An evolutionary theory killer

How to create biologically uninformed theorists

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Carl Woese was wrong

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

Celebrate Your Inner Virus

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

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

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

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

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

The MicroRNAome Strikes Back: A Sokalian hoax (9)

Summary: Darwin’s “conditions of life” link the creation of sunlight from the creation of ATP to the creation of microRNAs and RNA-mediated cell type differentiation in the context of biophysically constrained viral latency. There is no magical creation of an RNA force field or protein force field that could be used to link the magic of evolution to biologically-based diversity in species from microbes to humans.
RNA force field with accuracy comparable to state-of-the-art protein force fields

The complex and often highly dynamic 3D structures of RNA molecules are central to their diverse cellular functions. Molecular dynamics (MD) simulations have played a major role in characterizing the structure and dynamics of proteins, but the physical models (“force fields”) used for simulating nucleic acids are substantially less accurate overall than those used in protein simulations, creating a major challenge for MD studies of RNA. Here, we report an RNA force field capable of describing the structural and thermodynamic properties of RNA molecules with accuracy comparable to state-of-the-art protein force fields.

In the context of Jason D. Sanders adolescent fascination with the “Star Wars” movie series (see below), “May the magic of the mitochondrial force be with you!”
In the context of John Hewitt’s attempt to link the automagical creation of enzymes to all biodiversity outside the context of the anti-entropic virucidal energy of sunlight, see: Cell Surface Deformation during an Action Potential

A theoretical analysis demonstrates that this observation can be explained by a reversible change in the mechanical properties of the cell surface (transmembrane pressure, surface tension, and bending rigidity). Taken together, these findings contribute to the ongoing debate about the physical nature of cellular excitability.

The mechanical properties of reversible changes in the cell surface did not create themselves. There is also no such thing as RNA force field without the creation of sunlight, the creation of ATP and the creation of RNA. The energy-dependent creation of RNA is required for the biophysically constrained construction of all membranes in all cells. The article about the RNA force field appears to be another hoax akin to Nonomura’s article: Small RNA pathways responsible for non-cell-autonomous regulation of plant reproduction.
The pathways do not create themselves. The RNA force field does not create itself. There is no such thing as non-cell-autonomous regulation outside the context of the creation of sunlight, energy, ATP, and RNA, which biophysically constrains viral latency.
See also: Mitochondria–lysosome contacts regulate mitochondrial fission via RAB7 GTP hydrolysis

Mitochondria–lysosome contacts thus allow bidirectional regulation of mitochondrial and lysosomal dynamics, and may explain the dysfunction observed in both organelles in various human diseases.

Reported as: Study Reveals Direct Contact Between Mitochondria and Lysosome Within the Cell

“In some ways, we assume that scientists have discovered all the major inner workings of our cells in the 21st century. And yet in this work, we made a new observation that these two organelles are directly talking to each other,”

The increasing number of publications that claim to link new findings to energy-dependent biophysically constrained RNA-mediated cell type differentiation can be viewed in the context of publications that fail to link what is known to serious scientists and instead claim that “evolution did it.”
See for example: The Neuronal Gene Arc Encodes a Repurposed Retrotransposon Gag Protein that Mediates Intercellular RNA Transfer

These findings suggest that Gag retroelements have been repurposed during evolution to mediate intercellular communication in the nervous system.

Reported as: Interview with Jason D. Shepherd, PhD

Arc looks like and behaves like a virus. The protein “infects” nearby cells, in this case neurons, with instructions of how to make more of itself, i.e. it shuttles its own mRNA from one cell to another.

If you never looked at another published work, you might still know more than Jason D. Shepherd knows about protein biosynthesis and degradation. He skips the parts about the energy-dependent creation of ATP and RNA and proceeds to link a protein that behaves like a virus to mRNA communication among cell types.
See for comparison: Structure of the Deactive State of Mammalian Respiratory Complex I

Complex I (NADH:ubiquinone oxidoreductase) is central to energy metabolism in mammalian mitochondria. It couples NADH oxidation by ubiquinone to proton transport across the energy-conserving inner membrane, catalyzing respiration and driving ATP synthesis.

