The Light and Darkness of "Evolution 2.0"

The light of evolution in the oft-cited work by Dobzhansky (1973) is the energy from sunlight. The sun’s biological energy links its anti-entropic virucidal epigenetic effects to RNA-mediated amino acid substitutions that differentiate all cell types in all individuals of all living genera.
Excerpt from Dobzhansky (1973)

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

My comment: Viruses steal the energy that is required for nutrient-dependent RNA-mediated cell type differentiation in the context of RNA-mediated amino acid substitutions.
Authors’ comment on Koel et al., (2013): The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.
My comment: When a virus steals energy from a cell, it uses the energy to support viral replication, and viral replication perturbs nutrient-dependent cell type differentiation.
Excerpt from Taylor et al (2015):

After 96 hours of incubation of AR2 and Pf0-2x at room temperature on SMM, two breakout mutations were visible, conferring first slow (AR2S and Pf0-2xS) and then fast (AR2F and Pf0-2xF) spreading over the agar surface (Fig. 1A). The AR2F strain produces flagella, but we could not detect flagella in electron microscopy samples for AR2S (Fig. 1B). Genome resequencing revealed a single-nucleotide point mutation in ntrB in strain AR2S, causing an amino acid substitution within the PAS domain of the histidine kinase sensor NtrB [Thr97→Pro97 (T97P)] (13). The fast-spreading strain AR2F had acquired an additional point mutation in the σ54-dependent EBP gene ntrC, which alters an amino acid (R442C) within the DNA binding domain (Table 1 and table S2).

My comment: Collectively, three articles established the link from sunlight to RNA-mediated cell type differentiation via microRNAs and adhesion proteins linked to supercoiled DNA and chromosomal rearrangements in the context of the physiology of reproduction. But, they individually and collectively reported their findings in terms of mutations and evolution.
See for comparison: Feedback loops link odor and pheromone signaling with reproduction and What is Life?
My comment: An intelligent person need look no further than what is known about life in the context of the nutrient-dependent physiology of reproduction, which links all invertebrates to all vertebrates. After a brief review, they could still probably grasp the fact that supercoiled DNA protects organized genomes from virus-driven entropy. If an intelligent person did not look at the role of viruses, they might make the claims made by neo-Darwinian evolutionary theorists. That is why it is important to note 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… — Eugene Koonin

See also: Who’s Invited to the Royal Society Evolution Paradigm Shift Meeting? – The Unofficial List

I was informed by the Royal Society science program office that there will be no formal presentations on viruses, per se, which seems peculiar considering viruses are now understood to be the biggest part of the biosphere, and a key reason for paradigm shift. Viruses and microbes — both organisms — were left out of the modern synthesis.

My comment: Why is a meeting that supposedly will address the evolution paradigm shift not going to include anyone who knows about virus-driven genomic entropy? Most serious scientists already know that …gradual mutation followed by selection has not, as a matter of fact, been demonstrated to be necessarily a cause of speciation.
That fact makes the motives of the meeting organizers increasingly suspicious. Clearly, the role of virus-driven genomic entropy msut be discussed in the context of a paradigm shift. The paradigm shift must also include what is known about nutrient-dependent RNA-mediated DNA repair. The nutrient-dependent repair mechanisms link metabolic networks to genetic networks in all living genera via the innate immune system.
See: Noncoding RNA –NORAD– Regulates Genomic Stability by Sequestering PUMILIO Proteins

Interestingly, it was recently reported that NORAD (LINC00657) is induced by hypoxia in human endothelial cells (Michalik et al., 2014), suggesting broader roles for NORAD in cellular stress responses. How NORAD influences the functional outputs of these and other stress response pathways, and the broader roles of NORAD in normal physiology and disease, represent important areas for future research.

