Stress-promoted mutations that occur in nondividing cells (adaptive mutations) 
have been implicated strongly in causing genetic variability as well as in 
species survival and evolutionary processes. Oxidative stress-induced DNA damage 
has been associated with generation of adaptive His(+) and Met(+) but not Leu(+) 
revertants in strain Bacillus subtilis YB955 (hisC952 metB5 leuC427). Here we 
report that an interplay between MutY and MutSL (mismatch repair system [MMR]) 
plays a pivotal role in the production of adaptive Leu(+) revertants. 
Essentially, the genetic disruption of MutY dramatically reduced the reversion 
frequency to the leu allele in this model system. Moreover, the increased rate 
of adaptive Leu(+) revertants produced by a MutSL knockout strain was 
significantly diminished following mutY disruption. Interestingly, although the 
expression of mutY took place during growth and stationary phase and was not 
under the control of RecA, PerR, or σ(B), a null mutation in the mutSL operon 
increased the expression of mutY several times. Thus, in starved cells, 
saturation of the MMR system may induce the expression of mutY, disturbing the 
balance between MutY and MMR proteins and aiding in the production of types of 
mutations detected by reversion to leucine prototrophy. In conclusion, our 
results support the idea that MMR regulation of the mutagenic/antimutagenic 
properties of MutY promotes stationary-phase mutagenesis in B. subtilis cells.