Instead of the simple-minded approach taken by Jason D. Shepherd, these authors link the creation of ATP to the biophysically constrained creation of RNA via published works from 1964 and 1968.
See: Dependence of RNA synthesis in isolated thymus nuclei on glycolysis, oxidative carbohydrate catabolism and a type of “oxidative phosphorylation” (1964)
See also: Long-range coherence and energy storage in biological systems (1968)
Half a century later RNA Cloaking by Reversible Acylation (January 26, 2018)

We describe a selective and mild chemical approach to controlling RNA hybridization, folding, and enzyme interactions.

Control of RNA hybridation, folding, and enzyme interactions is energy-dependent. That is no secret to serious scientists!
Reported as:  A chemical cloak of invisibility could reveal RNA’s secrets

Biologists used to think they knew DNA’s less famous cousin, RNA, but in the last two decades it’s become clear the molecule is keeping far more secrets than it has ever revealed. Recent discoveries have it taking on never-before-anticipated roles in regulating how a cell functions.

Diagram: A hairpin loop from a pre-mRNA. Highlighted are the nucleobases (green) and the ribose-phosphate backbone (blue). Note that this is a single strand of RNA that folds back upon itself.
In the past two decades (January 26, 1998 to January 26, 2018) more than  62,000 published works mention “microRNAs,” which used to be called pre-mRNAs. In our 1996 Hormones and Behavior review, we linked the food energy-dependent creation of pre-mRNAs to the pheromone-controlled physiology of reproduction in all living genera via RNA-mediated cell type differentiation. The claim that “Recent discoveries have it [RNA] taking on never-before-anticipated roles in regulating how a cell functions”  is an insult to every serious scientist who has lived and or died during the past half century.

It is no secret that the creation of sunlight has been linked from the creation of ATP to the creation of RNA and all biophysically constrained biodiversity via the physiology of pheromone-controlled reproduction. The cell biology board game “Cytosis” is proof of the fact that anyone age 10+ who plays the game will know more about energy-dependent RNA-mediated cell type differentiation than anyone who reports their findings as if new information had recently become available.


Cancer: Evolution 2.0's Blind Spot

See also:
Hydrogen-atom transfer in DNA base pairs (5)

Hydrogen-atom transfer in DNA base pairs (5)

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

…methylation of the carbon-5 position of cytosine, which results in differences in 5hmCs, may be the most commonly studied type of nutrient-dependent pheromone-controlled structural and functional eukaryotic modification that results from organizing base pair changes.

Team uses internet network theory to decipher the first epigenetic communication network

… 5hmC regulates changes in the compaction of the chromatin, cellular differentiation processes and the energy metabolism in embryonic stem cells.

My comment: Energy metabolism and changes in chromatin compaction are nutrient-dependent in all cell types of all individuals of all living genera. They just reported my claims with no claim about where the energy came from or how the energy was biophysically constrained in the context of RNA-mediated protein folding chemistry that must be linked  from atoms to ecosystems via supercoiled DNA.
The journal article is free: Epigenomic Co-localization and Co-evolution Reveal a Key Role for 5hmC as a Communication Hub in the Chromatin Network of ESCs
Excerpt 1)

Proteins editing and reading 5hmC signals co-evolve

Excerpt 2)

We are still far from understanding the epigenomic “syntax” and how these and the other elements involved in epigenomic communication shape the functional landscape of mammalian genomes.

Excerpt 3)

This conceptual framework constitutes the first explicit formulation to study chromatin as a biological communication system.

My comment: We established a model of chromatin structure as a biological communication system in 1996 in the context of sex differences in cell types  “…in species as diverse as yeast, Drosophila, mice, and humans.”

Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes (Saunders, Chue, Goebl, Craig, Clark, Powers, Eissenberg, Elgin, Rothfield, and Earnshaw, 1993; Singh, Miller, Pearce, Kothary, Burton, Paro, James, and Gaunt, 1991; Trofatter, Long, Murrell, Stotler, Gusella, and Buckler, 1995). Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.

My comment: Our model, From Fertilization to Adult Sexual Behavior was extended across all living genera.
See: The Bull Sperm MicroRNAome and the Effect of Fescue Toxicosis on Sperm MicroRNA Expression.
Nutrient-dependent signals link the pheromone-controlled physiology of reproduction in soil bacteria to plant growth and transgenerational epigenetic inheritance in mammals. The signals do not evolve. Proteins don’t evolve. Bull sperm doesn’t evolve.

