In growing cells, apurinic/apyrimidinic (AP) sites generated spontaneously or 
resulting from the enzymatic elimination of oxidized bases must be processed by 
AP endonucleases before they compromise cell integrity. Here, we investigated 
how AP sites and the processing of these noncoding lesions by the AP 
endonucleases Nfo, ExoA, and Nth contribute to the production of mutations 
(hisC952, metB5, and leuC427) in starved cells of the Bacillus subtilis YB955 
strain. Interestingly, cells from this strain that were deficient for Nfo, ExoA, 
and Nth accumulated a greater amount of AP sites in the stationary phase than 
during exponential growth. Moreover, under growth-limiting conditions, the 
triple nfo exoA nth knockout strain significantly increased the amounts of 
adaptive his, met, and leu revertants produced by the B. subtilis YB955 parental 
strain. Of note, the number of stationary-phase-associated reversions in the 
his, met, and leu alleles produced by the nfo exoA nth strain was significantly 
decreased following disruption of polX. In contrast, during growth, the 
reversion rates in the three alleles tested were significantly increased in 
cells of the nfo exoA nth knockout strain deficient for polymerase X (PolX). 
Therefore, we postulate that adaptive mutations in B. subtilis can be generated 
through a novel mechanism mediated by error-prone processing of AP sites 
accumulated in the stationary phase by the PolX DNA polymerase.