Aim: The ssrA mutants were found to be more sensitive to mitomycin C (MMC) and our aim was to study this phenomenon in detail.
Materials & Methods: Strains were constructed by P1 transduction. pssrA plasmid was constructed by PCR-based cloning and transformation was done by CaCl method.
Very recently, we have reported about an unconventional mode of elicitation of Mitomycin C (MMC) specific resistance in lexA3 (SOS repair deficient) mutants due to a combination of Rif-Nal mutations (rpoB87-gyrA87). We have clearly shown that UvrB is mandatory for this unconventional MMC resistance in rpoB87-gyrA87-lexA3 strains and uvrB is expressed more even without DNA damage induction from its LexA dependent promoter despite the uncleavable LexA3 repressor. The rpoB87 allele is same as the rpoB3595 which is known to give rise to a fast moving RNA Polymerase and gyrA87 is a hitherto unreported Nal(R) allele.
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