My comment: The immune system is the interface between stress-related effects on cell types vs healthy longevity.  Stress-related proliferation of viruses links viral microRNAs to perturbed RNA-mediated protein biochemistry that is typically constrained by hydrogen-atom transfer in DNA base pairs. Constraint-breaking mutations show up quickly and are consistently linked to outcomes via changes in thermodynamic cycles of protein biosynthesis and degradation that can be measured via changes in the pH of human body fluids or via spectophotometry. Both types of measurements assess nutrient-energy theft by viruses.
See for example: Molecular requirements for a pandemic influenza virus: An acid-stable hemagglutinin protein

These studies link a fundamental property, activation energy of a fusion protein measured as its pH of activation (acid stability), to the ability of zoonotic influenza viruses to cause a human pandemic.

Reported as: Acid-sensitive molecular changes contribute to the emergence of pandemic influenza

“The hemagglutinin protein plays a central role in human flu pandemics, yet until now the molecular properties required for pandemic viruses have remained largely undefined,” Russell said. “Our findings suggested that one requirement for a pandemic influenza A virus was an acid-stabilized protein with an activation pH of 5.5 or less, which was sufficient to allow airborne human-to-human transmission at the start of the 2009 H1N1 pandemic.”

Koel et al., (2013) revisited: The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.
My comment: In the context of my model, virus-linked energy theft from specific cell types led to the stability of an acid-stabilized protein in the virus with an activation pH of 5.5 or less via a single amino acid, which allowed “…airborne human-to-human transmission at the start of the 2009 H1N1 pandemic.”
See also:  The Quest to End the Flu
My comment:

See also: “Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution”
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?

The comment above was also published to the “Science Magazine” comments section, but it was removed and replaced with the authors’ comment. Obviously, they knew that anyone familiar with the laws of physics and chemistry of nutrient-dependent RNA-mediated protein folding would link virus-driven constraint breaking mutations to the antigenic change in the virus without claims about evolution.
Viruses don’t evolve! Antigenic changes don’t evolve! Proteins don’t evolve! Researchers must make it clearer that they know the difference between neo-Darwinian theory and facts about cell type differentiation. That is the only way serious scientists can avoid being removed from positions where their ignorance may cause a pandemic.

See also: It is not clear in any representation that a virus-driven change in a base pair could be linked from the theft of energy and perturbed hydrogen-atom transfer in DNA base pairs in solutuion to pathology. Although only one base pair change and one amino acid substitution may make a difference to the cell type, nutrient-dependent RNA-mediated healthy longevity is not placed into the context of one amino acid substitution linked to pH and spectophotometric assays of hydrogen ion concentration in body fluids. Thus, the accumulated knowledge fron every test that I ever performed during ~60,000 hours of testing in my career as a medical laboratory scientist is dismissed by the claims of evolutionary theorists.
However, the changes in hydrogen-atom transfer in DNA base pairs in solution have now been placed into the context of bacteria the move towards the light.
See: How slime can SEE where it’s going: Single-celled pond bacteria act like ‘microscopic eyeballs’ to sense light and move towards it
Light induced change in bacteria
Previous studies have shown Synechocysti contain photosensors and that they are able to perceive the position of a light source and move towards it – a phenomenon called phototaxis. This study showed how this process works. Bacteria moving towards a light is pictured
See also:
Comparative Proteomics Reveals Important Viral-Host Interactions in HCV-Infected Human Liver Cells
Theoretical investigation of hydrogen atom transfer in the cytosine-guanine base pair and its coupling with electronic rearrangement. Concerted vs stepwise mechanism
Wheeler’s delayed-choice gedanken experiment with a single atom
Effect of Methylation on the Properties of the H-Bridges in DNA. A Systematic Theoretical Study on the Couples of Base Pairs
Photoinduced amino–imino tautomerism of 2-aminopyridine in a low-temperature argon matrix
My comment: Even those who claim to be trying to reconcile the differences between theorists and creationists contribute to ongoing misunderstanding.
See: Darwinists Underestimate Nature. Creationists Underestimate God

You say that “We can produce new species at will and it happens all the time”.

