fruit-dove

Happy Darwin Day (2017)

My series of blog posts about the refutation of theistic evolution by George Church led him to contact me via email.

  1. He asked why he would get credit for or against the refutations
  2. He claimed he was trained in quantum physics.
  3. He claimed that he has authored peer reviewed papers on protein folding, biodiversity, supercoiling, etc.
  4. He wanted to know more but did not know enough about my target audience to realize why I included information about the viral hecatomb.
  5. He also claimed to have written more on what is known about endogenous RNA interference than on exogenous RNA interference.

I invited him to discuss this further on my FB group, or on this domain. He declined. That was a great end to my 2017 Darwin Day.
See Evolution-guided optimization of biosynthetic pathways, which was co-authored by George Church and published December 1, 2014.
There is no such thing as evolution-guided optimization. Natural selection for energy dependent codon optimality is the only link from ecological variation to ecological adaptation in all living genera. That means we can move forward without George Church and still place his comments into the context of “Trust me, I’m a biologist.
I think that most serious scientists agree that you can’t trust evolutionary theorists For comparison, you can trust Darwin’s “conditions of life.”
Darwin’s “conditions of life” link the anti-entropic virucidal energy of sunlight to the physiology of reproduction in all living genera. Can you trust anyone who claims evolution did that?
See: RNA-Guided Human Genome Engineering 

Repetitive elements or endogenous viral elements can be targeted with engineered Cas+gRNA systems in microbes, plants, animals, or human cells to reduce deleterious transposition or to aid in sequencing or other analytic genomic/transcriptomic/proteomic/diagnostic tools (in which nearly identical copies can be problematic).

Nutrient energy-dependent microRNAs link natural selection for energy-dependent codon optimality to viral latency and protection of organized genomes from endogenous viral elements. Targeting endogenous viral elements with RNA-mediated amino acid substitutions is the key to biophysically constrained cell type differentiation. Fixation of amino acid substitutions prevents problematic nearly identical copies. There is no need for uncontrolled copies if there is no need to find another energy source. Uncontrolled copies link virus-driven energy theft from mutations to all pathology in all genera.
For example, energy theft from bacteria links messenger RNA degradation to morphological and behavioral phenotypes of archaea. Similarly, messenger RNA degradation in humans links the transgenerational epigenetic inheritance of Zika virus-damaged DNA to craniofacial morphology and brain development in infants.
Taken together with what is known about differences in energy-dependent endogenous RNA interference in nematodes, all ridiculous misrepresentations of Darwin’s works must be reversed to show the truth about what virus-driven energy theft does. It links RNA-mediated cell type differentiation from the energy-dependent creation of bacteria to the energy-dependent creation of humans and it links virus-driven energy theft to all pathology.
Riding the Evolution Paradigm Shift With Eugene Koonin

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… 

Is Eugene Koonin joking about what was left out? If not, big bang cosmologists and neo-Darwinian theorists have never tried to support their ridiculous theories with any experimental evidence of biologically based cause and effect. They never examined the role of energy-dependent microRNAs or virus-driven energy theft. Instead, they invented gene-centric theories of mutation-driven evolution.

See for comparison: Membrane Patterns Carry Ontogenetic Information that is Specified Independently of DNA
Reported as: Peer-Reviewed Paper: Development Needs Ontogenetic Information that Cannot Arise from Neo-Darwinian Mechanisms

With over 400 citations to the technical literature, this well-researched and well-documented article shows that embryogenesis depends on crucial sources of information that exist outside of the DNA.

A 16 page monograph with 12 pages of citations is an unparalleled achievement for anyone who is not a polymath or someone who has not already linked physics and chemistry from molecular epigenetics to all biophysically constrained cell type differentiation in all living genera via fixation of nutrient energy-dependent RNA-mediated amino acid substitutions in supercoiled DNA.
None of the cited works appear to link what is known about virus-driven energy theft to all pathology. Again, it is time to move forward.
See: Charles Darwin’s Ocean Upwelling

It’s hard to overstate how vital Darwin’s coral reef theory was in developing his career and thinking. It paved the way, conceptually and methodologically, for everything to come — particularly his transmutation theory [natural selection]. The likenesses startle. Like the transmutation theory, the coral reef theory described how small, virtually unnoticeable changes could create differences of essential type in seemingly immutable forms — and in doing so, account for broad patterns of development and difference.

Changes in coral reefs are nutrient energy-dependent and controlled by the physiology of reproduction. De vries defined “mutation” in 1902, which means that Darwin could not have had a transmutation theory. Also, Darwin repeatedly asserted the claim that his “conditions of life” must come before any claims about natural selection.
Darwin Day 2017 may become known as the day George Church refused to publicly discuss evolution or to admit there is no such thing as evolution outside the context of virus-driven energy theft and the evolution of  pathology. On the same day, The Smithsonian National Museum of Natural History blog site published a post that misrepresented everything known to serious scientists about biophysically constrained energy-dependent RNA-mediated cell type differentiation and healthy longevity.  Who could ask for a better Darwin Day than one during which Darwin’s “conditions of life” clearly triumphed over the ridiculous claims made by neo-Darwinian theorists and others who refuse to admit to the facts that link energy-dependent changes in chirality from autophagy to endogenous RNA interference and to supercoiled DNA, which prevents virus-driven energy theft from causing the mutations that all serious scientists have linked to all pathology?
 

IMG_3010

Bio-functional information

Peter Berean‘s attack on my model of energy as information led him to invent or re-introduce the term “Bio-Functional Information.” The comment from Greg Thurston (below) can be placed into the context of Schrodinger’s claims from “What is Life?”
For instance, Schrodinger challenged de Vries definition of the term mutation with this entry:

“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.) (pp. 73 and 74)”

Watch as Greg launches another personal attack against me because I refuse to allow Peter Berean‘s comments on my representations of energy as information to go unchallenged. In my model, for comparison,  the anti-entropic energy of sunlight is linked to all biodiversity,
See: What is life when it is not protected from virus driven entropy?
Greg makes it appear that I am the only person who knows Peter Berean is trying to introduce a term that must be defined before others realize it is synonymous with de Vries 1902 definition of mutation. Peter Berean’s treachery could conceivably delay scientific progress for at least one more generation if students are taught that “Bio-Functional Information” is different that energy as information.
The success of all threats to scientific progress depends on the misrepresentations of theorists, and definitions are one way to eliminate energy as information from biologically-based cause and effect. De Vries definition of mutation did that and his definition has served biologically uninformed theorists very well during the past 114 years.
Sudden energy jumps were used to link the assumptions of theorists to claims about mutation-driven evolution, which supposedly occurred via natural selection. All serious scientists have since realized that natural selection for energy as information must be linked from codon usage to energy-dependent changes, which link the physiology of reproduction to supercoiled DNA in all living genera.
Theorists are not likely to ever accept that fact. The levels of complexity are too difficult for pseudoscientists to integrate, which helps to explain why many of them are also atheists or agnostics. When creationists tout the same pseudoscientific nonsense, it shows why we have come so close to the virus-driven apocalypse.
———————————–
Greg Thurston wrote:
December 17 at 10:59am
James Kohl – it was nice to see your name in the comments on this thread when it first appeared. Then it was quite a surprise to see the nature of your comments. It’s been a while since we connected. I believe you are onto something, but somehow you are unable to convey it in a way that anyone (or at least most) can assimilate. As you may recall, I even thought for a while that I could help unpack it enough to make it clear (to me and then others), but the more I waded into it, the denser the thicket seemed to get, and I was overwhelmed. I don’t have the time. I am so disappointed to see the tone of your comment [to] Peter Berean. I thought you were above ad hominem et al. I hope you can take this as not an insult, but a caution from one who would like to be considered a friend, that it seems perhaps ego has clouded your ability to be gracious and have courteous discourse with others who see things differently. It is amazing to me how much ego commandeers intellect in so many instances. It is a threat to us all, of which we must be exceedingly diligent to resist.
———————–
See also: What is Life?
“How often do we still hear that quantum effects can have little relevance in the study of biology, or even that we eat food in order to gain energy?” — Roger Penrose (8 August 1991)
I get the impression that Greg Thurston might think Roger Penrose is an ego-maniacal threat to Peter Berean‘s intellect.
Perhaps, someone like Greg Thurston will first ask Peter Berean to tell others the difference between a “mutation” and “bio-functional information.” For contrast, in the context of my model, the fixation of energy-dependent RNA-mediated amino acid substitutions links biophysically constrained cell type differentiation to the physiology of reproduction in all living genera.
Theorists do not have a model for how that occurs in the context of biophysical constraints. They have theories, which helps to explain why Peter Berean is tweaking the theories via his usage of words. He knows nothing about natural selection for energy-dependent codon optimality. That requires the invention and/or reuse of the term “bio-functional information.” It is a great way for pseudoscientists to dismiss everything known to serious scientists via a vague term.
fruit-dove

Tasting light links energy from creation to adaptation

Biology to a Physicist
The C. elegans Taste Receptor Homolog LITE-1 Is a Photoreceptor

“In Brief: A taste receptor homolog absorbs UV light and mediates avoidance behavior in C. elegans in response to light exposure.”

