The magic of evolution times two

By: James V. Kohl | Published on: January 27, 2017

See: Stress and bacterial evolution

We try to understand the genetic mechanisms involved in genome stability in bacteria and their roles on evolution and adaptation

For comparison: No Genetics without Epigenetics? No Biology without Systems Biology?

Systems biology therefore focuses on the relations between data, on their system’s aspect, more than on the data themselves. It is on this basis that it proposes to generate an understanding on “how their maze of interactions in time and space govern life,”3 to genuinely “turn data into knowledge,” or else, to “bring genomes to life.”4,12–14

See also: Mae-Wan Ho: No Boundary Really Between Genetic and Epigenetic

…when we eat food nucleic acids can get into our cells. Also, there is a theory that our cells in the body keep sending out nucleic acids and one theory has it that it seems to correct the mistakes that other cells have suffered from mutations. . . .

A non-canonical mismatch repair pathway in prokaryotes

The phylogenetic analysis of NucS indicates a complex evolutionary process leading to a disperse distribution pattern in prokaryotes. Together, these findings indicate that distinct pathways for MMR have evolved at least twice in nature.

Characterization of the two NucS regions

To identify potential domains in NucS, we focused on the archaeal P. abyssi NucS, whose 3D structure was previously resolved (PDB 2VLD chain B)11. This structure is composed by two distinct regions: the N-terminal DNA-binding region (1–114 amino acids) and the C-terminal catalytic region (126–233 amino acids)11. Given the absence of structural data for the bacterial NucS protein, the M. tuberculosis NucS structure was modelled using the archaeal P. abyssi NucS as a template using I-TASSER16 and generated a reliable model (Supplementary Fig. 3). Template and model were structurally aligned using the Combinatorial Extension (CE) algorithm17, built-in with PyMOL, to identify relevant residues.

Reported as: ‘Survival gene’ stops strains of tuberculosis mutating into deadly ‘superbugs’

…the loss of this DNA repair process can cause a huge increase in the mutation rates…

The DNA repair process is nutrient energy-dependent and RNA-mediated. Amino acid substitutions in supercoiled DNA link the virucidal effects of ultraviolet light (UV) to all biodiversity via phosphorylation, which protects organized genomes from virus-driven energy theft and genomic entropy.
Claims about the loss of the DNA repair process fail to address the complexity of how it was created in the context of femtosecond blasts of UV light. They also fail to address facts about where the energy for DNA repair goes when it gets “lost.” The facts are lost in the pseudoscientific nonsense about “deep evolution.” For comparison, see
Bacteria ‘hotwire their genes’ to fix a faulty motor and see how my comments were dismissed by the biologically uninformed.
Nothing can convince theorists that the weekend resurrection of the bacterial flagellum is not an example of evolution. To a theorist, everything must be an example of evolution or they are forced to start thinking in terms of energy-dependent creation. They do not want to think about that.
Nobody wants to belong to the party of losers. One of the best strategies in such a case is evidently an interpretation of the change as a gradual accumulation of knowledge while their work has always been at the cutting edge. —  Kalevi Kull
 


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