Nutrient-dependent trophic analogs

By: James V. Kohl | Published on: November 27, 2015

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Adaptive Resistance in Bacteria Requires Epigenetic Inheritance, Genetic Noise, and Cost of Efflux Pumps

Excerpt:

Our results identify the molecular mechanism of epigenetic inheritance as the main target for therapeutic treatments against the emergence of adaptive resistance. Finally, our theoretical framework unifies known and newly identified determinants…

Conclusion:

Our model provides an explanation for the emergence of adaptive resistance based on the cost and benefit of the biological characteristics of an efflux pump system. It does not only predict the behavior of populations subjected to different antibiotic shocks and at different time, but also a number of different phenomena observed experimentally in bacterial populations, such as phenotypic reversibility, genetic assimilation, and even the survival rates of populations that have been pre-induced with non-lethal antibiotic concentrations (see S1 Text and S12 Fig.).

My comment: My model linked nutrient-dependent RNA-mediated amino acid substitutions to cell type differentiation in the context of ecological variation and ecological adaptations in all living genera.

See: Nutrient-dependent/pheromone-controlled adaptive evolution: a model.

See also:

Microbes are trophic analogs of animals

Excerpt:

Viewed under the lens of amino acid isotopic analysis, the bacteria, fungi, and animals in our study exhibited strikingly similar patterns of intertrophic 15 N-discrimination. Specifically, the consistent TDF glu-phe among all consumers reflected predictable patterns of 15N-discrimination in glutamic acid and phenylalanine, the two amino acids previously shown to be critically important to accurate TP estimation among animals (17, 20, 26, 33). The degree of intertrophic 15N-discrimination in glu was relatively high, whereas that of phe was characteristically low, which contrasted with the more variable patterns observed in the remaining amino acids. This glu-phe 15N-discrimination pattern held true across not only a broad phylogenetic spectrum (three biological kingdoms), but also a diversity of ecosystem types (terrestrial vs. aquatic) and trophic groups (plant- vs. animal-based diets). Trophically, therefore, the macro- and microfauna in our study were equivalent. Such constancy in the TDF glu-phe facilitates accurate, predictable trophic position estimation within the broader empire of heterotrophy.

Conclusion:

It is more parsimonious to conclude that the organisms in our study reflect real patterns within the broader heterotrophic empire and that microbes can be considered the trophic equivalents of animals within a food chain. For food web ecology, this reframes how the microbiome can be viewed and resolves long-standing questions as to where microbes fit within the food chain. Fungal, bacterial, and animal species can be integrated within a single trophic hierarchy, thereby uniting the macro- and microbiome and facilitating more comprehensive assessments of functional diversity within ecosystems.

Note: Phenylketonuria (PKU) Definition By Mayo Clinic Staff

“… is a rare inherited disorder that causes an amino acid called phenylalanine to build up in your body. PKU is caused by a defect in the gene that helps create the enzyme needed to break down phenylalanine.”

My comment: The inherited disorder links a single amino acid substitution to human brain development.
See also:

Viral Genome Junk Is Bunk

Excerpt:

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

My comment: I extended the examples from my 2013 across all genera via top-down causation that links ecological variation to ecological adaptation in trophic analogs of microbes and animals. The conserved molecular molecular mechanisms of nutrient dependent cell type differentiation in plants are the same.

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

My comment: Viruses are clearly linked to genomic entropy when the conserved moleular mehanisms of RNA-mediated DNA repair are disabled by the accumulation of viral microRNAs that perturb protein folding.