The neo-Darwinian “BS”  evolved into a theory about chromatin as a biological communication system two decades after we reported that chromatin is the biological communication system of molecular epigenetics. There is still no defined boundary between epigenetics and genetics, which suggests our 1996 review answered Schrodinger’s question in the context of Darwin’s “conditions of life.” Life is nutrient-dependent and controlled by the physiology of reproduction.
See: What is Life?

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)

I reiterate: “After utilizing it they return it in a very much degraded form -not entirely degraded, however, for plants can still make use of it.” Plants can make use of the BS, but neo-Darwinian theorists cannot use it to support their ridiculous theories. Nothing ecologically adapts without light. Nothing co-evolves. Nutrient-dependent co-adaptation may occur to establish slight differences in the construction of ecological niches. But BS and other nutrients used to feed plants are required for niche construction.
Everything that neo-Darwinian theories based on their BS and other inferences was placed into the context of my atoms to ecosystems model. It was also reported in the context of the Structural diversity of supercoiled DNA.

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.

My comment: The only way to understand any metaphorical epigenomic “syntax” is to start with the de novo creation of receptors that allow nutrients to enter cells.  If theorists start with a metaphorical cell, they must continue to infer that cellular metabolism automagically emerged and led to the differentiation of cell types. Theorists will then be asked to explain the emergence of metabolism and the circular arguments that link the emergence of metabolism to other ignorant inferences about biologically-based cause and effect.
How did sex differences co-evolve? How do inferences link biophysically constrained cell type proliferation and differentiation from ecological variation via the atoms to ecosystems they placed into the context of 5hmC as a “communication hub?” How did 5hmC become the link to the chromatin network of embryonic stem cells? How did that happen outside the context of nutrient-dependent cell type differentiation at the dawn of the de novo creation of receptors and cells?
See also: Discovered: How to unlock inaccessible genes

The researchers first mapped the location of several “chromatin-remodeller enzymes” across the entire genome of the embryonic stem cells of the mouse.

My comment: Chromatin remodelling is nutrient dependent and it links what they call “chromatin-remodeller enzymes” to RNA-mediated cell type differentiation in species from yeasts to mammals via the conserved molecular mechanisms we detailed in the molecular epigenetic section of our 1996 review.

Genome-wide nucleosome specificity and function of chromatin remodellers in ES cells [subscription required]

Two trends emerge: an activating [energy-dependent] remodeller in one class of genes is an inhibitor remodeller in the other class; and within the same class, an [energy-dependent] activating remodeller can be counteracted by an inhibitor remodeller. Taken together, [energy-dependent activating and inhibiting] remodellers work together at specific nucleosome positions adjacent to promoter region NFRs to elicit proper gene control.

The energy-dependent activating and inhibiting remodellers link hydrogen-atom transfer in DNA base pair in solution to the de novo creation of receptors in cell types. The failure to mention that everything above is based on the energy linked from ATP limits the explanatory power of their claims. If they included ATP it would become clear that nutient-dependent energy links everything currently known about hydrogen-atom transfer in DNA base pairs from ecological variation to ecological adaptation. The links have been established in the context of thermodynamic cycles of protein biosynthesis and degradation.
The cycles occur only when the DNA base pairs are in solutions with a properly controlled pH balance that protects supercoiled DNA from virus-driven entropy.
The de novo creation of receptors in the context of hydrogen-atom transfer in DNA base pairs is the starting point for the creation of different cell types. Creation of different cell types is nutrient energy-dependent RNA-mediated, and it links physics from chemistry to the conserved molecular mechanisms of life in all living genera
For example, see:
1) Non‐enzymatic glycolysis and pentose phosphate pathway‐like reactions in a plausible Archean ocean and
2) Conditional iron and pH-dependent activity of a non-enzymatic glycolysis and pentose phosphate pathway

We find reactions with the same pH optimum neighbor in an experimentally functional reaction network that shares topological similarity with modern cell’s glycolytic pathway and PPP. The coexistence of different pH optima in different parts of the network allows conditional activity, as it does in the modern cell. This implies that changing chemical conditions can, at least in a rudimentary sense, mimic an essential feature of the modern metabolic network, which is to regulate metabolism by the ability to turn metabolic pathways on and off.

