The SOS response is an essential process for responding to DNA damage in bacteria. The expression of SOS genes is under the control of LexA, a global transcription factor that undergoes self-cleavage during stress to allow the expression of DNA repair functions and delay cell division until the damage is rectified. LexA also regulates genes that are not part of this cell rescue program, and the induction of bacteriophages, the movement of pathogenicity islands, and the expression of virulence factors and bacteriocins are all controlled by this important transcription factor. Recently it has emerged that when regulating the expression of genes from mobile genetic elements (MGEs), LexA often does so in concert with a corepressor. This accessory regulator can either be a host-encoded global transcription factor, which responds to various metabolic changes, or a factor that is encoded for by the MGE itself. Thus, the coupling of LexA-mediated regulation to a secondary transcription factor not only detaches LexA from its primary SOS role, but also fine-tunes gene expression from the MGE, enabling it to respond to multiple stresses. Here we discuss the mechanisms of such coordinated regulation and its implications for cells carrying such MGEs.
- Bacterial Proteins/genetics
- DNA Damage
- Interspersed Repetitive Sequences
- SOS Response, Genetics
- Serine Endopeptidases/genetics
- Transcription, Genetic