Evolutionary resurrection of flagellar motility via rewiring of the nitrogen regulation system
Excerpt: The fast-spreading strain AR2F had acquired an additional point mutation in the σ54-dependent EBP gene ntrC, which alters an amino acid (R442C) within the DNA binding domain (Table 1 and table S2).
Reported as: Evolutionary Rewiring
Strong selective pressure can lead to rapid and reproducible evolution in bacteria.
| February 26, 2015
Excerpt: NtrC shares 30 percent amino acid identity with FleQ, suggesting the proteins may be able to minimally cross-react with each other’s target genes. Sure enough, the researchers determined that the initial mutations, which ramped up NtrC levels, enabled a minor upregulation of FleQ’s target genes. The second mutations to NtrC itself then improved the protein’s interaction with the FleQ targets, boosting their expression, and the bacteria’s ability to swim.
My summary: Researchers still seem to be very confused about the difference between amino acid substitutions, which stabilize RNA-mediated protein folding and mutations. Mutations perturb protein folding, which is why they are consistently linked to physiopathology and not linked from ecological variation to nutrient-dependent pheromone-controlled ecological adaptations via the physiology of reproduction in species from microbes to humans.
My comments on “Evolutionary Rewiring”:
Re: “…repurposing of a distantly related protein.”
1) The “repurposing” is nutrient-dependent and pheromone-controlled.
2) The repurposing exemplifies how ecological variation leads to nutrient-dependent RNA-directed DNA methylation and RNA-mediated amino acid substitutions that stabilize DNA in the organized genomes of species from microbes to man.
See how important it is to understand genomic stability in the context of “repurposing.” Biocontainment of genetically modified organisms by synthetic protein design. See also the importance of Combating Evolution to Fight Disease.
Richard Lenski and many others have been on the wrong side of this fight for several decades. See, for example: A single amino acid substitution differentiates cell types of E. coli
Re: “The results highlight the importance of gene duplication…”
Gene duplication is nutrient-dependent. Fixation of amino acid substitutions that stabilize the genome is controlled by the physiology of reproduction, which is controlled by the metabolism of nutrients to species-specific pheromones.
The RNA-mediated fixation of amino acid substitutions links metabolic networks to genetic networks. That fact explains why Church’s group has taken great care to address other facts that link physics, chemistry, and conserved molecular mechanisms to cell type proliferation, which theorists tend to attribute to mutations and evolution.
For constast to the claims of theorists, Christ and others: The Pharmacology of Regenerative Medicine are also attempting to link “… the salient features of diverse fields of research—ranging from materials chemistry and functionalized biomaterials to stem cells, organ/tissue regeneration, wound healing, and development biology…”
Accurate representations of nutrient-dependent biologically-based cause and effect during life history transistions also can be viewed in the context of heterochronic parabiosis, which links fixed amino acid substitutions in red blood cells to the delivery of nutrients to every cell in organisms with a circulatory system.
Mutations perturb the molecular mechanisms of the delivery system, which typically prevent sepsis caused by E. coli or other microbes that ecologically adapt to higher body temperatures than can be maintained by immunocompromised mammals (e.g., like your grandmother who may have died from complications of a urinary tract infection in the context of evolutionary theory).
The journal article reports the de novo origination of new functions via the nutrient-dependent creation and rewiring of gene networks linked to metabolic networks by the pheromone-controlled fixation of an amino acid substitution in the DNA of the organized genome of a microbe with a flagellum that enables it to find food. In their example of a starving microbe, the flagellum is first evolved then lost. A few days later it has re-evolved, and they place evolution and re-evolution of the structure and its function into the context of mutations and evolution via “…a highly repeatable two-step evolutionary pathway with the same point mutations often recurring in independent lineages.”
See also: Bacteria ‘hotwire their genes’ to fix a faulty motor.
Watch for more pseudoscientific nonsense as evolutionary theorists try to explain the nutrient-dependent breaking of Mendel’s “Law of Segregation” reported here R2d2 beats Mendel: Scientists find selfish gene that breaks long-held law of inheritance and why additions must be made to the second Law of thermodynamics, reported here: On quantum scales, there are many second laws of thermodynamics.
Obviously, they will keep trying to get others to believe that they have accurately represented biologically-based cause and effect that may or may not lead to evolution in 4 days or 2 billion years. See: Scientists discover organism that hasn’t evolved in more than 2 billion years. There only other choice is to join the serious scientists who are Combating Evolution to Fight Disease. However, recruits may now be required to pass an intelligence test, since nearly everyone will want to join serious scientists in combat. Those who have published papers about mutations and evolution during the past decade may be automatically excluded unless they can explain why they thought that evolution via mutations automagically occurred.