My comment: An intelligent medical laboratory scientist can link reactions in a plausible Archean ocean from differences in temperature and differences in pH to spectophotometric assays of chemicals in human body fluids. For example, I can also link the pH of blood agar used to grow pathogenic bacteria from their nutrient-dependent energy transfer to healthy longevity or to virus-driven pathology.
Pathology arises when embryonic stem cells do not turn off their metabolic pathways. It’s called cancer. Virus-driven energy theft causes the pathology of cancer. The viruses cause changes in pH in different cell types in tissues such as circulating blood. The circulating blood links energy-dependent hydrogen-atom transfer in DNA base pairs to ecological adaptation in all invertebrates and vertebrates with circulating cell types, except when viruses steal the energy that is required for cell type differentiation.
Serious scientists know what happens when viruses steal energy and temporarily alter the picture of health.
See: Molecular requirements for a pandemic influenza virus: An acid-stable hemagglutinin protein
They cite:
2007 A two-amino acid change in the hemagglutinin of the 1918 influenza virus abolishes transmission
2013 The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site
2014 A single amino acid in the stalk region of the H1N1pdm influenza virus HA protein affects viral fusion, stability and infectivity
1973 Nothing in Biology Makes Any Sense Except in the Light of Evolution
Excerpt 1)

 ….compared the amino acid sequences in cytochrome C in different branches of the living world. Most significant similarities as well as differences have been brought to light. The cytochrome C of different orders of mammals and birds differ in 2 to 17 amino acids, classes of vertebrates in 7 to 38, and vertebrates and insects in 23 to 41; and animals differ from yeasts and molds in 56 to 72 amino acids. Fitch and Margoliash prefer to express their findings in what are called “minimal mutational distances.” It has been mentioned above that different amino acids are coded by different triplets of nucleotides in DNA of the genes; this code is now known.

Excerpt 2)

…the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla. ( p. 127)

See also: Receptor binding and pH stability – how influenza A virus hemagglutinin affects host-specific virus infection
My comment: The nutrient-dependent innate immune system typically controls host-specific virus infection. Ongoing virus onslaughts require the more permanent nutrient-dependent protection of supercoiled DNA. However, the viruses that become retroviruses due to gene losses and gains in the chromosomes of different species, can be reactivated by nutrient-stress or by social stress. Both forms of stress are linked via the same pathways to virus-driven genomic entropy during life history transitions, or to healthy longevity in the absence of stress.
See:  Lineage-Specific Profiling Delineates the Emergence and Progression of Naive Pluripotency in Mammalian Embryogenesis

These results highlight metabolic differences, in particular with regard to amino acid biosynthesis, between the mouse and marmoset embryo.

Reported as: Shining light on the pathways that give rise to pluripotent cells in rodents and primates

This highly interdisciplinary study blends traditional embryology, genomics and bioinformatics.

My comment: Researchers who have not learned how energy theft by viruses is linked to pandemics in populations that have not ecologically adapted via RNA-mediated amino acid substitutions are pseudoscientists who also don’t know that the stability of supercoiled DNA protects organized genomes from virus driven entropy.
An accumulation of viruses causes a change in pH that alters thermodynamic cycles of protein biosynthesis and degradation. Stress-related reactivation of retroviruses links the change in pH from perturbed cycles of protein folding to all cancers via the return of somatic cell types to a pluripotent undifferentiated embryonic state.
See: Intrinsic retroviral reactivation in human preimplantation embryos and pluripotent cells
My comment: Energy theft by viruses either kill or are biophysically constrained by the nutrient-dependent immune system. But biophysically constrained viruses may still be part of lineage specific cell types. I cannot explain this further except via the use of a metaphor.  For example, I ride a smaller motorcycle than I once rode, with a smaller battery than any of the larger motorcycles I have ridden for the past 15 years. The battery was nearly dead, and I could not start my motorcycle yesterday. I put it on a “trickle” charger and started it today. The metaphor is that the charger provided a form of nutrient-like energy to the battery, which enabled me to use the fuel-injected gas energy that is required to run the engine that enables movement of what might in this case be considered a metaphorical life form.

