Fig. 3.

Model for activation or repression of QS, excision, and transfer of ICEMlSym^R7A. (A) In cells that are repressed for qseM expression by QseC (10), TraR complexed with N-(3-oxo-hexanoyl)-L-homoserine lactone (3-oxo-C6-HSL) activates expression from the traI1 promoter and from the promoter of traI2–msi172–msi171 (11). This activation leads to increased production of 3-oxo-C6-HSL, as observed in strain R7AΔqseM (10). Increased transcription of traI2–msi172–msi171 leads to increased translation of msi172–msi171. In 3.9–12.8% of translation events (Fig. 1C and Fig. S4), a PRF event occurs, resulting in the production of the master activator FseA. FseA activates transcription from the rdfS promoter, resulting in increased expression of the excisionase RdfS, the prepilin protease TraF, and the predicted murein hydrolase Msi107 (9). It remains unknown whether expression of other ICEMlSym^R7A transfer genes including rlxS (dotted line) is also activated. In the absence of qseM, activation by FseA leads to excision in 40–100% of cells (depending on growth phase) and a 1,000-fold increase in conjugative transfer (10). (B) In cells that contain insufficient QseC to repress qseM expression (10), QseM is expressed and interacts with TraR–3-oxo-C6-HSL, inhibiting transcription of traI1, 3-oxo-C6-HSL production, and transcription of traI2–msi172–msi171 (11). QseM also binds FseA (Fig. 2), preventing any activation of the rdfS promoter that might result from leaky expression of traI2–msi172–msi171.