thermodynamic stability of the plant extract was maintained for medicinal use.
Excerpt 2)

Tu pioneered a new approach to malaria treatment that has benefited hundreds of millions of people and promises to benefit many times more. By applying modern techniques and rigor to a heritage provided by 5000 years of Chinese traditional practitioners, she has delivered its riches into the 21st century.

My comment: Other researchers from China recently linked everything else known about RNA-mediated protein folding biochemistry via amino acid substitutions to the thermodynamic stability of all organized genomes. The “Holy Grail” of nutrient-dependent RNA-mediated protein folding is thermodynamically regulated.
Structural basis of pre-mRNA splicing 
Structure of a yeast spliceosome at 3.6-angstrom resolution
Reported as: Chinese Scientists Discover Structural Basis of Pre-mRNA Splicing

On August 21st, the research team led by Prof. Yigong Shi from School of Life Sciences, Tsinghua University in China published two side-by-side research articles in Science, reporting the long-sought-after structure of a yeast spliceosome at 3.6 angstrom resolution determined by single particle cryo-electron microscopy (cryo-EM), and the molecular mechanism of pre-messenger RNA splicing. Until now, decades of genetic and biochemical experiments have identified almost all proteins in spliceosome and uncovered some functions. Yet, the structure remained a mystery for a long time. The works, primarily performed by Dr. Chuangye Yan, and Ph.D students Jing Hang and Ruixue Wan under Prof. Yigong Shi’s supervision, settled this Holy Grail question and established the structural basis for the related area. This work was supported by funds from the Ministry of Science and Technology and the National Natural Science Foundation of China.

See also: Feedback loops link odor and pheromone signaling with reproduction and Sensory feedback shapes individuality to provide equal space for behavioral excellence
Other mainstream scientists continue attempts to genetically engineer mosquitoes to limit their nutrient-dependent physiology of RNA-mediated ecological adaptation. These mainstream scientists ignore the contribution of RNA-mediated amino acid substitutions reported in Amino Acid Residues Contributing to Function of the Heteromeric Insect Olfactory Receptor Complex.
They use viruses to genetically engineer mosquitoes with mutations that limit reproduction. See: orco mutant mosquitoes lose strong preference for humans and are not repelled by volatile DEET and Genome-engineering with CRISPR-Cas9 in the mosquito Aedes aegypti.
If this diagram looks impressively complex compared to claims that linked traditional medicine across 5000 years of what should have been advances in treatment of diseases made by mainstream scientists, realize is that mainstream scientists get paid to do work that is represented like this.



Do young neurons in the brain evolve?

Brain Gain

Young neurons in the adult human brain are likely critical to its function.

By Jef Akst | October 1, 2015


“The rate at which [new neurons] incorporate is dependent upon experience,” Gage says.

My comment: The experience-dependent de novo creation of olfactory receptor genes is the basis for the following representation of biologically-based cause and effect:
Feedback loops link odor and pheromone signaling with reproduction
Virus-perturbed nutrient-dependent RNA-mediated protein folding biochemistry is the clearest link from nutrient-stress and social stress to brain pathology and other pathology. The pathology is linked to viral microRNAs that steal the energy provided by nutrient-dependent microRNAs, which is essential for RNA-mediated DNA repair during the life history transitions of all living genera.
Neo-Darwinian theorists tend not to comment on that fact. Perhaps the problem is Eugene Koonin’s admission that:  “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…”


The bug in the "holy grail" of evolution

Evolution Bug

by Richard William Nelson, October 1, 2015

In one of the largest invertebrate amino acid sequences studies to date, Young and Hebert, found highly variable patterns of amino acid sequences in the enzyme known as cytochrome C between species. None of Charles Darwin’s continuous “successive, slight” evolutionary changes in more than 4,000 species of arachnids studied were found. The paper, published in the highly respected journal PLoS ONE, August, 2015, demonstrates the persistent bug in the theory of evolution – no common ancestor.

My comment: This is an unparalleled accurate representation of facts that link nutrient-dependent RNA-mediated gene duplication and RNA-mediated amino acid substitutions to all cell type differentiation in all living genera via metabolic networks linked to genetic networks. See also: Clinically Actionable Genotypes Among 10,000 Patients With Preemptive Pharmacogenomic Testing. Pharmacogenomic testing links nutritional epigenetics via metabolism to energy-dependent protein folding via amino acid substitutions that stabilize organized genomes.
In the same context, McEwen et al (2015) Mechanisms of stress in the brain  can be compared to Bohacek & Mansuy (2015) Molecular insights into transgenerational non-genetic inheritance of acquired behaviours
McEwen et al (2015) eliminates evolutionary theory via focus on the conserved molecular mechanisms that link nutrient stress and/or social stress from ecological variation to ecological adaptations in all living genera. Bohacek & Mansuy (2015) try to put what is known about the nutrient-dependent innate immune system, cell type differentiation, and the physiology of reproduction into the context of evolutionary theory.
All serious scientists know the outcome of the conflict between McEwen et al (2015) and evolutionary theory. It is not possible to put what is known about RNA-mediated gene silencing or any other aspect of RNA-mediated epigenetic regulation of gene expression into the context of ridiculous theories. The conflict ends when all serious scientists link the “holy grail” of biophysically constrained nutrient-dependent RNA-mediated amino acid substitutions and protein folding to an end to the search for the “holy grail” of evolution.
Simply put, the search for the last universal common ancestor (LUCA) has ended badly for theorists. What is known about molecular epigenetics links ecological variation to ecological adaptation via RNA-mediated amino acid substitutions, without LUCA. Without LUCA, there is no neo-Darwinism; no Modern Synthesis; no evolution industry, and no big bang cosmology industry.
Ecological adaptation starts with the required response of the innate immune system to viruses, which perturb protein folding.

