But of course you leave out the fact that there are only two mutations in a specific enzyme whose function is not known. That is not accidental. They tried to generate the activity by deleting both genes capable of producing the desired activity with no success. You also fail to point out that the two genes being discussed are very similar. The mutations are targeted to two specific locations on one specific gene.
A molecule hits a receptor that activates a transcriptional repressor that turns off a gene.
No, again you simplify.
To summarize: (i) PsiB appears to inhibit adaptive mutation when the LexA regulon is constitutively de-repressed in a lexADef mutant; and (ii) two proteins that modulate RecA* activity, DinI and PsiB, affect adaptive mutation positively and negatively. These data suggest that RecA* activity is critical in adaptive mutation, that if RecA* activity is either too high or too low, mutation is decreased. These results indicate a tight control over adaptive mutation by factors modulating the SOS response, and provide evidence of SOS regulation of adaptive mutation independent of particular LexA alleles.
In that particular case, sure.
But in general we see the overall trend whereby mutations can improve the catalytic efficiency of enzymes. Check out “directed evolution”.
And indeed there is tight control on the mechanisms that increase or decrease the mutation rate during the SOS response to stress. That control is control over the expression of error prone DNA polymerase, DNA mutation repair enzymes, etc. Control doesn’t imply that each mutation is part of some programmed response, the control is over the mechanisms that act over the entire genome increasing the RATE of mutation.
So now that we are deep into a discussion over how an organism controls its mutation rate; why do you suppose there might be ANY advantage to responses that INCREASE the mutation rate over the entire genome?