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. 2014 Sep;82(9):3636–3643. doi: 10.1128/IAI.01699-14

FIG 1.

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 PA promoter by binding to the high-affinity operator, O1, and two weaker operators, O2 and O3, whereas LexA inhibits transcription from PA by binding a single site (SOS box) that overlaps with the O2 operator. RstR (bound to O1) together with LexA activates transcription from PR, which controls the expression of rstR. When RstR levels become too high, RstR displaces LexA from DNA (occupying O2 and O3), and PR is repressed. DNA damage activates the SOS response, which causes RecA-mediated autocleavage of LexA, leading to repression of PR. Eventually, due to falling levels of RstR, derepression of both PA and PR 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).