DNA damage response and cell cycle regulation in bacteria: a twist around the paradigm.

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.