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

I wrote:

The idea of biophysical constraints seems antithetical to the idea of nature somehow selecting mutations that cause amino acid substitutions. However, I am not a biophysicist or evolutionary theorist.
The problem may be my focus on nutrient-dependent receptor-mediated amino acid substitutions in species from bacteria to humans (non-viral organisms). Since I am not a virologist or physicist, I’m not sure that the laws of physics apply to viruses and their replication.
If they do, natural selection for random mutations is not likely to result in amino acid substitutions because the thermodynamics of changes in organism-level thermoregulation preclude such randomness. Stability of protein biosynthesis and degradation that probably depends on protein folding must somehow be controlled. Besides, I don’t know how random mutations in viruses could be naturally selected for inclusion in the human virome (or in the virome of any organism capable of thermoregulating its thermodynamic intercellular signaling).
If the Second Law of Thermodynamics does not apply to viruses, which means the chemical bonds that enable the amino acid substitutions can form at random and somehow be naturally selected, the details of biophysical constraints in this article seems out of place, since I do not think in terms of constrained random mutations and natural selection in mutation-driven evolution.
Hopefully, someone with a background in biophysics will address my confusion in case others are confused. In addition, I wonder if the consequences of understanding the evolutionary mechanisms that govern viruses extend to consequences important to understanding the evolution of species from bacteria to humans via constrained random mutations and natural selection?

When my comment (above) was replaced by the author’s comment on Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution, the facts about evolution became perfectly clear.
Darwin claimed, “conditions of life” must come first. His conditions are nutrient-dependent and controlled by the physiology of reproduction. Top-down causation and the physiology of reproduction link ecological variation to ecological adaptations in all living genera via amino-acid substitutions the stabilize the organized genomes of all living genera.
See also: A universal trend of amino acid gain and loss in protein evolution

We cannot conceive of a global external factor that could cause, during this time, parallel evolution of amino acid compositions of proteins in 15 diverse taxa that represent all three domains of life and span a wide range of lifestyles and environments. Thus, currently, the most plausible hypothesis is that we are observing a universal, intrinsic trend that emerged before the last universal common ancestor of all extant organisms.

My comment: If you have not yet grasped the fact that the claim above means there is no such thing as neo-Darwinian evolution, it is because the neo-Darwinists refuse to admit that they know the facts. (Alternatively, they may not know any.) Like Eugene Koonin, other neo-Darwinists are Riding the Evolution Paradigm Shift to its death. But most others have not admitted that:

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…

That admission eliminates all the ridiculous claims made by neo-Darwinists who left more biological facts out of the “Modern Synthesis” than they included in the estimates of how long it might take for one species to evolve into another, which never happens. Ecological adaptations happen, not evolution of viruses, proteins, or people.
Patterns of Protein Evolution in Cytochrome c Oxidase 1 (COI) from the Class Arachnida

…cytochrome c oxidase 1 (COI) from more than 400,000 animal species…


…COI sequence data can provide an overview of patterns of amino acid evolution across both other groups of arthropods and animal life at large.

My comment: Animal life and plant life are linked to all biodiversity and all biomass by the conserved molecular mechanisms that link atoms to ecosystems via RNA-mediated epigenetic regulation of gene expression and RNA-mediated gene silencing.


Are mutations beneficial?

Researchers develop non-invasive method to detect tumor-causing mutations in saliva

