Vibrio cholerae LexA Coordinates CTX Prophage Gene Expression

Abstract

The filamentous bacteriophage CTX Phi transmits the cholera toxin genes by infecting and lysogenizing its host, Vibrio cholerae. CTX Phi genes required for virion production initiate transcription from the strong P(A) promoter, which is dually repressed in lysogens by the phage-encoded repressor RstR and the host-encoded SOS repressor LexA. Here we identify the neighboring divergent rstR promoter, P(R), and show that RstR both positively and negatively autoregulates its own expression from this promoter. LexA is absolutely required for RstR-mediated activation of P(R) transcription. RstR autoactivation occurs when RstR is bound to an operator site centered 60 bp upstream of the start of transcription, and the coactivator LexA is bound to a 16-bp SOS box centered at position -23.5, within the P(R) spacer region. Our results indicate that LexA, when bound to its single site in the CTX Phi prophage, both represses transcription from P(A) and coactivates transcription from the divergent P(R). We propose that LexA coordinates P(A) and P(R) prophage transcription in a gene regulatory circuit. This circuit is predicted to display transient switch behavior upon induction of CTX Phi lysogens.