See: Single neuron may carry over 1,000 mutations (with my comments),

 A natural history of neurons: Diverse mutations reveal lineage of brain cells (with my comments),

and Study examines scale of gene mutations in human neurons,

All three of the links above are to reports on the study results published as:

Somatic mutation in single human neurons tracks developmental and transcriptional history

Excerpt 1)

We also observed a signature of methylated cytosine (meC) to thymine (T) transitions (fig. S8), which can occur as a result of replication-independent deamination of meC, in single-neuron SNVs. Taken together, these data demonstrate that replication-independent mutational mechanisms generate more SNVs than does replication in human neurons, which are postmitotic and live long, transcriptionally active lives.

My comment: This is unadulterated pseudoscientific nonsense. They link RNA-directed DNA methylation from nutrient-dependent RNA-mediated gene duplication and RNA-mediated amino acid substitutions that differentiate all cell types in all living genera and report it in the context of replication-independent mechanisms, which they call mutations and they link the mutations to the stability of organized genomes.

Excerpt 2) 

Our work demonstrates that somatic mutations can be used to reconstruct the developmental lineage of neurons, suggesting a potential “population genetics” of brain cells and representing a durable record of the series of cell divisions that gives rise to the human brain.

My comment: Neo-Darwinian theory was based on assumptions about de Vries definition of “mutation.” The nonsense about mutations has no explanatory power. These researchers have been stuck with an outdated concept that has been replaced by what is known about the biophysically constrained nutrient-dependent RNA-mediated protein folding chemistry of cell type differentiation. RNA-mediated amino acid substitutions are linked to ecological adaptations via a well-detailed model of how the epigenetic landscape becomes the physical landscape of DNA in the context of the physiology of reproduction, which is perturbed by the accumulation of viruses.

See for comparison my invited review of nutritional epigenetics for the journal Nutrients.

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

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.

I mentioned before that Science Magazine replaced my comment on Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution with this comment from the authors:

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

My comment: With publication of the work by Walsh’s group and their links from “…replication-independent mutational mechanisms…” to the generation of more SNVs than those generated in the context of RNA-mediated cell type differentiation in human neurons, Science has taken the lead in the publication of more pseudoscientific nonsense than serious scientists would think was possible.

Here’s my published comment that was subsequently removed from 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?

Addendum: The comment by the authors, which replaced my comment, attests to the fact that they realized the laws of physics apply to viruses and their replication. However, there have been no subsequent attempts to end the confusion caused by the misrepresentations of biologically-based cause and effect published in Science Magazine. Even after accurate representations of protein folding biochemistry linked the “holy grail” of biology from physics to chemistry, we see this:

Ongoing random mutation of DNA ensures that no two cells in an individual are genetically identical (1). Some of these “somatic” mutations cause cancer or, when they occur in progenitors in the developing human brain, neurological diseases such as epilepsy and developmental brain malformations (2).

Having escaped from what is known to serious scientists about physics and chemistry with claims of “ongoing random mutations,” the authors proceed to link mutations to the development of the human brain in the context of our evolutionary lineage. That is the pseudoscience in this weeks edition of “Science Magazine.”

See also: A Review of the Book

Excerpt: The beauty of the evolutionary perspective (see Wilson, Geher, & Waldo, 2009) is that evolution is an all-encompassing, interdisciplinary idea from the outset.

My comment: The horror of all self-aggrandizing claims made by ethologists, or other bird-watchers / butterfly collectors, is that Eugene Koonin admitted their ridiculous theories did not include the role of viruses in the context of the RNA-mediated gene duplication and RNA-mediated amino acid substitutions, which are required to link ecological variation to ecological adaptation via what serious scientists know about metabolic networks and genetic networks. See these four responses to the ridiculous claim about the beauty of the evolutionary perspective as: “…an all-encompassing, interdisciplinary idea from the outset.”

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

“…evolutionary science has now “moved on to such an extent” that she and Peter Saunders don’t really care anymore about “trying to convince the neo-Darwinists.”–Mae-Wan Ho, (reported by Suzan Mazur)

The idea is that when you look at the early history of life and the origin of the cell, you really can’t track linearly from primitive form through changes in the genome to later forms because entities are now understood to be coming in laterally from other forms. It’s new thinking and I have no disagreement with it. — Stuart Newman

[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. — Lynn Margulis (reported by Suzan Mazur)

Summary: The most recent citation to my most recent published work is

“The OL acting as control centre may be target organ for metabolic hormones such as leptin like and insulin like peptides, and olfactory organ could exert regulatory action on the OL via epigenetic effects of nutrients and pheromones on gene expression (Kohl, 2013; Elekonich and Robinson, 2000).” Role of olfaction in Octopus vulgaris reproduction (p. 61)

The octopus genome sequencing has since linked our claims in From Fertilization to Adult Sexual Behavior to RNA-mediated cell type differentiation in all cell types of all individuals of all living genera.

Keep Reading