Witkin E M, Kogoma T
Proc Natl Acad Sci U S A. 1984 Dec;81(23):7539-43. doi: 10.1073/pnas.81.23.7539.
DNA damage activates RecA protein of E. coli to a form (RecA*) that promotes proteolytic cleavage of LexA protein, the repressor of at least 17 DNA damage-inducible genes, resulting in expression of the SOS response. In addition to this known role, RecA* performs another function necessary for expression of SOS mutagenesis [Blanco, M., Herrera, G., Collado, P., Rebollo, J. & Botella, L. M. (1982) Biochimie 64, 633-636]. The additional role of RecA* could be (i) cleavage of another repressor, (ii) proteolytic processing of one or more proteins, or (iii) mechanistic interaction with DNA or with one or more other proteins. We describe experiments designed to test the first possibility. Our results suggest that neither SOS mutator activity nor ultraviolet mutagenesis requires induction by RecA* of any gene(s) outside the LexA regulon and that the additional role of RecA* is not cleavage of another repressor. We show that stable DNA replication, another DNA damage-inducible function [Kogoma, T., Torrey, T. A. & Connaughton, M. J. (1979) Mol. Gen. Genet. 176, 1-9], shares with SOS mutagenesis the requirement for RecA* activity, even in a strain constitutively expressing all LexA-controlled genes. In this strain, conditions that activate RecA initiate expression of stable DNA replication in the presence of chloramphenicol, without an intervening period of protein synthesis. We conclude that the additional function of RecA* in stable DNA replication is not another antirepressor activity.
DNA损伤会将大肠杆菌的RecA蛋白激活为一种形式（RecA*），这种形式会促进LexA蛋白的蛋白水解切割，LexA蛋白是至少17个DNA损伤诱导基因的阻遏物，从而导致SOS应答的表达。除了这个已知作用外，RecA还执行SOS诱变表达所必需的另一个功能[布兰科，M.，埃雷拉，G.，科利亚多，P.，雷博洛，J. & 博特拉，L.M.（1982年）《生物化学》64卷，633 - 636页]。RecA的额外作用可能是：（i）切割另一种阻遏物；（ii）对一种或多种蛋白质进行蛋白水解加工；或者（iii）与DNA或一种或多种其他蛋白质发生机制性相互作用。我们描述了旨在测试第一种可能性的实验。我们的结果表明，SOS诱变活性和紫外线诱变都不需要RecA诱导LexA调控子之外的任何基因，并且RecA的额外作用不是切割另一种阻遏物。我们表明，稳定DNA复制是另一种DNA损伤诱导功能[小滨，T.，托里，T.A. & 康诺顿，M.J.（1979年）《分子与普通遗传学》176卷，1 - 9页]，即使在组成型表达所有LexA控制基因的菌株中，它与SOS诱变一样需要RecA活性。在该菌株中，激活RecA的条件会在氯霉素存在的情况下启动稳定DNA复制的表达，而无需中间的蛋白质合成期。我们得出结论，RecA在稳定DNA复制中的额外功能不是另一种抗阻遏物活性。