Excerpt: Light sensation is critical for all phyla of life, ranging from bacteria to humans (Wang and Montell, 2007; Yau and Hardie, 2009). Organisms have evolved various types of photoreceptor proteins…

Photoreceptors are G protein-coupled receptors (GPCRs). No experimental evidence of biologically-based cause and effect links the evolution of any type of photoreceptor to any other type of G protein-coupled receptor (GPCR). Nothing except energy-dependent hydrogen-atom transfer in DNA base pairs in solutions like sea water and blood links the de novo creation of olfactory receptor genes, which are GPCRs, to all biodiversity via the physiology of reproduction and supercoiled DNA in all living genera.
The facts about supercoiled DNA link energy-dependent RNA-mediated amino acid substitutions to cell type differentiation in all cells of all individuals of all living genera via the claim that “…a taste receptor homolog absorbs UV light and mediates avoidance behavior in C. elegans in response to light exposure.”
That claim can be readily linked to the energy-dependent experience-dependent nutrient-dependent RNA-mediated de novo creation of all GPCRs and experience-dependent behavior that links chemotaxis from the de novo creation of olfactory receptor genes to phototaxis via the nutrient energy-dependent de novo creation of photoreceptors and/or all other receptors.
Reported as: Tasting light: New type of photoreceptor is 50 times more efficient than the human eye

1) …within the protein, having the amino acid tryptophan in two places was critical to its function.

2) Breaking it apart, or “denaturing” it, completely stops its ability to absorb light, rather than just diminishing it — showing that it really is a different model, Xu said.

The two nutrient energy-dependent RNA-mediated amino acid substitutions link UV light from DNA repair to all biophysically constrained pheromone-controlled biodiversity via the innate immune system and supercoiled DNA, which protects all organized genomes from virus-driven energy theft and genomic entropy. The claim that the are using a different model to do that should be placed into the context of the only model that links angstroms to ecosystems in all living genera to all nutrient energy-dependent RNA-mediated amino acid substitutions and pheromone-controlled biodiversity.
Also reported as: Powerful New Photoreceptor Found in Roundworms

Because the “genetic code” of these photoreceptor proteins are so much different than that of other photoreceptors found in the animal kingdom, there is a ton of untapped potential in this discovery.

There is only one genetic code. It links the epigenetic landscape to the physical landscape of supercoiled DNA via energy-dependent changes in base pairs, which link natural selection for codon optimality to the physiology of reproduction by protecting the organized genomes of all living genera from virus-driven energy theft.
See: Nutrient-dependent/pheromone-controlled adaptive evolution: a model
Conclusion:

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

See also: Meaning = Information + Evolution

Notions like meaning, signal, intentionality, are difficult to relate to a physical word. I study a purely physical definition of “meaningful information”, from which these notions can be derived. It is inspired by a model recently illustrated by Kolchinsky and Wolpert, and improves on Dretske classic work on the relation between knowledge and information. I discuss what makes a physical process into a “signal”.

Energy as information becomes a signal via its effect on hydrogen-atom transfer in DNA base pairs in solution. The information links the anti-entropic virucidal energy of sunlight to all biophysically constrained cell type differentiation in all living genera via the innate immune system, which links the physiology of reproduction to supercoiled DNA.
For more experimental evidence of this established link to biologically-based cause and effect, which was not presented in the context of my model from 2013, see:
Dynamic control of chirality and self-assembly of double-stranded helicates with light
Physicochemical mechanism of light-driven DNA repair by (6-4) photolyases

Clearly, if one photon provides just enough energy to perform repair, two photons are even better. However,
these are speculations…

UV-Induced Charge Transfer States in DNA Promote Sequence Selective Self-Repair
Control of pH responsive peptide self-association during endocytosis is required for effective gene transfer
Analysis of Viral and Cellular MicroRNAs in EBV-Infected Cells
A Framework for integrating multiple biological networks to predict microRNA-disease associations
Without a framework that links energy-dependent changes from angstroms to ecosystems in all living genera via their physiology of reproduction and fixation of RNA-mediated amino acid substitutions in supercoiled DNA, which protects organisms from virus-driven energy theft and genomic entropy, all that’s left is the pseudoscientific nonsense of neo-Darwinian theories.
For comparison, with a framework that links the sun’s anti-entropic virucidal energy to cell type differentiation in all genera, it is likely that the cure for all pathology is within sight. For example all pathology appears to be is epigenetically controlled at the level of quantized energy.
See also: Melanocytic Nevi and the Genetic and Epigenetic Control of Oncogene-Induced Senescence
Melanocytic nevi represent benign clonal proliferations of the melanocytes in the skin that usually remain stable in size and behavior or disappear during life. Infrequently, melanocytic nevi undergo malignant transformation to melanoma. Understanding molecular and cellular mechanisms underlying oncogene-induced senescence should help identify pathways underlying melanoma development, leading to the development of new strategies for melanoma prevention and early detection.
See also: microRNA
More than 55,000 published works link energy-dependent changes in the microRNA/messenger RNA balance to the framework that links amino acid substitutions to cell type differentiation and healthy longevity compared to virus-driven energy theft, which has been linked to all pathology by amino acid substitutions that stabilize viruses.
Here is some background on the concept of sunlight as energy that links information to all biodiversity via natural selection for energy-dependent RNA-mediated codon optimaility.
Light Absorption, Reflection, and Transmission

If a light wave of a given frequency strikes a material with electrons having the same vibrational frequencies, then those electrons will absorb the energy of the light wave and transform it into vibrational motion. During its vibration, the electrons interact with neighboring atoms in such a manner as to convert its vibrational energy into thermal energy. Subsequently, the light wave with that given frequency is absorbed by the object, never again to be released in the form of light. So the selective absorption of light by a particular material occurs because the selected frequency of the light wave matches the frequency at which electrons in the atoms of that material vibrate. Since different atoms and molecules have different natural frequencies of vibration, they will selectively absorb different frequencies of visible light.

The absorption of ultraviolet light links the anti-entropic virucidal energy of the sun to all biophysically constrained biodiversity.

What is life when it is not protected from virus driven entropy

The anti-entropic force of virucidal ultraviolet light (UV) links guanine–cytosine (G⋅C) Watson–Crick base pairing from hydrogen-atom transfer in DNA base pairs in solution to supercoiled DNA, which protects the organized genomes of all living genera from virus-driven entropy. For example, protection of DNA from permanent UV damage occurs in the context of photosynthesis and nutrient-dependent RNA-directed DNA methylation, which links RNA-mediated amino acid substitutions to DNA repair. In the context of thermodynamic cycles of protein biosynthesis and degradation, DNA repair enables the de novo creation of G protein coupled receptors (GPCRs). Olfactory receptor genes are GPCRs. The de novo creation of olfactory receptor genes links chemotaxis and phototaxis from foraging behavior to social behavior in species from microbes to humans. Foraging behavior links ecological variation to ecological adaptation in the context of this atoms to ecosystems model of biophysically constrained energy-dependent RNA-mediated protein folding chemistry. Protein folding chemistry links nutrient-dependent microRNAs from microRNA flanking sequences to energy transfer and cell type differentiation in the context of adhesion proteins, and supercoiled DNA that protects all organized genomes from virus-driven entropy.