Excerpt: “…a multiplexible electrochemical sensor uses electrode chips to enable vesicular entities in saliva called exosomes to rapidly release molecular constituents (DNA, RNA and proteins) while simultaneously detecting any mutations in tumor-causing DNA sequences. The total detection time is less than 10 minutes and required a small saliva sample.”
My comment: This news about multiplexing attests to the complexity of systems biology, which links amino acid substitutions to mutated DNA in cancer, and also links amino acid substitutions from nutrigenomics and pharmacogenomics (e.g., Alpha Genomix) to cancer treatment.
For example, metabolic profiling links EGFR tyrosine kinase inhibitors to amino acid substitutions via the monooxygenase, cytochrome P450 3A4 (CYP3A4). This links thermodynamic cycles of protein biosynthesis and degradation from RNA-mediated events to amino acid substitutions in cancer and to its effective treatment.
The link from physics to the chemistry of protein folding is less likely to be considered by those who were taught to believe that mutations in DNA are more important than the RNA-mediated events, which are directly linked to the bio-physically constrained thermodynamic stability of metabolic and genetic networks. Physics, chemistry, and molecular biology are all considered in the context of metabolic profiling that links metabolic and genetic networks.
This profiling is currently available in the US, and it is typically covered by Medicare — given the appropriate diagnosis codes. The profiling links the epigenetic landscape to the physical landscape of DNA via nutrient-dependent amino acid substitutions that differentiate healthy and cancerous cell types. The epigenetic/metabolic link to the physical landscape of DNA attests to the relative stability of healthy organized genomes. That healthy genomic stability can be compared to the genomic and metabolic instability associated with pathology.
Evolutionary theorists continue to tout pseudoscientific nonsense that links mutations to increasing organismal complexity without the requirement for genomic stability. Their theories link mutations to natural selection, which eliminates “less fit” or diseased organisms from populations at a faster rate than the rate at which healthy organisms with organized genomes can reproduce. In their ridiculous theories, mutations associated with cancer, starvation, and/or predation may be beneficial.
Intelligent people who have not been taught to believe in theoretical nonsense are less likely to believe that mutations are beneficial. They are more likely to believe that nutrient-dependent amino acid substitutions are beneficial to all organisms because all organisms must eat and reproduce to stabilize the organized genomes or their species.
News that evolutionary theory will be taught to younger students in Israel included this intelligent perspective. “…learning about evolution is not the primary function of the decision, but rather to use it as a building block for students to learn more about their ecology.
There was no intelligent perspective in the news from the UK. Preparing local schools for teaching evolution in the classroom
Excerpt: Workshops included creating a “washing line of time”; discussing whether this is at odds with ‘religious time’ and the biblical explanation of how Earth developed, making rockets to explore the Big Bang theory and analysing fossils to ask whether, and how, science is compatible with creation and religious faith.
My comment: Discussing the Big Bang theory and analyzing fossils has contributed to the pseudoscientific nonsense taught by evolutionary theorists who invented neo-Darwinism. “[W]hat Haldane, Fisher, Sewell Wright, Hardy, Weinberg et al. did was invent…. The anglophone tradition was taught. I was taught, and so were my contemporaries, and so were the younger scientists. Evolution was defined as “changes in gene frequencies in natural populations.” The accumulation of genetic mutations was touted to be enough to change one species to another…. No, it wasn’t dishonesty. I think it was wish fulfillment and social momentum. Assumptions, made but not verified, were taught as fact.”
Haldane, whose works led to the teaching of assumptions, also said this: I suppose the process of acceptance will pass through the usual four stages:
1. This is worthless nonsense,
2. This is an interesting, but perverse, point of view,
3. This is true, but quite unimportant,
4. I always said so.
(Review of The Truth About Death, in: Journal of Genetics 1963, Vol. 58, p.464)” ― J.B.S. Haldane
Similarly, Neil de Grasse Tyson said: “Every great scientific truth goes through three phases. First, people deny it. Second, they say it conflicts with the Bible. Third, they say they’ve known it all along.
For contrast, Max Planck said: “A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die, and a new generation grows up that is familiar with it.
Theodosius Dobzhansky said:  The notion has gained some currency that the only worthwhile biology is molecular biology. All else is “bird watching” or “butterfly collecting.” Bird watching and butterfly collecting are occupations manifestly unworthy of serious scientists!
Unfortunatelym, the words of Planck and Dobzhansky suggest that evolutionary theorists will not accept the truth individually. They will wait until it is forced on them, collectively. Until then, serious scientists have a problem.
The UK school system seems intent on teaching the ridiculous bastardized version of Darwin’s theory, at the same serious scientists are Combating Evolution to Fight Disease by including what is currently known about RNA-mediated cell type differentiation. See, for example: RNA and dynamic nuclear organization.
Unfortunately, despite my attempts to include a common sense perspective on what has been known since Darwin included his ‘conditions of life’ in his theory, I was overwhelmed by the pseudoscientific nonsense of the participants in the discussion of teaching evolution in the classroom. That nonsense seems to be encouraged by the moderators at News.
Fortunately, although cell type differentiation in this video is placed into the context of millions of years of co-evolution, no one is ignorant enough to continue putting evolution into the context of mutations that somehow lead to increasing organismal complexity. Thus, it will be only a matter of months until evolution is eliminated from any further consideration whatsoever as all experimental evidence continues to link ecological variation to ecological adaptations via nutrient-dependent RNA-mediated amino acid substitutions that differentiate cell types via their pheromone-controlled fixation in the DNA of organized genomes of species from microbes to man.