Hecatombic non-specific mutation-driven evolution
These findings provide new evidence for a possible link between viral infections and chemoautotrophic production in the microbial food web. Viral-mediated mortality of bacteria and archaea may stimulate heterotrophic metabolism. This, in turn, may enhance nitrogen regeneration processes, supporting ammonia-dependent chemoautotrophic production. This biological feedback could have important consequences for C and N cycling.
My comment: This is an open-access article… You can cite it and help others to learn what the findings mean by placing one-carbon metabolism into the context of nutrient energy-dependent links from sunlight to all biodiversity via so called chemoauthotrophic production of signals the control the nutrient-dependent physiology of reproduction in the context of pheromones that link quorum-sensing from one-carbon metabolism to the molecular epigenetics of all cell type differentiation in the microbial food web.
For example, ultraviolet (UV) light kills viruses. That fact links quantised energy as information from Thomas Hunt Morgan’s claims about chromosomes as the biophysically constrained link from angstroms to ecosystems via transgenerational epigenetic inheritance in species from microbes to humans.
But Thomas Hunt Morgan did not win the 1933 Nobel Prize in Physiology or Medicine for detailing that fact. His experimental evidence of biologically-based cause and effect had to be interpreted by others to arrive a logical conclusion. For comparison, claims about mutation-driven evolution are straight-forward. They do not need to be interpreted and they do not allow any serious scientist to make a logical conclusion about the origins of life or how biodiversity arose. It life did not automagically emerge and lead from mutation-driven evolution to all biodiversity, the works of the Nobel Prize winners in Physiology or Medicine in 1933, 2004, and 2016 cannot be placed into the context of any model of biologically-based cause and effect. That explains why no experimental evidence of biologically-based cause and effect exists to show how mutation-driven evolution might occur. That’s because it doesn’t occur.
See: One-carbon metabolism and epigenetics: understanding the specificity
One-carbon metabolism utilizes a variety of nutrients, such as glucose, vitamins, and amino acids, to fuel a variety of metabolic pathways that utilize these one-carbon units. These pathways include nucleotide metabolism, maintenance of cellular redox status, lipid biosynthesis, and methylation metabolism.
See for comparison: Mutation-Driven Evolution (p. 196)
(1) Mutation is the source of all genetic variation on which any form of evolution is dependent. Mutation is the change of genomic structure and includes nucleotide substitution, insertion/deletion, segmental gene duplication, genomic duplication, changes in gene regulatory systems, transposition of genes, horizontal gene transfer, etc. (2) Natural selection is for saving advantageous mutations and eliminating harmful mutations. Selective advantage of the mutation is determined by the type of DNA change, and therefore natural selection is an evolutionary process initiated by mutation. It does not have any creative power in contrast to the statements made by some authors.
My comment: The theories that collectively led to publication of Mutation-Driven Evolution on Jun 14, 2013 were placed into the context of this review: Nutrient-dependent/pheromone-controlled adaptive evolution: a model, which also was published on Jun 14, 2013.
See also: Criticisms of the nutrient-dependent pheromone-controlled evolutionary model, which was published on June 4, 2014
Andrew Jones cited Mutation-Driven Evolution in his criticisms of my model.
…James Kohl presents an unsupported challenge to modern evolutionary theory and misrepresentations of established scientific terms and others’ research. It was a mistake to let such a sloppy review through to be published.
My comment: No experimental evidence of biologically-based cause and effect linked the claims in Mutation-Driven Evolution to the nutrient-dependent pheromone-controlled ecological adaptations manifested in all living genera. Instead of linking energy-dependent one-carbon metabolism from the innate immune system to RNA-mediated amino acid substitution in supercoiled DNA, which protect all organized genomes from virus-driven entropy, Mutation-Driven Evolution was an attempt to link metabolic networks to genetic networks via the selective advantage of a mutation, which is determined by the type of DNA change.
The claim that damaged DNA could provide a selective advantage should be considered only in the context of virus-driven energy theft and one-carbon metabolism. When a virus uses the cell’s metabolism to support it’s replication, energy is used by the virus, not by the cell.
The damage to DNA is due to virus-driven energy theft, and energy theft is never beneficial.
That’s why I asked for an alternative model in my conclusion from Nutrient-dependent/pheromone-controlled adaptive evolution: a model
…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’.
There is still no alternative model.
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)].”
My comment: Masatoshi Nei and Masafumi Nozawa put the links from virus-driven energy theft to all pathology into the same context of “space limitations” in Roles of Mutation and Selection in Speciation: From Hugo de Vries to the Modern Genomic Era
…we will not consider geographical and ecological factors because of space limitation. Our primary purpose is to clarify the roles of mutation and selection in the evolution of reproductive isolation and show that the molecular basis of speciation is more complicated than generally thought at present.
For example the hecatombic virus-driven “slaughter” of 100 energy-dependent microRNAs may be pleasing to the gods one worships, if that is all that it takes to link all biodiversity via mutations and natural selection. But if the hecatombic slaughter is not considered in the context of healthy longevity and the energy-dependent weekend resurrection of the bacterial flagellum, it is more difficult to compare with models of how natural selection for nutrient energy-dependent codon optimality and fixation of RNA-mediated amino acid substitutions in supercoiled DNA prevent virus-driven entropy in all organized genomes.
When studying regulation of host- or virus-encoded RNA targets by miRNAs, the “abundance problem” needs to be considered. Based on studies in cell lines, it has been argued that approximately 100 copies of a miRNA are needed to affect host transcripts and, depending on the number and activity of viral genomes in the cell, likely a higher number to affect viral transcripts (78). Thus, expression changes of low copy number miRNAs during infection may be of little functional consequences. Studies on regulation of host miRNAs in infection often ignore this potentially important issue.
My comment: Virus-driven energy theft linked from viral microRNAs to amino acid substitutions in viruses is clearly linked to the stability of their organized genomes. Eliminating consideration for nutrient energy-dependent microRNAs in the context of healthy longevity via the stability of organized genomes in all living genera is the only way to keep supporting the pseudoscientific nonsense of neo-Darwinian theory.