See also: Royal Society: The Public Evolution Summit  Page 12
Witzany is organizing a conference symposium for July 2018 “Evolution-genetic innovations without error replication”
The title may change to “You are what you eat.” He has already linked energy and information-dependent changes from physics to chemistry and all the biodiversity of life.
See also: Life is physics and chemistry and communication

Manfred Eigen extended Erwin Schroedinger’s concept of “life is physics and chemistry” through the introduction of information theory and cybernetic systems theory into “life is physics and chemistry and information.” Based on this assumption, Eigen developed the concepts of quasispecies and hypercycles, which have been dominant in molecular biology and virology ever since. He insisted that the genetic code is not just used metaphorically: it represents a real natural language. However, the basics of scientific knowledge changed dramatically within the second half of the 20th century. Unfortunately, Eigen ignored the results of the philosophy of science discourse on essential features of natural languages and codes: a natural language or code emerges from populations of living agents that communicate. This contribution will look at some of the highlights of this historical development and the results relevant for biological theories about life.

Biological facts about life link energy-dependent changes from angstroms to ecosystems in all living genera via the physiology of reproduction and supercoiled DNA, which protects all organized genomes from virus-driven energy theft and genomic entropy. Why hasn’t everyone already accepted the facts that Schrodinger helped to detail in 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.) (pp. 73 and 74)

See also from the forward to the reprint edition:

“How often do we still hear that quantum effects can have little relevance in the study of biology, or even that we eat food in order to gain energy?” (Roger Penrose 8 August 1991)

Eliminating energy-dependent creation and Darwin’s “conditions of life” was probably not de Vries intention when he defined the term mutation in 1902. But, neo-Darwinian theorists took his claims about sudden energy jumps and assumed the jumps could explain what would happen if accumulated random mutations had somehow caused one species to evolve into another.
In that view of evolution, millions of years are required to link the sudden energy jumps to all morphological and behavioral diversity. Serious scientists have since learned that all energy-dependent changes in organized genomes link what organisms eat to their physiology of reproduction. That is how biodiversity is biophysically constrained by the availability of food and how food odors and pheromones are linked to the physiology of reproduction by feedback loops.
See: Feedback loops link odor and pheromone signaling with reproduction
Neo-Darwinian theorists eliminated energy and the nutrient energy-dependent feedback loops that link odors and pheromones to biophysically constrained biologically based cause and effect.
See for comparison: Scientists Seek to Update Evolution and Genetic and mechanistic diversity of piRNA 3′-end formation.
The news article by Carl Zimmer and the journal article ignore all accumulated experimental evidence of biologically-based energy-dependent top-down causation. The authors of the journal article invent the term “egoistic genes” as if no one had refuted the pseudoscientific nonsense of Richard Dawkins’ “The Selfish Gene.”
Pseudoscientists seem to think that serious scientists must prove their pseudoscientific nonsense is nonsense. Serious scientists do not try to do that because they are not taught to believe in theories. Serious scientists are taught to find experimental evidence of biologically-based cause and effect that supports their claims.

See for an example of the energy-dependent de novo creation of G protein-coupled receptors: Soft X-Ray Tomography Reveals Gradual Chromatin Compaction and Reorganization during Neurogenesis In Vivo

See for comparison: Mutation-Driven Evolution

…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world. In this view of evolution there is no need of considering teleological elements” (p. 199).

See also: 30 Reasons to Never Put Another M&M in Your Mouth Ever Again
See also: The Sea Slug That Eats The Sun
See also: Sci-hub  Our mission is to remove any barrier which impeding the widest possible distribution of knowledge in human society!
See also: Purkinje effect: Physiology:
The effect occurs because the color-sensitive cones in the retina are most sensitive to green light, whereas the rods, which are more light-sensitive (and thus more important in low light) but which do not distinguish colors, respond best to green-blue light.[4] This is why humans become virtually color-blind under low levels of illumination, for instance moonlight.
The effect links the sun’s anti-enrtopic virucidal biological energy to all biophysically constrained cell type differentiation via the physiology of reproduction in all living genera.
Light and Color – Detailed Help

Jack is wearing a red shirt. The shirt is illuminated with white light. Jill views Jack’s shirt while looking through a magenta filter. To Jill, Jack’s shirt will appear ____.

If you look at a red shirt through a red filter, you will most likely claim that the shirt is white. If you eliminate the sun’s biological energy from your claims about evolution, you will eliminate everything known to serious scientists about the energy-dependent creation of all biodiversity.
The fact that light and color are clearly linked to the morphological and behavioral phenotypes of the fruit dove, pictured above, is hard to dismiss, no matter how biologically uninformed others are.

Alternative splicing of pre-mRNA

Energy-dependent coulombic, autophagic, polycombic healthy longevity

Mitophagy is the selective degradation of mitochondria by autophagy.
See also this excerpt:

Disorders in energy creation by mitochondria can cause cellular degeneration…

Mitochondria do not create energy.  They link the creation of the sun’s anti-entropic virucidal energy to RNA-mediated cell type differentiation via biophysically constrained DNA repair. Energy-dependent autophagy links mitophagy to supercoiled DNA via the innate immune system and RNA-mediated repair of damaged DNA.
Repair is nutrient-energy dependent. Separating mitophagy from autophagy is one way to prevent people from realizing how energy-dependent viral latency and healthy longevity is typically achieved outside the context of ridiculous neo-Darwinian theories. Mitophagy and autophagy are two terms used to describe the same energy-dependent molecular mechanisms. In this case, we see the claim that energy creation by mitochondria obfuscates the fact that energy cannot be created or destroyed in the context of what is known about how quantum physics must be linked from quantized energy to biologically-based cause and effect.
Selective removal of deletion-bearing mitochondrial DNA in heteroplasmic Drosophila
Re:  mtDNA deletion (mtDNAΔ) in adult Drosophila muscle.
Excerpt:

Stimulation of autophagy, activation of the PINK1/parkin pathway or decreased levels of mitofusin result in a selective decrease in mtDNAΔ.

Conclusion:

A key question is whether occasional manipulations of cell physiology that promote mtDNA quality control, in otherwise healthy individuals, can bring about a more general ‘housecleaning’ that keeps the frequency of mutant DNA below the threshold for causing cellular dysfunction in diverse tissues without incurring other organismal costs.

My comment: The innate immune system links selective removal of dysfunctional mitochondria to nutrient energy-dependent healthy longevity via the physiology of reproduction in all living genera. Everything known to all serious scientists about energy-dependent thermodynamic cycles of protein biosynthesis and degradation should not lead to the “key question” above. It is too obvious that virus-driven energy theft stimulates autophagy, which typically allows natural selection for nutrient energy-dependent codon optimality to repair damaged DNA.
For example, energy-dependent changes in base pairs link single nucleotide polymorphisms (SNPs) to fixation of RNA-mediated amino acid substitutions in supercoiled DNA via successful reproduction. Fixation of the amino acids substitutions in different cell types of different species is the hallmark of successful reproduction. For contrast, de Vries (1902) defined the term “mutation” in the context of what he claimed were sudden “jump-like” changes in energy. His definition became the basis for the invention of neo-Darwinian pseudoscientific nonsense, which has prevailed among the biologically uninformed.
For comparison, serious scientists have learned that virus-driven energy theft prevents fixation of the amino acid substitutions in host populations. Energy theft facilitates fixation of amino acid substitutions in viruses. For example, fixation via energy-dependent viral replication contributes to the stability of the viral genome via a single amino acid substitution in the influenza virus.
See: The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.
The increasing instability of the human host’s organized genome can be viewed in the context of accumulated mutations caused by virus-driven energy theft. That instability eventually leads to all virus-driven pathology. The innate immune system is compromised by virus-driven energy theft, and that biological fact also is a historical fact.
See: Analysis of 6,515 exomes reveals the recent origin of most human protein-coding variants
Excerpt:

Of the putatively deleterious protein-coding SNVs, 86.4% arose in the last 5,000 to 10,000 years, and they are enriched for mutations of large effect (Supplementary Fig. 14) as selection has not had sufficient time to purge them from the population.

