RNA-mediated gene duplication, fixation, and ecological adaptation

By: James V. Kohl | Published on: July 11, 2015

Chromosomal Arrangement of Phosphorelay Genes Couples Sporulation and DNA Replication

The simplicity of this coordination mechanism suggests that it may be widely applicable in a variety of gene regulatory and stress-response settings.

Reported as:

Bacteria use DNA replication to time key decision


“Successful sporulation requires two complete copies of the bacterial chromosome, so coordination between the sporulation decision and the completion of DNA replication is very important,” Narula said. “A good analogy might be a semester-long course in biology.

My comment: If, at the end of the semester, you believed that these bacteria “evolved” their ability to choose when to sporulate, you might continue to ignore this fact: Their biophysically constrained nutrient-dependent RNA-mediated thermodynamic cycles of protein biosynthesis and degradation are controlled by the physiology of their reproduction in the context of fixed RNA-mediated amino acid substitutions and gene duplication.
The fact that gene duplication is nutrient-dependent is difficult to ignore even when it is referred to as DNA replication. It is also difficult to ignore the fact that no experimental evidence of biologically-based cause and effect has ever linked mutations to the creation of new genes. That means mutations cannot be linked from genes to the chromosomal rearrangements that link RNA-mediated amino acid substitutions to biodiversity via the conserved molecular mechanisms of nutrient-dependent biophysically constrained RNA-mediated protein folding chemistry.
If you, like the atheist blogger PZ Myers and his idiot minions, continue to attack anyone who provides experimental evidence that links the creation of new genes to chromosomal rearrangements and to biodiversity in species from microbes to man, you will be more than 30 years behind the experimental evidence that links viruses to genomic entropy and the anti-entropic epigenetic effects of nutrients to RNA-mediated cell type differentiation in species from microbes to man.

See: One crank dies, another rises to take his place

Behold James Vaughn Kohl.

Ecological adaptation occurs via the epigenetic effects of nutrients on alternative splicings of pre-mRNA which result in amino acid substitutions that differentiate all cell types of all individuals of all species. The control of the differences in cell types occurs via the metabolism of the nutrients to chemical signals that control the physiology of reproduction.
These facts do not refute evolution; they simply refute the ridiculous theory of mutation-initiated natural selection that most people here were taught to believe is the theory of evolution.

PZ Myers did not like my accurate representation of biologically-based cause and effect, which he linked to the accurate representations by others who he attacked in the past. Others did not like my accurate representations, either. In his Criticisms of the nutrient-dependent pheromone-controlled evolutionary model, Andrew Jones included a citation to PZ Myers blog.

A multitude of misconceptions and misunderstandings can be seen in his comments on Dr. PZ Myers’ blog, Pharyngula (Kohl, 2014b).

My comment: Everything known about ecological variation and biologically-based ecological adaptation links RNA-mediated events to metabolic networks and genetic networks. The metabolic networks and genetic networks link RNA-directed DNA methylation to gene duplication via the fixation of RNA-mediated amino acid substitutions. The nutrient-dependent amino acid substitutions are linked to healthy longevity. Mutations are linked to pathology. Everything published by serious scientists during the past 30 years also links RNA-mediated gene duplication from metabolic networks to genetic networks and the biodiversity of all extant species. Species that failed to ecologically adapt became extinct. For example, when they ran out of food, they did not evolve into another species because gene duplication is nutrient-dependent.

See also: RNA-Mediated Gene Duplication and Retroposons: Retrogenes, LINEs, SINEs, and Sequence Specificity (2013) and RNA-mediated gene duplication: the rat preproinsulin I gene is a functional retroposon (1985)
My comment: Serious scientists have known for more than 30 years that gene duplication is RNA-mediated. If they don’t know that gene duplication is nutrient-dependent, they are not serious scientists.  Moving forward, let’s look at what serious scientists know about gene duplication. We can forget about PZ Myers and his idiot minions or anyone else who was taught to believe in ridiculous theories about mutations and evolution.
Synthetic success:
Rewriting the blueprint of life by synthetic genomics and genome engineering

The engineered E. coli incorporated non-standard amino acids into its proteins and showed enhanced resistance to bacteriophage T7 [25].

Natural failure
Elephantid Genomes Reveal the Molecular Bases of Woolly Mammoth Adaptations to the Arctic

…we functionally annotated fixed, derived amino acid and loss-of-function (LOF) substitutions in woolly mammoths.

How to ecologically adapt:
Transposon-mediated rewiring of gene regulatory networks contributed to the evolution of pregnancy in mammals
My comment: To ecologically adapt, species must reproduce.
How to become extinct:
Popping the Cork on a microbiome alliance
Excerpt 1)

While most people are familiar with human viruses, it is not as well known that bacteria also have viruses which can drastically influence bacterial populations. These bacterial viruses are necessary for a balanced ecosystem, which is vital for the overall health of the host,” said Hill.