My comment: February 7, 2016 at 7:21 am
Like many others, you seem to be confused about what can happen in the lab compared to what does not happen outside the lab.
For example: Re: “1) Hybrids, where Species 1 crossed with Species 2 gives you Species 3. ”

For comparison: Species of Drosophila


Hybrids of Drosophila pseudoobscutra and D. persirnilis are easily obtainable in the laboratory, but they are absent in localities where both species occur side by side (14).

See also: The Myopics of Darwinism, Dawkinsism and Blind Faith – Enter Evolution 2.0

My comments: Perry Marshall seems to be siding with those who think hybrids are proof that evolution may occur over millions of years, albeit without the pseudoscientific nonsense about mutations and natural selection.

James V. Kohl says: January 26, 2016 at 3:24 pm
My 2012 Templeton Grant Proposal:

Nutrient chemicals are required to sustain life and for transgenerational epigenetic inheritance of biological populations. This fact is exemplified in the honeybee model organism and other model organisms. The nutrient chemicals cause receptor-mediated events. The receptor-mediated events allow nutrient chemicals to enter though the cell wall. Electrostatic changes then alter intracellular signaling as nutrient chemicals are metabolized to species-specific chemicals called pheromones.
The metabolism of nutrient chemicals to pheromones exemplifies the apparent design of biology. Bottom-up (genetically predisposed organization) and top-down reciprocity via sensory activation is what allows nutrient chemicals and pheromones to control survival of the species. The nutrient chemicals support individual fitness and the pheromones control reproduction. From the bottom up, their ability to control species survival is enabled by their epigenetic effects of nutrient chemicals that cause stochastic gene expression. Similarly, from the top down, pheromones epigenetically effect stochastic gene expression (in cells of organisms from microbes to man).
All extant organisms show a clear pattern of genetic predispositions that enable nutrient chemical-dependent and pheromone-dependent adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction. Adaptive evolution is facilitated via the expression of new genes, including those that are important to the development of language abilities and human brain development.
The ability of cells containing genes to produce de novo genes does not seem to have developed via random mutations. Although gene expression is stochastic, organisms that choose the wrong nutrient chemicals are less reproductively fit and doomed to suffer and die. One organisms choice also may determine downstream down-stream epigenetic effects on other organisms that selfishly compete for life-sustaining nutrient chemicals in same ecological niche. Only when some level of cooperation is achieved can individuals or species survive in the same ecological niche, and species-specific pheromones ensure that two species do not share the same social niche.
Ecological and social niche construction collectively enabled evolved nutrient-dependent and pheromone-dependent neurogenic niche construction, which is exemplified in vertebrates by conservation of the GnRH molecule, and diversification of its receptor across 400 million years of adaptive evolution that first required nutrient-dependent and pheromone-dependent sexual reproduction in unicellular and multicellular organisms, with molecular origins as the alpha-mating pheromone in brewer’s/baker’s yeast.
The ecological and social niches constructed by one species that eats another exemplify how that advent of multicellularity and cooperation in different species enabled the cascade of diversity that is readily evidenced across Creation, as it always has been. When viewed from a model of complexity, Creation of the diversity of life does not appear to involve random events, but instead involves the common molecular biology of receptor-mediated events is species from microbes to man.
The concept that is extended is the epigenetic tweaking of immense gene networks in ‘superorganisms’ that ‘solve problems through the exchange and the selective cancellation and modification of signals. It is now clearer how an environmental drive probably evolved from that of food ingestion in unicellular organisms to that of socialization in insects. It is also clear that, in mammals, food odors and pheromones cause changes in hormones that have developmental affects on sexual behavior in nutrient-dependent, reproductively fit individuals across species of vertebrates.
Thus, simply put: “Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans.” And there is nothing random about that!

