The disruption of ung, the unique uracil-DNA-glycosylase-encoding gene in 
Bacillus subtilis, slightly increased the spontaneous mutation frequency to 
rifampin resistance (Rif(r)), suggesting that additional repair pathways 
counteract the mutagenic effects of uracil in this microorganism. An alternative 
excision repair pathway is involved in this process, as the loss of YwqL, a 
putative endonuclease V homolog, significantly increased the mutation frequency 
of the ung null mutant, suggesting that Ung and YwqL both reduce the mutagenic 
effects of base deamination. Consistent with this notion, sodium bisulfite (SB) 
increased the Rif(r) mutation frequency of the single ung and double ung ywqL 
strains, and the absence of Ung and/or YwqL decreased the ability of B. subtilis 
to eliminate uracil from DNA. Interestingly, the Rif(r) mutation frequency of 
single ung and mutSL (mismatch repair [MMR] system) mutants was dramatically 
increased in a ung knockout strain that was also deficient in MutSL, suggesting 
that the MMR pathway also counteracts the mutagenic effects of uracil. Since the 
mutation frequency of the ung mutSL strain was significantly increased by SB, in 
addition to Ung, the mutagenic effects promoted by base deamination in growing 
B. subtilis cells are prevented not only by YwqL but also by MMR. Importantly, 
in nondividing cells of B. subtilis, the accumulations of mutations in three 
chromosomal alleles were significantly diminished following the disruption of 
ung and ywqL. Thus, under conditions of nutritional stress, the processing of 
deaminated bases in B. subtilis may normally occur in an error-prone manner to 
promote adaptive mutagenesis.