One of the proposed mechanisms for generating adaptive mutations is down regulation of mismatch-repair system (MMR). Our focus was to investigate how mutation rate of the Gram-positive model Bacillus subtilis changes when it is exposed to nutritional and hyperosmotic stress.
We also studied expression of MMR genes on these conditions. The mutation rate was measured as frequency of rifampicin or spectinomycin-resistant cells arising during growth.
Expression of mutSL operon (coding for both known components of MMR) was monitored by measuring the activity of beta-galactosidase, whose gene was fused to the promoter of this operon. We confirm that complete inactivation of MMR results in one hundred-fold increase in mutation rate, When carried out using hyperosmotic shock, mutation rates remained essentially the same, suggesting fully functional MMR.
Our results suggest that stresses we tested do not trigger any large-scale mutagenesis in B. subtilis.