Evidence for a weak adaptive response to alkylation damage in Vibrio cholerae.

Wild-type Vibrio cholerae cells, when adapted by a stepwise treatment with sub-lethal concentrations of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), acquired resistance to killing and mutagenesis by subsequent challenges with higher concentrations of MNNG. This was also seen in the rec isogenic strain indicating that the observed phenomenon was not due to the induction of SOS functions. Further, the adapted cells of both the wild-type and rec strains could reactivate lethally alkylated phages with equal efficiency. Increased resistance of adapted cells correlated with the induction of a 17-kDa DNA methyltransferase, capable of repairing O6-methylguanine lesions in DNA. This induced methyltransferase was found to be antigenically unrelated to the Escherichia coli methyltransferase (Ada protein) as determined by Western blotting with polyclonal antiserum raised against the E. coli protein. Even though no counterpart of the constitutively expressed methyltransferase (Ogt) of E. coli could be detected in V. cholerae, several lines of evidence pointed towards the presence of an E. coli alk A-like gene in the organism.