My comment: No experimental evidence of biologically-based cause and effect suggests that mutations are purged by selection. Natural selection for energy-dependent codon optimality clearly shows that virus-driven energy theft is biophysically constrained. The biophysical constraints link viral latency to healthy longevity in species from microbes to humans. Bacteria are more ecologically adapted than archaea, for example.
See: Virus-mediated archaeal hecatomb in the deep seafloor
Concluding sentence:

We show here for the first time the crucial role of viruses in controlling archaeal dynamics and therefore the functioning of deep-sea ecosystems, and suggest that virus-archaea interactions play a central role in global biogeochemical cycles.

My comment: Virus-human interactions clearly play the central role in the history of all life-sustaining cycles of protein biosynthesis and degradation. The transgenerational epigenetic inheritance of Zika virus-damaged DNA is the only proof of that fact that any serious scientist needs.
See for example: Small non-coding RNAs associated with viral infectious diseases of veterinary importance: potential clinical applications (April 4, 2016)
Excerpt:

The emerging correlation between miRNA expression and disease pathogenesis and outcomes suggests the potential use of miRNAs as biomarkers.

See also: MicroRNAs in the Host Response to Viral Infections of Veterinary Importance (October 17, 2016)
Excerpt:

Viruses, particularly DNA viruses [Marek’s disease virus (MDV), bovine herpesvirus] and even retroviruses (e.g., bovine leukemia virus), can also encode their own miRNAs, but due to space limitations, this topic is not emphasized in this review, and we refer the reader to excellent existing reviews [e.g., Ref. (8, 9)].

See also this invited (unpublished) review of nutritional epigenetics. Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems  (It was returned without review.)

This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent pheromone-controlled ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity in species from microbes to man.

See for comparison: Turning back the aging clock

Most people start off life with some level of heteroplasmy, and the levels of mutant mtDNA increase throughout life. When a critical threshold level of mutant mtDNA is passed, cells become nonfunctional or die.

The accumulation of mutant mtDNA over a lifetime is thought to contribute to aging and degenerative diseases of aging such as Alzheimer’s, Parkinson’s, and sarcopenia—age-related muscle loss and frailty. Inherited defects in mtDNA are also linked to a number of conditions found in children, including autism.

My comment: Virus-driven energy theft is clearly linked from changes in the nutrient energy-dependent microRNA/messenger RNA balance to all pathology. The most recent example of this was reported a few days ago in the context of autism: Shared epigenetic changes underlie different types of autism.
See also: Energy-dependent purifying selection / autophagy (2)
See also: Controlled amino acid treatment of all pathology

rp_levels-of-organization.jpg

Magic, Miracle, or Molecular Mechanism?

The Miracles of Smell and Taste: Evolutionists Cannot Account for the Origin of the Sense of Smell

Excerpt:

Professor of Biology John T. Caprio of Louisiana State University states that initially, the sense of smell developed in order to identify amino acid-like chemical substances soluble in water. The ability to determine molecules floating in the air is an adaptation of that original mechanism.96 (p. 106)

How The Nose Knows: Research On Smell Boosted

Excerpt:

In an interesting side note, Caprio observed that a pheromone which excites sex in an elephant is the same one that excites sex in a moth.

Origins of magic: review of genetic and epigenetic effects

What is already known on this topic

  • Magical abilities may be heritable

  • Complete family lineages to study this topic have only recently become available

What this study adds

  • Some components of magical ability clearly have a genetic basis

  • This is not a simple single gene effect and may be related to “magical enhancer” elements

My comment: Is life about miracles or about magic?
See also: What is Life? (1944)

Excerpt:

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)

See also: What is Life?: The Intellectual Pertinence of Erwin Schrödinger with a forward by Roger Penrose
Excerpt:

How often do we still hear that quantum effects can have little relevance in the study of biology, or even that we eat food in order to gain energy?

My comment: Is life supported by “magical enhancer” elements, or by photosynthesis and nutrition in accord with Schrodinger, Penrose, and Darwin’s nutrient-dependent “conditions of life?” Darwin’s “conditions of life” also are controlled by the energy-dependent physiology of reproduction.

Will debate over the facts that link angstroms to ecosystems via energy-dependent changes in hydrogen-atom transfer in DNA base pairs in solution lead to resolve of any issues invented by pseudoscientists. See, for example: Watch the Great Debate on Connectomics (April 7, 2016 – video)

Excerpt:

On one side was Moritz Helmstaedter of the Max Planck Institute, arguing that understanding neuronal circuit structure is key to modeling the mind. On the other side was Anthony Movshon of NYU, arguing that functional models that carefully analyze behavior are the key.

See also: Toward Predicting Personalized Neural Responses (April 7, 2016)

Excerpt:

Individual brains differ in shape, architecture, and connectomes, impacting how different parts of the brain communicate. A long-standing question in neurobiology is to what extent brain architecture and/or neural connections underlie behavioral differences observed among people.

My comment: Who is questioning whether the conserved molecular mechanisms of nutrient-dependent pheromone-controlled cell type differentiation extend from C. elegans to the morphological and behavioral differences of P. pacificus (a predatory nematode with teeth) and humans?

What aspect of the biophysically constrained chemistry of RNA-mediated protein folding, which links the innate immune system to supercoiled DNA in all living genera, do pseudoscientists think is questionable?

At a time when all models are supported by experimental evidence of biologically-based cause and effect that links angstroms to ecosystems, who wonders if energy-dependent hydrogen-atom transfer in DNA base pairs in solution links the anti-entropic energy of the sun from the morphological and behavioral phenotypes of microbes to humans?

See also: What is life when it is not protected from virus driven entropy? (6 minute video)

See also:  The science behind bodily secretions (April 5, 2016)

Excerpt: “…all four parts must be activated (turned on) for calcium to increase in a cell and start processes like fluid secretion.”
My comment: The four parts are nutrient-dependent and controlled by the physiology of reproduction, which links RNA-mediated events to transgenerational epigenetic inheritance of cell type differentiation via the biophysically constrained four parts in species from microbes to humans.
All four parts of the biophysically constrained receptor-mediated events involve the sensing and secreting of molecules that allow different cell types and organisms to achieve the versatile social behaviors, which are controlled by the metabolism of nutrients to species-specific pheromones in species from microbes to humans.
See also my comment on:Secreting and Sensing the Same Molecule Allows Cells to Achieve Versatile Social Behaviors

Re: “Evolution appears to favor efficient circuits and signaling elements that can accomplish many different tasks…”
That was inferred in our 1996 Hormones and Behavior review: From Fertilization to Adult Sexual Behavior. We started with the conserved molecular epigenetics of yeasts and extended nutrient-dependent genetic diversity from the metabolism of nutrients to the pheromone-controlled physiology of reproduction in species from microbes to man.
Four years later our yeast-to-mammalian model was extended by others to hormone-organized and hormone-activated invertebrate behavior, and 5 years after that to the life history transitions of the honeybee model organism.
Since then, “Signaling Crosstalk: Integrating Nutrient Availability and Sex” has linked yeasts to “Feedback loops link odor and pheromone signaling with reproduction” in other species and to “Nutrient-dependent/pheromone-controlled adaptive evolution: a model”
Placing all these published works into the context of evolution as Youk and Lim have done seems somewhat problematic for some evolutionary theorists. The conserved molecular mechanisms appear to represent adaptations to ecological variation via nutrient-dependent secretion of pheromones and the sensing of pheromones.
That links the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man.
The fact that ecological adaptations occur via a nutrient-dependent signaling pathway, which regulates a pheromone-controlled signalling pathway shows how unicellular and multicellular organisms produce a coordinated response to multiple stimuli with no consideration for mutations or for natural selection of anything except food.
That does not present a problem in the context of biologically-based food odor- and social odor-driven cause and effect, but it makes mutation-driven evolution appear to be not only biologically implausible but also to not be an ecologically valid approach to species diversity.

See also: Modern men lack Y chromosome genes from Neanderthals, researchers say

Excerpt:

…a woman’s immune system might attack a male fetus carrying Neanderthal H-Y genes. If women consistently miscarried male babies carrying Neanderthal Y chromosomes, that would explain its absence in modern humans. So far this is just a hypothesis, but the immune systems of modern women are known to sometimes react to male offspring when there’s genetic incompatibility.

