Quillardet P, Hofnung M
J Bacteriol. 1984 Jan;157(1):35-8. doi: 10.1128/jb.157.1.35-38.1984.
The influence of the nucleotide excision repair system on the induction by UV irradiation of the SOS function sfiA has been investigated. The level of sfiA expression was monitored by means of a sfiA::lacZ operon fusion in both the wild-type strain and a uvrA mutant. We found that the initial steady rate of sfiA expression was proportional to the UV dose and was identical in uvr+ and uvrA backgrounds. This suggests that the initial steady rate of sfiA expression is determined by the initial number of lesions and before any effect of excision repair. We confirmed that after 2 h of expression the net synthesis of sfiA product is, for the same UV dose, about five times lower in uvr+ than in uvrA strains. We show that this is due to earlier repression of the SOS system in uvr+ than in uvrA strains and not to different initial rates.
已对核苷酸切除修复系统对紫外线照射诱导SOS功能sfiA的影响进行了研究。通过在野生型菌株和uvrA突变体中使用sfiA::lacZ操纵子融合来监测sfiA的表达水平。我们发现,sfiA表达的初始稳定速率与紫外线剂量成正比,并且在uvr+和uvrA背景中相同。这表明sfiA表达的初始稳定速率由损伤的初始数量决定,且在切除修复产生任何影响之前。我们证实,在表达2小时后,对于相同的紫外线剂量,uvr+菌株中sfiA产物的净合成比uvrA菌株低约五倍。我们表明,这是由于uvr+菌株中SOS系统的抑制比uvrA菌株更早,而不是由于初始速率不同。