My comment: I did not receive the grant and as of 2/9/16, I had not received a response from Perry Marshall to my post, which addresses many of his claims. I held this blog post for several weeks to give Marshall and others a chance to respond to what is currently known to serious scientists about how physics, chemistry, and molecular epigenetics must be linked to healthy longevity or to virus-driven pathology.  Obviously, it is not only the neo-Darwinists and theoretical physicists who want to continue to ignore the obvious links from atoms to ecosystems via the sun’s anti-entropic energy.

Perry Marshall says:

February 9, 2016 at 3:39 pm

No argument that living things use sunlight in processing of information.Show me a non-living thing that turns sunlight or chemicals into code and then we’ll have something to talk about. Thus far nothing you have presented so far meets the specification of the prize.

James V. Kohl says:

February 9, 2016 at 5:51 pm
Thanks. I think others can see what is happening with the specifications of the prize.
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.”
Sunlight is the energy that links information to matter. Now it’s not a formula that you want; it’s an example of a non-living thing that links sunlight from quantum physics to the chemistry of protein folding via the de novo creation of nucleic acids.
Why not simply admit that you will not accept any accurate representation of biological facts that link the de novo creation of nucleic acids (the code) to all RNA-mediated biodiversity. You’re stuck with your claims about hybrids and Shapiro’s nonsense.
Addendum: Shapiro’s nonsense was published as Evolution: A View from the 21st Century
Excerpt: Proteins operate as conditional microprocessors in regulatory circuits.
Excerpt: The concept of most proteins as systems of domains exemplifies the new combinatorial thinking frequently emphasized in this book. It makes good sense a priori to expect that a protein will make a successful functional change by acquiring an existing intact binding or catalytic capability. Intuitively, this has a far higher probability of proving effective than does a random process of changing one amino acid at a time and gradually selecting modest improvements in catalysis or binding specificity.
My comment: The processes that link RNA-mediated amino acid substitutions to cell type differentiation in all living genera via the physiology of reproduction are nutrient-dependent. They are not random processes that change amino acids one at a time. The processes link atoms to ecosystems via hydrogen-atom transfer in DNA base pairs in solution in the context of microRNAs, adhesion proteins, DNA repair, and the stability of organized genomes that links supercoiled DNA to protection against virus-driven entropy.
Shapiro’s book (2011) and Nei’s book (2013) Mutation-Driven Evolution were more than a decade past their due dates. As is common with all textbooks, by the time they are published, new information makes them increasingly worthless to anyone who needs to learn more about what is known to serious scientists. For that knowledge, you must follow the extant literature and try to keep up. Good luck catching up before you try to keep up with what is being published on the role of microRNAs in cell type differentiation.
See, for example: Items: 1 to 20 of 47233

Perry Marshall says:

February 9, 2016 at 9:45 pm

James, if you think you have a solution then fill out a proper prize submission and show that you have met the specification.
My comment: Perry Marshall removed my response. I asked where to find the prize submission form and asked again about the Non-Disclosure Agreement (NDA), which he claims is not yet available. He contacted me via email. He claimed that he would send the submission form and asked me to be patient while waiting for the NDA. It seems clear to me that the prize is part of a scam. One that provides an opportunity for Perry Marshall to market his book with his opinions about how biologically-based cause and effect are linked to nutrient-dependent biodiversity. But, as every serious scientist knows, Perry Marshall’s opinions are worth no more than the opinions of others who are biologically uninformed.

James V. Kohl says:

Your comment is awaiting moderation.

February 10, 2016 at 2:30 am

Thanks. I’m disgusted by your claims and the missing “proper prize submission” form, and the unavailable non-disclosure agreement.
The delay has left others with the opportunity to move forward with publications that address your questions in the context of the same experimental evidence I intended to provide several weeks ago.
You should have admitted that the forms weren’t available, so that everyone would be aware of the delay you caused in my attempt to win the prize.

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