My comment: The innate immune system links ecological variation to ecological adaptation in species from microbes to humans via RNA-mediated events that link amino acid substitutions to supercoiled DNA, which protects all organized genomes from virus-driven energy theft and entropy. Energy theft links mutations to all pathology.

See: Species of Drosophila (1972)
Excerpt 1)

A biological species concept is therefore necessary. Its beginning goes back to John Ray, who stated in 1686 that “one species never springs from the seed of another” [quoted in (1)].

Excerpt 2)

They [species] are separated by any one, or by a combination of several, reproductive isolating mechanisms, (1, 4-7). Hybrid inviability and sterility are among such mechanisms, but there are others (for example, ethological and ecological isolations) which may be just as effective in nature.

My comment: Nutrient-dependent pheromone-controlled cell type differentiation links supercoiled DNA and  chromosomal rearrangements to protection against virus driven entropy in all vertebrates. That is why modern men lack Y chromosome genes from Neanderthals. The experience-dependent de novo creation of olfactory receptor genes links chemotaxis and phototaxis to other sensory input and to behavior via supercoiled DNA, which protects organized genomes from virus-driven entropy.
See also: Natural Selection on the Olfactory Receptor Gene Family in Humans and Chimpanzees (2003) — co-authored by Carlos D. Bustamante
Conclusion:

…humans may identify the selected changes and shed light on what olfactory stimuli have exercised selective pressures on the human OR gene repertoire.

My comment: Food odors and pheromones exercise selective pressure that enable the olfactory receptor gene repertoire, which links supercoiled DNA to protection against virus-driven entropy in the organized genomes of all living genera. As it always has been, supercoiled DNA is the link from metabolic networks to genetic networks that typically prevents hybridization. By preventing hybridization, food odors and pheromones establish the niche construction that is exemplified in every species.
See also:  The Divergence of Neandertal and Modern Human Y Chromosomes (2016) — co-authored by Carlos D. Bustamante
My comment: Scientific progress has led all serious scientists to explanations that link angstroms to ecosystems in all living genera. Serious scientists have linked what is known about molecular diagnostics across all species. When will neo-Darwinian theorists admit that they have known how odors and pheromones link biophysically constrained RNA-mediated cell type differentiation to supercoiled DNA in all living genera?
Obviously, not all theorists are committed to telling “Just So” stories about mutations and human evolution. For example, see: Clustered mutations in hominid genome evolution are consistent with APOBEC3G enzymatic activity, which was reported as: Human evolution fast-tracked by mutations from anti-viral enzyme
Excerpt (with my emphasis):

…when examining the locations of the clustered mutations, the researchers found they were enriched in transcriptionally active and regulatory regions of the human genome. Over a third of mutations overlapping coding regions led to amino acid changes, and in several cases an entire mutation cluster overlapped, resulting in up to five amino acid substitutions in a single exon.
Our results are at odds with assumptions of mutational models that are at the basis of most genetic analyses, including in medical genetics, evolutionary genetics, and population genetics,” co-corresponding author Keinan said.

My comment: Those assumptions were based on de Vries 1904 definition of mutation.  [W]hat Haldane, Fisher, Sewell Wright, Hardy, Weinberg et al. did was invent…. 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…. Assumptions, made but not verified, were taught as fact.
The facts have since been repeatedly stated and often succinctly stated, as in:  Feedback loops link odor and pheromone signaling with reproduction; and in Combating Evolution to Fight Disease and in MicroRNA-Based Single-Gene Circuits Buffer Protein Synthesis Rates against Perturbations. 
In my invited review of nutritional epigenetics I placed the facts into the context of nutrient-dependent pheromone-controlled biophysically constrained cell type differentiation and changes in the microRNA/messenger RNA balance, which are linked from RNA-mediated amino acid substitutions to cell type differentiation in all living genera.
See: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems (April 11, 2014)
Abstract excerpt:

This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent pheromone-controlled ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity in species from microbes to man.

My comment: My invited review was promptly returned without review.

For comparison, see this award-winning invited review: The Mind’s Eyes: Human pheromones, neuroscience, and male sexual preferences

In his review of my award-winning review, David A. Puts wrote:

James Kohl authors the Handbook’s final chapter, “The mind’s eyes: Human pheromones, neuroscience, and male sexual preferences.” Kohl posits innate sex differences in preferences for sexually dimorphic pheromones. These sex pheromones act as unconditioned stimuli that become associated with visual and tactile stimuli through classical conditioning. Consequently, men with innate preferences for women’s odors come to prefer the appearance and feel of women, for example. Homosexuality results from incomplete sexual differentiation of the olfactory system.

Kohl marshals supporting evidence, though it is often subject to alternative interpretation. For example, Kohl suggests that exposure to sex pheromones is “the most likely explanation for the recent finding that saliva [testosterone] levels in men increase with exposure to a young woman, but do not increase with exposure to a young man” (p. 327). Is it not likely that the young woman’s appearance raised men’s testosterone levels?

Multiple studies by independent researchers leave little doubt that odor affects human mate choice, but Kohl probably grossly overstates its importance. Why postulate that humans evolved only obligate olfactory/pheromonal preferences? Isn’t there likely to be useful information about mates that is better obtained through vision and touch than through smell? If so, selection would probably favor more reliable developmental patterns for visual and tactile preferences than classical conditioning to olfactory ones. Moreover, there is a trend among anthropoid primates, including humans, for reduced olfaction and increased reliance on vision for locating food and mates. This is witnessed in our tiny olfactory bulbs, which are relatively many times smaller than in rats; and our apparent lack of a functional vomeronasal organ, which is used by many mammals to detect pheromones.

Ironically, a seemingly fatal blow follows from a condition that Kohl presents in support of his hypothesis. Prior to treatment, people with Kallmann Syndrome (KS) lack both a sense of smell and much of a libido. Superficially, these facts appear to support Kohl’s hypothesis that olfaction is primary in sexual interest. However, the relation between olfaction and libido here is not causal. In most fetuses, some cells in the olfactory placode develop into olfactory cells while others migrate to the hypothalamus to become cells that trigger sex hormone secretion by the gonads. A mutation in one of three known genes can disrupt the development of these cells, so that a person not only lacks a sense of smell but also has gonads that do not produce sex hormones. It is the low sex hormone levels, rather than a lack of olfaction, that leads to reduced libido in adults with KS: Testosterone treatment at least partially restores libido in men with KS, but there is no known treatment for their anosmia.

My comment: David A. Puts is one of the most personable and intelligent antagonists I have ever met, but he failed to realize that I was not detailing a hypothesis. The model I detailed has been supported by all experimental evidence of biologically-based cause and effect since the time I first presented it in 1992, and subsequently co-authored The Scent of Eros: Mysteries of Odor in Human Sexuality (1995/2002).

See also: On April 9, 2016 at 1145 AM, on the sexnet listserver, David A. Puts, PhD (Associate Professor, Department of Anthropology, Center for Brain, Behavior, and Cognition, Center for Human Evolution and Diversity, Penn State University, University Park, PA 16802, wrote:

“Modern humans may also have abducted Neandertal females, so that the flow of Neandertal genes into modern human populations was primarily through females. Hypergynous marriage along the lines that Ray describes is also a possibility, but my gut is that relations between “us” and “them” weren’t so civil.
A less sexy possibility that the authors mention is simply that the Neandertal Y was lost due to drift. (The effective population size of Y chromosomes is half that of autosomes, and drift is stronger in smaller populations.)
Gene flow primarily through females and loss of Neandertal Y’s through drift are not mutually exclusive, but drift seems more consistent with also losing Neandertal mtDNA.

And of course there could be selection against the Neandertal Y in human-Neandertal hybrids, as the authors suggest.”

My comment: None of his claims are supported by experimental evidence of biophysically constrained biodiversity in any species.
For comparison, see: Formation of novel PRDM9 allele by indel events as possible trigger for tarsier-anthropoid split
Abstract excerpt:

The first mutation event interrupts the reading frame and function while the second compensates both. The fixation of this peculiar allele variant in tarsiers led to hypothesize that de- and reactivation of the zinc finger domain drove the speciation in early haplorhine primates.