Excerpt 2) The role of phage in shaping the microbiota in health and disease is relatively unexplored…
My comment on excerpt 1) Accumulation of viral microRNAs links bacterial viruses to perturbed protein folding and unbalanced ecosystems that lead to extinction. Without the anti-entropic epigenetic effects of nutrient-dependent microRNAs, all species would have long-ago become extinct.
My comment of excerpt 2) The role of phages has been explored in the context of what has been learned about virus-driven genomic entropy, which is prevented by the anti-entropic epigenetic effects of nutrients on DNA repair. Fixation of nutrient-dependent amino acid substitutions links RNA-mediated cell type differentiation and biodiversity in all genera. Mutations are linked to pathology.
See for example:

Analysis of 6,515 exomes reveals the recent origin of most human protein-coding variants

Excerpt: Of 1.15 million single-nucleotide variants found among more than 15,000 protein-encoding genes, 73% in arose the past 5,000 years, the researchers report. 164,688 of the variants — roughly 14% — were potentially harmful, and of those, 86% arose in the past 5,000 years.
My comment: The harmful variants link mutations to pathology. That is the reason they are called harmful variants. Amino acid substitutions are linked to healthy longevity, which is why they should not be called mutations.
For example, Evolutionary resurrection of flagellar motility via rewiring of the nitrogen regulation system, claims that two mutations enabled the bacterial flagella of a species to “re-evolve” over-the-weekend. They called the fixed amino acid substitutions that enabled food finding mutations. Sulfur-cycling fossil bacteria from the 1.8-Ga Duck Creek Formation provide promising evidence of evolution’s null hypothesis linked the lack of mutations and/or amino acid substitutions to the evolution that did not occur in ~2 billion years.
In reality, which for most people is what happens to them during their life-time, mutations are bad, and fixation of nutrient-dependent RNA-mediated amino acid substitutions is good.
For example: DNA methylation and single nucleotide variants in the brain-derived neurotrophic factor (BDNF) and oxytocin receptor (OXTR) genes are associated with anxiety/depression in older women.
RNA-directed DNA methylation links fixed amino acid substitutions to hormones and behavior during life history transitions of all genera. Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults.
The failure of RNA-mediated fixation that is required for brain development during the transition from adolescence to adulthood, is linked to behavioral instability by hormones, which are also associated with anxiety/depression in older women. However, linking the hormones to the evolution of personality is a ridiculous misrepresentation of biologically-based cause and effect. See for example: Neuroendocrine mechanisms underlying behavioral stability: implications for the evolutionary origin of personality.
The neuroendocrine mechanisms are nutrient-dependent and they require gene duplications to link the biophysically constrained chemistry of nutrient-dependent RNA-mediated protein folding to behavioral changes during life history transitions.
For example, see: Brain feminization requires active repression of masculinization via DNA methylation

 Our observation that Dnmt inhibition reduced a substantial number of genes in females reveals an additional layer of complexity for which there is no current explanation.

My comment: They cannot explain why the lack of gene duplication led to changes in behavior.  Oddly, they appear to have learned nothing about how the anti-entropic epigenetic effects of RNA-mediated amino acid substitutions explain all links from genes to the hormones that affect behavior. Evidently, the RNA-mediated gene duplication and RNA-directed demethylation that links RNA-mediated amino acid substitutions to the development of behavior is too complex for them to comprehend.
See, instead: From Fertilization to Adult Sexual Behavior.
Our section on molecular epigenetics links everything currently known about RNA-mediated cell type differentiation to the development of morphological and behavioral phenotypes in all genera. However, we did not mention the fact that RNA-mediated gene duplication must come first. We assumed that serious scientists knew that, and that only pseudoscientists would continue to tout their ridiculous theories about mutations and evolution.
We were wrong. Our facts about RNA-mediated cell types were ignored. For contrast: [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 assumptions taught to biologically uninformed theorists have continue to plague serious scientists who present experimentally established facts.
See for example, the discussions at: Researchers find the organization of the human brain to be nearly ideal and at ‘Map of life’ predicts ET. (So where is he?)
No matter how much experimental evidence is cited, the assumptions prevail. See also discussions of Learning categorical information gives children a feeling of deja vu and of Researcher disputes claim that humans can distinguish one trillion odors.
Pseudoscientists have successfully convinced many people that mutations can be linked to evolution without consideration of RNA-mediated gene duplication or the RNA-mediated events that link the metabolism of nutrients to cell type differentiation via fixation of amino acid substitutions in the context of the biophysically constrained chemistry of protein folding.

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