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 t he 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 c orrelated with the induction of a 17-kDa DNA methyltransferase, capabl e of repairing O-6-methylguanine lesions in DNA. This induced methyltr ansferase was found to be antigenically unrelated to the Escherichia c oli methyltransferase (Ada protein) as determined by Western blotting with polyclonal antiserum raised against the E. coli protein. Even tho ugh no counterpart of the constitutively expressed methyltransferase ( Ogt) of E. coli could be detected in V. cholerae, several lines of evi dence pointed towards the presence of an E. coli alkA-like gene in the organism.