My comment: Only if you believe that mutations are fixed in organized genomes can you link virus-driven energy theft from pathology to neo-Darwinian pseudoscientific nonsense in which alleles are somehow formed outside the context of the nutrient-dependent physiology of reproduction. Only if you believe that mutations are fixed in organized genomes can you link weekend evolution of the bacterial flagellum from mutations the evolution of primates. But as all serious scientists know, those who link mutations to the evolution of microbes into primates never learned the difference between mutations and nutrient-dependent RNA-mediated amino acid substitutions that link de novo gene creation to biodiversity in the context of the innate immune system and supercoiled DNA.
 
 

Filtering light through a prism to identify tissue type

Creating nutrient-dependent life with enough genes to survive

Design and synthesis of a minimal bacterial genome

Excerpt:

Cells are the fundamental units of life. The genome sequence of a cell may be thought of as its operating system. It carries the code that specifies all of the genetic functions of the cell, which in turn determine the cellular chemistry, structure, replication, and other characteristics. Each genome contains instructions for universal functions that are common to all forms of life, as well as instructions that are specific to the particular species. The genome is dependent on the functions of the cell cytoplasm for its expression. In turn, the properties of the cytoplasm are determined by the instructions encoded in the genome. The genome can be viewed as a piece of software; DNA sequencing allows the software code to be read.

My comment: What is currently known to serious scientists about molecular epigenetics lies beyond this simplistic explanation of gene-centric cell type differentiation. Most of the article’s attempts to link nutrient-dependent biologically-based cause and effect do not address the fact that there is no defined boundary between epigenetic and genetic. Similarly, they do not address most of the extant literature that has defined biodiversity in the context of terms used to describe the magic of evolution.
Reported on 3/24/16 as:

The creators of the first ‘synthetic life’ made a cell with just enough genes to survive

Excerpt:
You have to define what life is going to mean each time,” Venter told The Post. In this case, life meant a bacterial cell that could grow rapidly in a glucose culture. If speed hadn’t been a priority, they could have trimmed the genome down a bit smaller. And if they’d wanted the cell to survive in conditions less sweet than a petri dish, they would have needed to give it a bigger genomic arsenal. “As soon as you want the cell to adapt to some environmental stress, it might not do it with the genes it has, it might just die,” he said.
This post was originally published on March 24th. On March 25th, Rachel Feltman changed her ridiculous title to this: This man-made cell has the smallest genome ever – but a third of its genes are a mystery. My post from yesterday about this was removed from the Evolutionary Psychology News group.  There will be much more spin-doctoring in attempt to try to avoid the intelligent conclusion that must be made by all serious scientists. If theorists must “…define what life is going to mean each time…” experimental evidence will continue to show why definitions of “mutation” have only been used by the biologically uninformed.

My comment: Hugo de Vries 1904 definition of mutation is the basis for all assumptions made by theorists who still claim that accumulated mutations could lead to the creation of a new species. Venter just placed that neo-Darwinian pseudoscientific nonsense into the context of ecological variation and nutrient-dependent pheromone-controlled ecological adaptations.

All serious scientists know that nutrient-dependent RNA-mediated amino acid substitutions link biophysically constrained protein folding chemistry to supercoiled DNA, which protects the organized genomes of all living genera from stress-induced virus-driven entropy.

Thus, Venter helped to take us forward with the sequencing of the human genome. Now, he takes us back to Darwin’s ‘conditions of life.’ Life must be defined in the context of energy-dependent microRNA biogenesis for comparison to virus-driven energy theft, which is linked to all pathology and death.

See also: Replace the Modern Synthesis (Neo-Darwinism): An Interview With Denis Noble

Excerpt:

[W]hat Haldane, Fisher, Sewell Wright, Hardy, Weinberg et al. did was invent…. 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….  Assumptions, made but not verified, were taught as fact.

My comment: How to define evolution becomes a problem in the context of the report the the bacterial flagellum evolved over the weekend compared to no change in ~2 billion years in bacteria living in ocean sediments at depths that prevent UV light-induced hydrogen-atom transfer in DNA base pairs in solution from leading to the cell type differentiation that occurs in all other ecologically adapted living genera.

See also:

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

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

terrarium-eco-system

Epigenetic (re)programming of behavior

Epigenetic (re)programming of caste-specific behavior in the ant Camponotus floridanus

Excerpt:

Our results suggest that behavioral plasticity in animals may be regulated in an epigenetic manner via histone modification.

My comment: Experimental manipulation of a single gene changed behavior. The evidence suggests all invertebrate and all vertebrate morphological and behavioral phenotypes can be linked via nutrient-dependent changes in microRNAs, adhesion proteins, and supercoiled DNA.

See: The phylogenetic utility and functional constraint of microRNA flanking sequences
My comment: Nutrient-dependent RNA methylation, RNA-directed DNA methylation, and RNA-mediated amino acid substitutions in the histones link microRNAs and adhesion proteins to supercoiled DNA in the context of chromosomal rearrangements and the physiology of species-specific reproduction linked to the stability of organized genomes in all living genera via protection from virus-driven entropy.
The results from ants extend what is known about how nutrient-dependent pheromone-controlled weekend evolution of the bacterial flagellum occurred via two amino acid substitutions.
See: Evolutionary resurrection of flagellar motility via rewiring of the nitrogen regulation system
Excerpt: 

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: Neo-Darwinian theorists do not seem to know the difference between the definition of mutation, which is linked to pathology, and how nutrient energy-dependent amino acid substitutions are typically linked to healthy longevity. They bastardized Darwin’s “conditions of life” by placing de Vries “jump-like” changes in energy (i.e., mutations) into the context of natural selection and evolved biodiversity.
Serious scientists have linked atoms to ecosystems within the biophysical constraints of Darwin’s “conditions of life” and everything known about nutrient-dependent pheromone-controlled biodiversity in species from microbes to humans.
See: Structural diversity of supercoiled DNA
Conclusion:

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

My comment: I cannot put that conclusion into the context of neo-Darwinian theories. And, neo-Darwinists do not seem willing to address the speed at which weekend evolution of the bacterial flagellum occurred.
As more examples from other species show that experimental manipulation of a single gene changes behavior, other model organisms can be linked to human behavior via as little as a single base pair substitution and single RNA-mediated amino acid substitution. Changes that would typically only occur during life history transitions can be linked from animal models, which are often used to model human physical and mental disorders.
For example: 

The honeybee already serves as a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, the development of the brain and behavior, mental health, longevity, diseases of the X chromosome, learning and memory, as well as conditioned responses to sensory stimuli (Kohl, 2012).

The molecular mechanisms continue to be detailed in disparate reports that make evolutionary theorists seem to become more desperate to change their theories each week. They have run out of “wiggle room.”
See also: An Illuminated State of Mind
Excerpt:

“A subsequent study demonstrated that scientists can even implant — we call it ‘incept’ — false memory in the mouse brain,” added Tonegawa. “The challenge is how to extend the information obtained in animal models to human models. The invention of revolutionary noninvasive or low-invasive technologies will be needed, and God knows when that will happen.”

My comment: I wonder how many minds need to be illuminated before everyone accepts the extension of information obtained in animal models to human behavior.
Additional illumination comes from several other articles published today in Science.
Sperm RNA fragments modify offspring metabolism (subscription required)
Excerpt(s)
…two new studies highlight a different class of RNAs, transfer RNAs, carried by sperm.
The effects of the RNA fragments don’t have to be harmful, Chen notes. “If a bad diet can influence us, I think a healthy diet can do it in the same way,” he predicts.
Seeing mTORC1 specificity (subscription required)
Excerpt:

On page 48 of this issue, Aylett et al. (1) help uncover the molecular underpinnings of mTORC1, while on pages 43 and 53, Wolfson et al. (2) and Saxton et al. (3), respectively, make strides in determining how mTORC1 is regulated by the amino acid leucine.