See also: The Cellular and Molecular Landscapes of the Developing Human Central Nervous System


We will next detail the current understanding of the transcriptional, epigenomic, and regulatory landscapes of the developing human neocortex and other regions of the CNS, noting the essential conserved features, as well as clade and species-specific differences, revealed by these studies.

See: Genomic Determinants of Vitamin D-Regulated Gene Expression
Abstract excerpt:

These studies highlight the role of chromatin in the expression of genes and the dynamic impact of the epigenetic landscape that contextualizes individual gene loci thus influencing the VDR’s transcriptional actions.

In my 2014 review of nutritional epigenetics I wrote:

Because vitamin C and other vitamins appear to epigenetically effect nutrient-dependent methylation at the level of single-base resolution in mammals, it has become more important to determine how base-pair changes alter intracellular interactions in embryonic stem cells or intercellular interactions in other cells that result in cascades of downstream intracellular and intercellular organizing interactions throughout life. Other vitamins, such as vitamin D, and metal ions such as calcium, iron, lead and manganese also appear to epigenetically alter these organizing interactions. Therefore, a biophysically constrained, nutrient-dependent, epigenetically-effected, receptor-mediated recognizable organized pattern of emergence can be viewed in the context of ecological variations and ecological adaptations.

In my 2014 review of nutritional epigenetics I wrote:

…calcitriol is the active form of vitamin D. Its effects on the microRNA(miRNA)/messenger RNA (mRNA) balance appear to protect against perturbed protein folding, which is associated with colorectal cancer. MiRNA-627 targets the mRNA that encodes an enzyme linked to histone demethylation and amino acid substitutions that increase stability of hydrogen bonds in DNA, which are important to protein folding (Padi, Zhang, Rustum, Morrison, & Guo, 2013).

My comment: Each day, others exemplify their ignorance of obvious links from atoms to ecosystems via what is currently known about hydrogen-atom transfer in DNA base pairs in solution that link RNA-mediated amino acid substitutions to cell type differentiation and the stability of organized genomes in all living genera.
For example, see this Nature Podcast on Ageing
My comment: Dr. Stroustrup isn’t sure whether the molecular mechanisms of RNA-mediated lifespan are the same in C. elegans and humans. I suspect that everything known to others about physics, chemistry, and the conserved molecular mechanisms of cell type differentiation, which links octopuses to primates, would convince Dr. Stroustrup and others to learn about what others already know. Simply put, the conserved molecular mechanisms that link C. elegans to humans are the same. That’s why they are called conserved molecular mechanisms. If the nutrient-dependent molecular mechanisms were not conserved, RNA-mediated differences in life span could be explained in the context of mutations and evolution.
See: The temporal scaling of Caenorhabditis elegans ageing
My comment: Stroustrup et al., (2016) used UV light and mutations to differentiation cause and effect in the context of the life-span of the model organism C. elegans. UV light was used to deactivate the bacteria fed to one population of organisms, which extended their lifespan, and disruption of feeding behavior by a mutation reduced the lifespan of another population of organisms.
In my model, cause and effect extends the anti-entropic virucidal effects of UV light from the death of viruses in the bacteria to the “inactivation” of the food. Inactivation in linked to increased lifespan in the context of thermodynamic cycles of protein biosynthesis and degradation that are not perturbed by the energy theft viruses use to support their replication, which changes the pH of cell types and limits nutrient-dependent RNA-mediated DNA repair of virus-driven damage.  In that context, albeit apparently without knowing it, Stroustrup et al., (2016) link insulin/IGF receptor daf-2 to the activity of the heat shock factor hsf-1. They link disruption of hsf-1 to temporal rescaling and reduced longevity (i.e., lifespan). They do not link the population-wide changes in different organismal physiological states to nutrient-dependent genome organization, vitality, organ reserve, or resilience. They do not link resilience to nutrient-dependent pheromone-controlled ecological speciation, which was reported in System-wide Rewiring Underlies Behavioral Differences in Predatory and Bacterial-Feeding Nematodes.
That was reported as: The neurobiological consequence of predating or grazing

The patterns of synaptic connections perfectly mirror the fundamental differences in the feeding behaviours of P. pacificus and C. elegans”, Ralf Sommer concludes. A clear-cut result like that was not what he had necessarily expected. Previous studies in much simpler neural circuits – as in the marine snail Aplysia – had indicated that changes in behaviour do not have to coincide with changes in number and location of synapses. Differences in physiological properties of neurons or in their modulation by neurotransmitters can be sufficient to effect behavioural changes.

