Characterization of a putative DNA-repair mechanism in Corynebacterium

快速有效地修复DNA损伤对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，许多成分，如RecA/Rad51，从细菌到人类无处不在。已经进化出几种不同的系统，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）如果不进行修复，总是致命的，因此对任何细胞来说都是一个严重的问题。重要的是，当DNA复制分叉停止时，dsb也会出现。因此，细胞编码有效的修复机制来抵消这些细胞毒性病变。细菌细胞编码一个复杂的反应机制，DNA损伤称为SOS反应。SOS诱导的细胞信号是异常高水平的单链DNA。我们已经在谷氨酸棒状杆菌中发现了一个LexA调控的操纵子，称为DipABCD。Dip蛋白与极性支架蛋白DivIVA相互作用，并在丝裂霉素C诱导的DNA胁迫或由内源性氨基酸（I-SceI）引入的DSBs时上调。我们将分析谷氨酸酵母中Dip蛋白的功能，并揭示它们的亚细胞动力学。谷氨酰胺是研究DNA修复的一个特别有趣的模型系统，因为它是DNA修复系统的一个不同寻常的子集，并且缺乏非同源末端连接（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.