DNA damage-induced SOS response elicits the induction of cell-division suppressor as well as DNA repair genes. In Gram-positive bacteria, cell-division suppressor genes, so far characterized from Bacillus subtilis (yneA) and Mycobacterium tuberculosis (rv2719c), share limited homology, but are both located in the vicinity of lexA on their respective genomes. Using this proximity to lexA, Corynebacterium glutamicum R divS (cgR1759) was identified as an SOS-inducible cell-division suppressor in this study. The amino acid sequence of DivS showed no homology to that of YneA and Rv2719c. divS expression was markedly induced by DNA-damaging mitomycin C treatment in wild-type cells, but not in its DeltarecA mutant cells, which are unable to induce the SOS response. Wild-type C. glutamicum R cells exposed to DNA-damaging mitomycin C exhibited elongated morphology that, using green fluorescent protein-FtsZ fusion protein, was attributed to defects in FtsZ ring assembly. Cells defective in FtsZ ring assembly were subsequently incapable of septum wall synthesis. In the presence of mitomycin C, divS mutant cells did not exhibit this elongated morphology, whereas cells overexpressing divS were elongated and abnormally branched.

译文

DNA损伤诱导的SOS反应引发细胞分裂抑制因子以及DNA修复基因的诱导。在革兰氏阳性细菌中,到目前为止,以枯草芽孢杆菌(yneA)和结核分枝杆菌(rv2719c)为特征的细胞分裂抑制基因具有有限的同源性,但都位于各自基因组的lexA附近。使用这种接近lexA的方法,谷氨酸棒杆菌R divS(cgR1759)被确定为SOS诱导的细胞分裂抑制剂。 DivS的氨基酸序列与YneA和Rv2719c没有同源性。 DNA破坏性丝裂霉素C处理可在野生型细胞中显着诱导divS表达,而在不能诱导SOS应答的DeltarecA突变细胞中则不会。暴露于破坏DNA的丝裂霉素C的野生型谷氨酸棒状杆菌R细胞表现出细长的形态,该形态使用绿色荧光蛋白-FtsZ融合蛋白归因于FtsZ环装配中的缺陷。 FtsZ环组件中有缺陷的细胞随后无法进行隔壁合成。在存在丝裂霉素C的情况下,divS突变细胞没有表现出这种拉长的形态,而过表达divS的细胞则拉长且异常分支。

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