Arthur H M, Cavanagh D R, Finch P W, Emmerson P T
J Bacteriol. 1987 Aug;169(8):3435-40. doi: 10.1128/jb.169.8.3435-3440.1987.
The roles of two putative promoter sequences, P1 and P2, and a potential antiterminator sequence found in the uvrD control region were examined in vivo. Constitutive and SOS-induced levels of uvrD mRNA were determined by S1 mapping, and it was shown that the majority of uvrD transcripts are from P1, while P2 plays only a minor role. A series of increasing deletions from the 5' end of the uvrD gene was used to assay transcription in the promoterless vector pKO-1. Loss of just the -35 region of P1 was sufficient to switch off detectable transcription from both P1 and P2. Disruption of the antiterminator by site-specific mutagenesis had no effect on constitutive levels of transcription, but led to a significant increase over wild-type levels following SOS induction. This suggests that the attenuator comes into play following DNA damage to moderate the increase in UvrD protein synthesis.
在体内研究了uvrD调控区中两个假定的启动子序列P1和P2以及一个潜在的抗终止子序列的作用。通过S1作图确定了uvrD mRNA的组成型和SOS诱导水平,结果表明,大多数uvrD转录本来自P1,而P2仅起次要作用。使用从uvrD基因5'端开始的一系列递增缺失来检测无启动子载体pKO-1中的转录。仅P1的-35区域缺失就足以关闭来自P1和P2的可检测转录。通过位点特异性诱变破坏抗终止子对组成型转录水平没有影响,但在SOS诱导后导致转录水平比野生型水平显著增加。这表明衰减子在DNA损伤后发挥作用,以调节UvrD蛋白合成的增加。