My comment: Nutrient-dependent immune system function is regulated by one amino acid substitution. Researchers seem to have difficulty placing that fact into the context of how ecological variations are linked to ecological adaptations manifested in supercoiled DNA that protects organized genomes from virus-driven entropy.
There seems to be a disconnect between theories and what is know about the theft of nutrient energy by viruses.
For example, I keep reminding people of this claim: The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.
It replaced this comment, which I fortunately had also posted to The Atlantic before it was removed by Science

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?

 

 

Physics

Hydrogen-Atom Transfer in DNA Base Pairs (3)

Video of our insignificance
The video can be compared to what is known to serious scientists about the answer to Schrodinger’s question: What is Life?
Excerpt: 

But about forty years ago the Dutchman de Vries discovered that 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. But quantum theory was but two years old when de Vries first published his discovery, in 1902. Small wonder that it took another generation to discover the intimate connection! (page 33-34)

My comment: See also: What is Life?: With Mind and Matter and Autobiographical Sketches (Canto Classics) Reprint Edition
Roger Penrose who has co-authored with cosmologist George F.R. Ellis and theoretical physicist Stephen Hawking, asks:

How often do we still hear that quantum effects can have little relevance in the study of biology, or even that we eat food in order to gain energy?

My comment: The video about our insignificance can be compared in the context of a need shared by all living genera. They need to eat to gain energy and prevent the theft of energy by viruses.
Darwin’s “conditions of life” were removed when neo-Darwinian theorists put natural selection first. That replaced the anti-entropic virucidal force of the sun’s biological energy with de Vries (1904) definition of “mutation” and assumptions about how long it might take the accumulation of “jump-like” changes to cause one species to evolve into another species.
Serious scientists know how to link the energy from the sun to hydrogen-atom transfer in DNA base pairs and to all cell type differentiation via biophysically constrained nutrient-dependent RNA-mediated protein-folding chemistry. For comparison, the biologically uninformed masses continue to tout neo-Darwinian nonsense.
This educational video informs intelligent people who want to become biologically informed. It also presents a threat to those who prefer to believe in ridiculous theories.

For an example of an ongoing threat to anyone who prefers to believe in theories see the link to this claim:

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

My comment: The theft of energy by the influenza virus is linked to DNA damage by a single amino acid near the receptor binding site, which can be linked to the entry of the virus into the cell and to antibiotic resistance in bacteria without invoking any neo-Darwinian nonsense. Viruses do not mutate and natural selection does not cause them to evolve. Theorists who claim that the evolution of anything can be linked to the evolution of antibiotic resistance or to the evolution of a new species from a different species are among the biologically uninformed. For example, aging theorists often cite the works of Richard Lenski et al., and claim that his experiments and others like them are proof of evolution.
See: The Man Who Bottled Evolution

See for comparison: Escape from Lethal Bacterial Competition through Coupled Activation of Antibiotic Resistance and a Mobilized Subpopulation

Excerpt 1)

Bacteria use these systems to sense and respond to their environment, which include stresses and nutrient conditions, but also include other bacteria and their antagonistic enzymes and specialized metabolites.

Excerpt 2)

To identify the active molecule, we analyzed the HPLC-purified sample by UV absorbance and ESI-mass spectrometry. The molecule showed strong UV absorbances at 319, 333, and 351 nm, indicative of a conjugated pentaene moiety [33].

My comment: UV absorbances are linked to measurable spectophotometric differences in concentrations of metabolites in body fluids. The measurements link metabolic networks to genetic networks and cell type differentiation associated with visually perceived differences in morphology via links to plumage color or skin color, or other types of changing colors in eyes, hair, skin etc..
See for comparison:

Don’t It Make Your Brown Eyes Blue?

Excerpt:

Researchers have finally located the mutation that causes blue eyes, and the findings suggest that all blue-eyed humans share a single common ancestor born 6000 to 10,000 years ago.

My comment: The ideas that mutations are linked to changes in eye color or that mutations are linked to the changes in octopuses that enable them to camouflage themselves in rapidly changing ecological conditions are equally ridiculous. The color changes in octopuses link their nutrient-dependent pheromone-controlled physiology of reproduction from the microbes in their digestive system to the feedback loops that link odors and pheromones to nutrient-dependent reproduction in species from microbes to humans.
See: Feedback loops link odor and pheromone signaling with reproduction
See also: “Is UV light what Dobzhansky saw?”

human-evolution

A genetic variant refutes neo-Darwinism

Summary: They link a single nucleotide polymorphism (SNP) to a genetic variant that decreases viability of an embryo, without linking a nutrient-dependent RNA-mediated amino acid substitution to pheromone-controlled cell type differentiation that begins in the embryo and continues throughout the life history transitions of invertebrates and vertebrates.

A Benefit of Failed Pregnancy?

This genome-wide association study revealed “…a striking link between mitotic aneuploidy and a single nucleotide variant (SNP rs2305957) on chromosome 4 of maternal genomes.”
Excerpt: “There’s this genetic variant that they’ve been able to identify with very nice evidence for positive selection, but that has a fitness consequence, a fecundity consequence . . . that decreases the viability of an embryo,” said evolutionary geneticist Ed Green of the University of California, Santa Cruz, who was not involved in the work. “It flies in the face of what we think of in terms of positive Darwinian selection and demands an explanation.”
My comment: The “flies in the face” comment reminds me of a work from this same group on fertility in flies. Strong Purifying Selection at Synonymous Sites in D. melanogaster
Excerpt: “Regulation of gene expression may be acting at the level of mRNA structures, mRNA stability, miRNA binding sites, and the modulation of translation rate [91]–[104].”
My comment: If so, fixation of nutrient-dependent amino acid substitutions can be linked to invertebrate cell type differentiation, but mutations, which are lethal or are not fixed, cannot be linked to biophysically constrained biodiversity. That attests to the fact that what most people think of in terms of positive Darwinian selection has no explanatory power. However, the thoughts of most theorists can be placed into the context of Dobzhansky’s claim: “…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). Nothing in Biology Makes Any Sense Except in the Light of Evolution
To make sense of how a single amino acid substitution in the developing embryo of a mammal or larvae of an invertebrate determines an organism’s fate, see also:
The smelling of Hedione results in sex-differentiated human brain activity
Section title: “3.1. mRNA of all intact VN1Rs is present in human olfactory mucosa”
See: 3.2. “Genetic variations of chemoreceptors caused by single nucleotide polymorphisms (SNPs) that result in an amino acid change…”
Wallrabenstein et al (2015) link what are obviously nutrient-dependent changes in the microRNA/messenger RNA (mRNA) balance to sexual differentiation of cell types and human communication with pheromones in adults. Greg Bear did this for a general audience in his science fiction novels “Darwin’s Radio” and “Darwin’s Children.” See, for example, this review of Darwin’s Radio.
In Kohl (2013) I wrote: “…ingested plant microRNAs influence gene expression across kingdoms (Zhang et al., 2012). In mammals, this epigenetically links what mammals eat to changes in gene expression (McNulty et al., 2011) and to new genes required for the evolutionary development of the mammalian placenta (Lynch, Leclerc, May, & Wagner, 2011) and the human brain…”
Simply put, ecological variation is linked to ecological adaptation that revolves around the conserved molecular mechanisms of nutrient-dependent RNA-directed DNA methylation and RNA-mediated events.
My model links RNA-mediated events to amino acid substitutions via natural selection based on food odors and the metabolism of nutrients to species-specific pheromones that control fixation of amino acid substitutions in the context of the nutrient-dependent physiology of reproduction. Chemical signaling among the rapidly differentiating cell types of embryos helps to ensure error recognition. If nutrient-dependent DNA repair mechanisms cannot immediately repair the errors that lead to perturbed protein folding, spontaneous abortion helps to ensure that the biological energy required to bring a mammalian pregnancy to a beneficial outcome is not wasted on a non-viable embryo.
For comparison to RNA-mediated biologically-based cause and effect that requires fixation of amino acid substitutions, when placed into the context of evolutionary theory, these “…findings seem “so paradoxical,” said Green, “I fear that any theory one can come up with is going to feel wrong in some way.
I agree. Theories that fail to include what is known about RNA-mediated amino acid substitutions and cell type differentiation have no explanatory power. They will invariably be wrong compared to any model that incorporates what is known about top-down causation, which is that “Feedback loops link odor and pheromone signaling with reproduction.”
For comparison, see: Possible creatures by Andreas Wagner

Introduction: “It seemed Darwin had banished biological essences – yet evolution would fail without nature’s library of Platonic forms”

My comment: The number of possible creatures is nutrient-dependent and the biodiversity of all animal species is pheromone-controlled. Nutrient-dependent RNA-directed DNA methylation is linked to the diversity of cell types in all organisms of all species via the biophysically constrained chemistry of RNA-mediated protein folding.