My comment: The consistency of what is being reported in the context of UV light altered diets compared to mutations the disrupt feeding behaviors becomes clear in the mouse model. Nutrient-dependent RNA-mediated amino acid substitutions are linked to morphological and behavioral phenotypes in Stress dynamically regulates behavior and glutamatergic gene expression in hippocampus by opening a window of epigenetic plasticity.
Abstract excerpt:

Excitatory amino acids play a key role in both adaptive and deleterious effects of stressors on the brain, and dysregulated glutamate homeostasis has been associated with psychiatric and neurological disorders. Here, we elucidate mechanisms of epigenetic plasticity in the hippocampus in the interactions between a history of chronic stress and familiar and novel acute stressors that alter expression of anxiety- and depressive-like behaviors.

My comment: Nutrient-dependent RNA-mediated amino acid substitutions continue to be linked across species from microbes to humans via the conserved molecular mechanisms that link epigenetic to genetics with no defined boundary between epigenetics and genetics in the context of biophysically constrained cell type differentiation and the physiology of reproduction. It will not become clearer that the physiology of reproduction links RNA-mediated amino acid substitutions to supercoiled DNA and the chromosomal rearrangements linked from pheromones to biodiversity in species from microbes to man.  However, the need for a model that links metabolic networks to genetic networks has become clear, as has the fact that the model will continue to be ignored.
For example, watch Perry Marshall ignore my model in my posts to his blogs.

Darwinists Underestimate Nature. Creationists Underestimate God

The lowest common denominator is nutrient-dependent RNA-mediated DNA repair. In the context of the physiology of reproduction, it links atoms to ecosystems via the innate immune system. Fixed amino acid substitutions stabilize all organized genomes.
See: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems.
Now see: “Team uses internet network theory to decipher the first epigenetic communication network” January 28, 2016
They are reporting what I detailed in an invited review of nutritional epigenetics. But they place it into the context of nutrient-dependent epigenomic co-localization and co-evolution. They don’t seem to realize the communication hub in the chromatin network of embryonic stem cells does not automagically evolve.

Intelligent Design’s Blind Spot

Yes, I understand that chemicals affect cells, and cells change their code as a result. But you’re putting the cart before the horse because none of this matters before you have a first cell.
Thanks. You are speculatively interpreting my works when you have not accepted part 1 or part 2 of the submission. Why do you think I have not addressed the creation of the first cell?
Today, others reported everything I reported in what could have been part 1 of a 2 part submission.
Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems.
Now see: “Team uses internet network theory to decipher the first epigenetic communication network” January 28, 2016
In part 2 of my submission, I will detail the origin of the code and explain how information leads to the de novo creation of receptors and all cell types in all living genera.
If you want part 2, accept part 1. If not, others will keep reporting the details I want to report in the context of mutations and evolution.
You prevented my reply to your reply (below).
I’m willing to proceed if you make a “good faith” effort to show that after I provide part 2, you will not claim I did not prove anything about the origin of the first cell.
From page 206 of “Evoluton 2.0.”
You wrote: “But I could find no formula or transformation that turns matter or energy into information. This is precisely what the Evolution 2.0 Prize seeks to discover.”
Perhaps I’m mistaken, but it appears that you’ve changed the goal. What does the first cell have to do with the origin of the code?
Neo-Darwinists do this. I showed that chromosomal rearrrangements are linked to ecological adaptation and PZ Myers ignored weekend evolution of the bacterial flagellum.
Like PZ Myers, others simply tell me (and you) that we misunderstood something they had claimed. They won’t make any claims that link physics, chemistry, and conserved molecular mechanisms from the origin of the code to the complexity of ecosystems. That complexity links atoms to ecosystems via examples of rapid adaptation.
My mistake. I apologize. I thought you had ended our discussion. After I posted my reply, I see that it was added below yours. PZ Myers biased my impression of what happened. Every time he has no response to a logical claim or assertion, he terminates the discussion.