PDF(Pubmed)
Abstract：
The co-protease activity in the RecA-ssDNA complex cleaves the autorepressor LexA, resulting in the derepression of a large number of genes under LexA control. This process is called the SOS response, and genes that are expressed in response to DNA damage are called SOS genes. The proteins encoded by the SOS genes are involved in both DNA repair and maintaining the functions of crucial cell division proteins (e.g., FtsZ) under check until the damaged DNA is presumably repaired. This mechanism of SOS response is the only known mechanism of DNA damage response and cell cycle regulation in bacteria. However, there are bacteria that do not obey this rule of DNA damage response and cell cycle regulation, yet they respond to DNA damage, repair it, and survive. That means such bacteria would have some alternate mechanism(s) of DNA damage response and cell cycle regulation beyond the canonical pathway of the SOS response. In this study, we present the perspectives that bacteria may have other mechanisms of DNA damage response and cell cycle regulation mediated by bacterial eukaryotic type Ser/Thr protein kinases as an alternate to the canonical SOS response and herewith elaborate on them with a well-studied example in the radioresistant bacterium Deinococcus radiodurans.
摘要：
RecA-ssDNA复合物中的共蛋白酶活性裂解自抑制因子LexA，导致LexA控制下的大量基因的抑制。这个过程称为SOS响应，响应DNA损伤而表达的基因称为SOS基因。SOS基因编码的蛋白质参与DNA修复和维持关键细胞分裂蛋白的功能（例如，FtsZ）进行检查，直到可能修复了受损的DNA。这种SOS应答机制是细菌中唯一已知的DNA损伤应答和细胞周期调控机制。然而,有些细菌不遵守DNA损伤反应和细胞周期调控的规律，然而它们对DNA损伤有反应，修复它,和生存。这意味着此类细菌将具有超出SOS应答的典型途径的DNA损伤应答和细胞周期调节的一些替代机制。在这项研究中,我们提出了细菌可能具有由细菌真核类型Ser/Thr蛋白激酶介导的DNA损伤反应和细胞周期调节的其他机制的观点，作为经典SOS反应的替代，并在此以放射性抗性细菌中充分研究的例子来阐述它们。
