Markham B E, Harper J E, Mount D W, Sancar G B, Sancar A, Rupp W D, Kenyon C J, Walker G C
J Mol Biol. 1984 Sep 15;178(2):237-48. doi: 10.1016/0022-2836(84)90142-6.
Escherichia coli responds to impairment of DNA synthesis by inducing a system of DNA repair known as the SOS response. Specific genes are derepressed through proteolytic cleavage of their repressor, the lexA gene product. Cleavage in vivo requires functional RecA protein in a role not yet understood. We used mRNA hybridization techniques to follow the rapid changes that occur with induction in cells with mutations in the recA operator or in the repressor cleavage site. These mutations allowed us to uncouple the induction of RecA protein synthesis from its role in inducing the other SOS functions. Following induction with ultraviolet light, we observed increased rates of mRNA synthesis from five SOS genes within five minutes, maximum expression ten to 20 minutes later and then a later decline to near the initial rates. The presence of a recA operator mutation did not significantly influence these kinetics, whereas induction was fully blocked by an additional mutation in the repressor cleavage site. These experiments are consistent with activation of RecA protein preceding repressor cleavage and derepression of SOS genes. The results also suggest that the timing and extent of induction of individual SOS genes may be different.
大肠杆菌通过诱导一种称为SOS应答的DNA修复系统来应对DNA合成的损伤。特定基因通过其阻遏物(lexA基因产物)的蛋白水解切割而解除阻遏。体内切割需要功能性的RecA蛋白,但其作用尚不清楚。我们使用mRNA杂交技术来追踪recA操纵子或阻遏物切割位点发生突变的细胞在诱导时所发生的快速变化。这些突变使我们能够将RecA蛋白合成的诱导与其在诱导其他SOS功能中的作用分离开来。用紫外线诱导后,我们观察到五个SOS基因的mRNA合成速率在五分钟内增加,十到二十分钟后达到最大表达,然后在稍后下降至接近初始速率。recA操纵子突变的存在对这些动力学没有显著影响,而阻遏物切割位点的额外突变则完全阻断了诱导。这些实验与阻遏物切割和SOS基因去阻遏之前RecA蛋白的激活一致。结果还表明,各个SOS基因诱导的时间和程度可能不同。