Mutations perturb protein folding. Amino acid substitutions stabilize protein folding in organized genomes.

The biological essence of an organism is the stability of its organized genomes. That stability is linked from ecological variation to ecological adaptations by selection against mutations in species from microbes to man. Selection against mutations links the de novo creation of light-induced amino acids to RNA-mediated amino acid substitutions that differentiate all cell types in all genera.

The entropic elasticity attributed to viral microRNAs is linked from the anti-entropic energy of the sun to amino acid-dependent protein biosynthesis and degradation via everything currently known about physics, chemistry, and the conserved molecular mechanisms that Dobzhansky (1973) linked to cell type differentiation in primates via identical sequences of amino acids in man and the chimpanzee that differ in one single amino acid (out of 141) in the gorilla.

Alternatively, in theory:  “…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world. In this view of evolution there is no need of considering teleological elements.” Mutation-Driven Evolution (p. 199)

For comparison, see: “… the massive creative power of a cooperative RNA consortium (QS-C) remains crucial for life. QS-C was made known to us only recently by virus evolution (e.g., HIV-1). Its role in the origin of life, the emergence of complexity and the creation of group identity should now receive our combined attention.” Force for ancient and recent life: viral and stem-loop RNA consortia promote life (p. 8).

My comment: The likelihood that viruses “evolved” can be placed into the context of Andreas Wagner’s book: Arrival of the Fittest: Solving Evolution’s Greatest Puzzle and/or the context of creationist literature.

From an Editorial Review: Andreas Wagner presents a compelling, authoritative, and up-to-date case for bottom-up intelligence in biological evolution, and it sticks.’ — George Dyson, author of Turing’s Cathedral ‘

From the creationist literature: Viral Genome Junk Is Bunk “So, where do viruses come from that essentially share the same sequences as those found in their host genomes? Perhaps the evolutionists have placed the cart before the horse on this issue, as proposed by several creationist scientists.4,6 In fact, in an ironic twist, the evidence mentioned above indicates that viruses likely arose from their hosts and not the other way around. As molecular biologist and biochemist Peter Borger notes, “The most parsimonious answer is: the RNA viruses got their genes from their hosts.”6”

The questions arise: Did viruses “evolve?” Are changes in their virulence caused by “mutations?” How much longer will theorists be stuck with de Vries definition of “mutation” and the assumptions made by population geneticists about the time it might take for a different species to “evolve?”

See also: A universal trend of amino acid gain and loss in protein evolution. 

Excerpt: “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.”

See also: “There is a Corrigendum (26 May 2005) associated with this document. We have since discovered that a similar scenario for protein evolution was proposed by Zuckerkandl and colleagues more than thirty years ago1.”

My comment: It has now been nearly 45 years since publication of Mutational trends and random processes in the evolution of informational macromolecules.

Theorist who still can’t explain anything about how mutations might somehow be linked to the evolution of different species via differences in their life history transitions should ask: Why did Israeli middle schools begin teaching the theory of evolution last year? Serious scientists will understand this answer to that question: “…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.”

Serious scientists are Combating Evolution to Fight Disease and they may be interested in recruiting intelligent combatants.

Creationists, it seems, have always been fighters. See also: Neo-Darwinism’s Catch-22: Before Evolving New Features, Organisms Would Be Swamped by Genetic Junk

Excerpt: “When it comes to generating viable living systems, it’s pretty much damned if you do, damned if you don’t. The bottom line seems to be that whatever cause generated the biological features we observe, unguided Darwinian evolution is not it.”

poster-from-jesse

Silencing genes and serious scientists

Silencing genes — to understand them

Excerpt: “RNAi and other processes may help science understand how life works at the most basic level.”
My comment: Serious scientists already understand how life works at the most basic level.  Viral microRNAs perturb protein folding that links nutrient-dependent microRNAs to DNA repair via the conserved molecular mechanisms that link amino acid substitutions to the biophysically constrained chemistry of protein folding, which is required for genomic stability and increasing organismal complexity.
Fixation of the amino acid substitutions occurs via the nutrient-dependent physiology of reproduction. The physiology of nutrient-dependent reproduction links the light-induced de novo creation of amino acids to RNA-mediated events and cell type differentiation in all cells of all individuals of all genera. The balance of viral microRNAs and nutrient-dependent microRNAs is the key to increasing organismal complexity and physiopathology.
Without mentioning microRNAs, this article refers to them as ‘triggering molecules’ that contain a string of 21 or 22 nucleotides. For comparison, see: MicroRNA control of protein expression noise.
Theoretical physicists and evolutionary theorists seem to consistently ignore the established links from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man.  They are foolish if they think serious scientists will continue to ignore the role of microRNAs that link physics to chemistry and molecular biology. Serious scientists have had enough of pseudoscientific nonsense. Theorists explain nothing, but see:

This explains everything

Excerpt: “If scientists cannot communicate a concept without falling back on maths, they don’t truly grasp what it is they are trying to talk about. It is a failure of the communicator, not of the audience.
My comment: It is the failure to communicate without using maths that led to acceptance of the assumptions of population geneticists and their idiot minions. They based their ridiculous theories on de Vries definition of mutation and ideas about how long it would take an accumulation of mutations to lead to a new species. Their theories led to the stagnation of research that finally links microRNAs to cell type differentiation via the biophysically constrained chemistry of nutrient-dependent RNA-mediated protein folding and fixation of amino acid substitutions via the physiology of reproduction.
Weinberg, and others like him, think that maths can explain top-down causation in the context of biology and the controlled physiology of reproduction. They explain nothing and tout only pseudoscientific nonsense. For contrast, see:
1996  “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…”
2003 “First, more sophisticated models of nonsynonymous evolution are required, specifically those that allow a limited number of sites to accumulate the vast majority of changes, as may be true of viruses in nature, as well as those that take account of RNA and protein secondary structure (15).”

New target for anticancer drugs—RNA

Excerpt 1 with my emphasis) “Our new results indicate that a number of key cancer-causing genes – genes that under normal circumstances keep cells under control – are held in check before the proteins are made,” Cate said. “This new control step, which no one knew about before, could be a great target for new anticancer drugs.
Excerpt 2) While our genes reside inside the cell’s nucleus, the machinery for making proteins is in the cytoplasm, and mRNA is the messenger between the two. All the DNA of a gene is transcribed into RNA, after which nonfunctional pieces are snipped out to produce mRNA. The mRNA is then shuttled out of the nucleus to the cytoplasm, where a so-called initiation complex gloms onto mRNA and escorts it to the ribosome. The ribosome reads the sequence of nucleic acids in the mRNA and spits out a sequence of amino acids: a protein.

My comment: What they claim is a new control step is the balance of viral microRNAs to nutrient-dependent microRNAs controls cell type differentiation via RNA-directed DNA methylation and RNA-mediated amino acid substitutions. Misrepresenting the control of cell type differentiation by RNA as a “…new control step, which no one knew about before…” is a continuation of the nonsense that keeps funding directed to those who deny what has been known about cell type differentiation for nearly two decades.
Clinically Actionable Genotypes Among 10,000 Patients With Preemptive Pharmacogenomic Testing establishes the obvious links between RNA-mediated metabolic networks and genetic networks.
Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults places what is known about cell type differentiation into the context of a single amino acid substitution that affects RNA-mediated metabolic networks; RNA-mediated genetic networks; and human behavior.
Stop the nonsense. Serious scientists are Combating Evolution to Fight Disease.
Pseudoscientists are telling you there is a “…new control step, which no one knew about before…” to get funding for anticancer drugs by ignoring what has been known for decades about RNA-mediated amino acid substitutions and cell type differentiation.
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).