Pheromone killing of multidrug-resistant Enterococcus faecalis V583 by native commensal strains
From their conclusion:
Irrespective of mechanism, the incompatibility between V583 and commensal strains of E. faecalis provides clear support for the hypothesis that this MDR hospital strain and commensal enterococci do not occupy the same habitat (20) and begins to shed light on differences in the colonization properties of hospital and commensal lineages of enterococci.
Reported as: Pheromones produced by gut bacteria found to kill resistant variants of its own kind
Excerpt:
…bacteria are winning the war against them by us humans—as we develop new agents to kill them, they develop new ways to avoid being killed by them, some of which include mobile elements that encode virulence and antibiotic resistance traits and new metabolic pathways. In this new effort, the researchers were investigating the ways that bacteria evolve to cause themselves to become resistant to new antibiotics…
My comment: They study and reporting ignore what is known to serious scientists about the nutrient-dependent pheromone-controlled links to antibiotic resistance and place the biophysically constrained chemistry of nutrient-dependent RNA-mediated protein folding into the context of evolution.
Irrespective of mechanism and the ways that bacteria evolve to cause themselves are the key phrases that cause serious scientists to shudder in disbelief as evolutionary theorists continue to contribute to disease.
My comment: See also: Combating Evolution to Fight Disease
Excerpt:
Molecular biology and evolutionary biology have been separate disciplines and scientific cultures: The former is mechanistic and focused on molecules; the latter is theoretical and focused on populations.
My comment: The molecular mechanisms of bacterial resistance to damage by viral microRNAs extend from microbes to humans. They are nutrient-dependent and pheromone-controlled. Nutrient-dependent microRNAs and RNA-mediated events linked to DNA repair defend the integrity of organized genomes in all genera. The nutrient-dependent innate defenses of the bacteria and their pheromone-controlled physiology of reproduction are linked from the bioluminescent bacteria in the light organ of the squid to the squid’s nutrient-dependent pheromone-controlled reproduction via the conserved molecular mechanisms that link ecological variation to ecological adaptations in all genera. The molecular mechanisms integrate what is currently known about the biophysically constrained chemistry of nutrient-dependent RNA-mediated protein folding.
Irrespective of mechanism and the ways that bacteria evolve to cause themselves exemplifies the lack of respect that evolutionary biologists/population geneticists have for serious scientists who know that bacteria and people do not evolve themselves.
See also: Searching journal content for alternative splicing in full text.
Why do researchers who report that “unknown mechanisms” link evolution to antibiotic resistance think they can report pseudoscientific nonsense, when others, like Bonnie Bassler have provided detailed explanations of biologically-based cause and effect?
See for instance: From Fertilization to Adult Sexual Behavior
Excerpt:
Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.