FIG 1.

Genetic switch of the CTX phage lysogen, based on previous work (13, 16, 35), and role of the antirepressor RstC (this study). Under normal growth conditions, the phage repressor RstR inhibits transcription from the P_A promoter by binding to the high-affinity operator, O1, and two weaker operators, O2 and O3, whereas LexA inhibits transcription from P_A by binding a single site (SOS box) that overlaps with the O2 operator. RstR (bound to O1) together with LexA activates transcription from P_R, which controls the expression of rstR. When RstR levels become too high, RstR displaces LexA from DNA (occupying O2 and O3), and P_R is repressed. DNA damage activates the SOS response, which causes RecA-mediated autocleavage of LexA, leading to repression of P_R. Eventually, due to falling levels of RstR, derepression of both P_A and P_R occurs. When the levels of LexA return to normal, the switch is reestablished (16, 35). The presence of high levels of the antirepressor RstC is expected to delay the reestablishment of CTX lysogeny (this study).