Decoding Bacterial Methylomes (5/25/13)
Methylation is nutrient-dependent and pheromone-controlled in microbes. This article suggested to me that antibiotic resistance is altered by nutrient-dependent thermodynamically controlled changes in the microRNA/messenger RNA balance. In a comment to The Scientist that has since been removed, I claimed that nutrient-dependent changes in the microRNA/messenger RNA balance could cause differences in intracellular signaling, internuclear interactions, chromatin remodeling, stochastic gene expression, and changes in seemingly futile cycles of nutrient-dependent de novo protein biosynthesis and degradation.
I added that successful metabolism of nutrients and protein biosynthesis results in protein degradation to species-specific pheromones that control reproduction by enabling quorum sensing (i.e., the pheromones epigenetically effect organism-level and colony-wide thermoregulation). The ability of one microbial ‘species’ to incorporate nutrient availability and to also withstand nutrient-dependent thermodynamically-controlled increased ‘heat’ is then associated with the species-wide ability to communicate successful competition for nutrients via pheromone production that controls colony growth (and antibiotic resistance in Escherichia coli, for example).
I asked, if anyone understands how what I just suggested may explain nutrient-dependent pheromone-controlled adaptive evolution via ecological and social niche construction in microbes, comments are welcome.
In 2013, I did not have the interdisciplinary expertise to move forward with anything more than just a model of cause and effect. I published Nutrient-dependent/pheromone-controlled adaptive evolution: a model (6/14/13), but received almost no positive feedback on any aspect of the model or its extension across species from microbes to man via nutrient-dependent / pheromone-controlled thermodynamics and thermoregulation. I was forced to retire from work as a medical laboratory scientist and my official retirement was effective during the month after The Scientist published the nonsense about Decoding Bacterial Methylomes.
I began to think that, perhaps I missed something that is obvious to others. Second thoughts led me to question my assessment of Mutation-driven evolution, a textbook that was published on the same day as my model of ecological adaptations. I asked several very intelligent people: “Could the claim that evolution is dependent on mutations that cause all genetic variation be correct?”
All of them said, “No!” It has since become obvious that Masatoshi Nei and others like him are biologically uninformed theorists.
The first page of the Main Text is displayed and the following claim is made:
…there are 20,418 protein-coding genes; 15,195 pseudogenes, and 22,107 ncRNAs. NcRNAs include 4,871 small ncRNAs [e.g., small nuclear RNAs (snRNAs), small nucleolar RNAs (snoRNA), microRNAs (miRNAs), tRNAs]…
McEwen et al., (1964) claimed that:
The synthesis of RNA in isolated thymus nuclei is ATP dependent.
See for comparison: A universal trend of amino acid gain and loss in protein evolution (2005)
Amino acid composition of proteins varies substantially between taxa and, thus, can evolve.
See for comparison: Single nucleotide polymorphism, a putative driver for the role of long intergeneric non-coding RNA (2018)
Some SNPs may serve as the risk factors for the development of various disorders, especially of cancers, and act as important regulatory signature involved in the modulation of lincRNAs in a tissue or disorder-specific manner. It indicates that lincRNA SNPs would potentially provide additional options for genetic testing, disease risk assessment, and RNA targeting therapeutics in the personalized medicine era.
In this 2018 review of nutritional epigenetics, I linked everything known about how light-activated microRNA biogenesis from energy-dependent changes in angstroms to changes in ecosystems via changes in SNPs linked to the ATP-dependent creation of RNA.
Why ask how?
Intelligent people know that organisms must eat and reproduce for species to adapt. Some theorists realize they must accept that fact and try to portray ecological variation and ecological adaptations in the context of evolution.
It has always been obvious to all serious scientists that those theorists exemplify human idiocy.