Abstract
The influence of the nucleotide excision repair system on the inducation by UV irradiation of the SOS function sfiA was investigated. The level of sfiA expression was monitored by means of a sfiA::lacZ operon fusion in the wild-type strain and a uvrA mutant. The initial steady rate of sfiA expression was proportional to the UV dose and was identical in uvr+ and uvrA backgrounds. Evidently, the initial steady rate of sfiA expression is determined by the initial number of lesions and before any effect of excision repair. After 2 h of expression the net synthesis of sfiA product is, for the same UV dose, 5 times lower in uvr+ than in uvrA strains. This is due to earlier repression of the SOS system in uvr+ than in uvrA strains and not to different initial rates.