N. Bhasin et A. Ghosh, EVIDENCE FOR A WEAK ADAPTIVE RESPONSE TO ALKYLATION DAMAGE IN VIBRIO-CHOLERAE, Mutation research. DNA repair, 336(1), 1995, pp. 79-89
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.