Characterization of a putative DNA-repair mechanism in Corynebacterium

DNA损伤的快速有效修复对于所有细胞恢复生长和防止致命突变至关重要。由于DNA修复对所有细胞的普遍重要性，许多组分，如RecA/Rad 51，从细菌到人类无处不在。几种不同的系统已经进化，用于修复不同的DNA损伤，如碱基损伤，链交联，DNA-蛋白质交联或单链和双链断裂。双链断裂（DSB），如果不修复，总是致命的，因此，对任何细胞都是一个严重的问题。重要的是，DSB也可以出现在DNA复制过程中，当复制叉停止时。因此，细胞编码有效的修复机制，以抵消这些细胞毒性病变。细菌细胞编码一种复杂的DNA损伤反应机制，称为SOS反应。SOS诱导的细胞信号是不寻常的高水平单链DNA。我们已经在谷氨酸棒杆菌中鉴定了一个莱克萨调节的操纵子，称为DipABCD。Dip蛋白与极性支架蛋白DivIVA相互作用，并在由丝裂霉素C或由内切核酸酶（I-SceI）引入的DSB诱导的DNA应激后上调。我们将分析Dip蛋白在C.并解开它们的亚细胞动力学。C.谷氨酸是研究DNA修复的特别有趣的模型系统，因为其不寻常的DNA修复系统子集和不存在非同源末端连接（NHEJ）修复机制。

The fast and efficient repair of DNA damage is essential for all cells to resume growth and prevent lethal mutations. Because of the universal importance of DNA repair to all cells, many components, such as RecA/Rad51, are ubiquitously found from bacteria to man. Several different systems have evolved that serve to repair different DNA damages, such as base lesions, strand cross-links, DNA-protein crosslinks or single – and double strand breaks. Double strand breaks (DSB) are, when left unrepaired, always lethal and, hence, a severe problem to any cell. Importantly, DSBs can also appear during DNA replication, when replication forks are stalled. Thus, cells encode efficient repair mechanisms to counteract these cytotoxic lesions. Bacterial cells encode a sophisticated response mechanism to DNA damage termed SOS response. The cellular signal for SOS induction is an unusual high level of single stranded DNA. We have identified a LexA regulated operon, termed DipABCD, in Corynebacterium glutamicum. Dip proteins interact with the polar scaffold protein DivIVA and are upregulated upon DNA stress induced by mitomycin C or introduced DSBs by endonulceases (I-SceI). We will analyze the function of the Dip proteins in C. glutamicum and unravel their subcellular dynamics. C. glutamicum is a particularly interesting model system to study DNA repair, because of its unusual subset of DNA repair systems and the absence of a non-homologous end-joining (NHEJ) repair mechanism.