FIGURE 1.

SOS pathway activation and inhibition. At left, under non-stressed conditions the intact LexA dimer binds to the SOS promoter region and tightly represses SOS protein production. Upon DNA damage RecA binds to DNA fragments to form RecA^∗ filaments that stimulate free LexA to undergo auto-proteolysis. Auto-proteolysis of LexA renders it unable to bind to the SOS promoters leading to expression of the effectors of the SOS pathway. These effectors promote DNA repair, accelerate gene transfer and mutagenesis, and contribute to virulence. At right, genetic inhibition of the SOS response has been shown to antagonize these antibiotic-evasion associated phenotypes and small molecule inhibition of the pathway is therefore a viable pathway for improving the efficacy of antibiotics or targeting virulence.