UV-repair and mutagenesis in Azotobacter vinelandii. I. Repair of UV-induced damages.

UV-irradiated Azotobacter vinelandii OP cells were found to be sensitive to dark repair-inhibitors, like caffeine and acriflavine. Sensitivity to both the inhibitors started to decrease at a fast rate immediately following UV-irradiation, when incubated in Burk's broth in dark. Total insensitivity to caffeine was attained at a time that was approximately double the time of the corresponding ribonucleic acid synthesis-inhibition and less than one generation time of the unirradiated cells. Nearly at the same time the rate of loss of sensitivity to acriflavine became much slower and total insensitivity to acriflavine occurred after relatively prolonged incubation. The protein synthesis inhibitor, streptomycin, reduced UV-survival, but after a time lag. The organism did not show liquid holding recovery and its UV-survival was not affected by components of complex medium. It is proposed that A. vinelandii OP possesses at least two dark-repair pathways: pre replication (acts immediately after UV exposure and is faster) and post replication (delayed and slower) repair. The first one is inhibited by caffeine and acriflavine and the second by acriflavine and streptomycin. The latter therefore requires de novo protein synthesis after UV-irradiation and may be inducible.