Regulation of the SOS response in Bacillus subtilis: evidence for a LexA repressor homolog.
Regulation of the SOS response in Bacillus subtilis: evidence for a LexA repressor homolog.
复制标题
枯草芽孢杆菌中 SOS 反应的调节：LexA 阻遏物同系物的证据。
DOI：
10.1128/jb.173.20.6489-6498.1991
复制
发表时间：
1991
影响因子：
3.2
通讯作者：
Love,PE
中科院分区：
文献类型：
--
作者：
Wojciechowski,MF;Peterson,KR;Love,PE
枯草杆菌中DNA修复和突变的诱导型SOS反应类似于大肠杆菌的广泛表征的SOS系统。在这份报告中，我们证明了细胞阻遏物的E。coli SOS系统中，莱克萨蛋白在B中被特异性切割。在将细胞暴露于诱导SOS反应的DNA损伤处理后，将细胞与枯草芽孢杆菌的DNA结合。体内莱克萨的切割依赖于E.大肠杆菌RecA蛋白同源物在B中。枯草芽孢杆菌（B. subtilis RecA）中产生相同的两个切割片段。在SOS反应诱导后，我们还表明，一个突变形式的E。coli RecA蛋白（RecA 430）可部分替代B中无功能的细胞RecA蛋白。subtilis recA 4突变体，与其在大肠杆菌中的已知活性和缺陷一致。杆菌RecA 430蛋白在大肠杆菌中具有受损的阻遏物切割（莱克萨、UmuD和噬菌体λ cI）功能，部分恢复了与B的遗传交换。subtilis recA 4菌株，但与野生型E. coli RecA蛋白，在B中不能诱导SOS功能（DNA损伤诱导型[din：：Tn 917-lacZ]操纵子的表达或RecA合成）。枯草芽孢杆菌对DNA损伤剂的反应或通常伴随生理能力发展的那些功能。我们的研究结果为B中存在细胞阻遏物提供了支持。subtilis功能上与E. coli莱克萨A阻遏蛋白的表达，并提示B. subtilis RecA蛋白（与E.大肠杆菌）被激活以促进SOS反应的诱导也是保守的。
The inducible SOS response for DNA repair and mutagenesis in the bacterium Bacillus subtilis resembles the extensively characterized SOS system of Escherichia coli. In this report, we demonstrate that the cellular repressor of the E. coli SOS system, the LexA protein, is specifically cleaved in B. subtilis following exposure of the cells to DNA-damaging treatments that induce the SOS response. The in vivo cleavage of LexA is dependent upon the functions of the E. coli RecA protein homolog in B. subtilis (B. subtilis RecA) and results in the same two cleavage fragments as produced in E. coli cells following the induction of the SOS response. We also show that a mutant form of the E. coli RecA protein (RecA430) can partially substitute for the nonfunctional cellular RecA protein in the B. subtilis recA4 mutant, in a manner consistent with its known activities and deficiencies in E. coli. RecA430 protein, which has impaired repressor cleaving (LexA, UmuD, and bacteriophage lambda cI) functions in E.coli, partially restores genetic exchange to B. subtilis recA4 strains but, unlike wild-type E. coli RecA protein, is not capable of inducing SOS functions (expression of DNA damage-inducible [din::Tn917-lacZ] operons or RecA synthesis) in B. subtilis in response to DNA-damaging agents or those functions that normally accompany the development of physiological competence. Our results provide support for the existence of a cellular repressor in B. subtilis that is functionally homologous to the E. coli LexA repressor and suggest that the mechanism by which B. subtilis RecA protein (like RecA of E. coli) becomes activated to promote the induction of the SOS response is also conserved.