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Journal of Bacteriology, November 2009, p. 6788-6795, Vol. 191, No. 22
0021-9193/09/$08.00+0 doi:10.1128/JB.00682-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Channing Laboratory, Brigham and Women's Hospital, and Howard Hughes Medical Institute, Boston, Massachusetts 02115
Received 26 May 2009/ Accepted 1 August 2009
The filamentous bacteriophage CTX
transmits the cholera toxin genes by infecting and lysogenizing its host, Vibrio cholerae. CTX
genes required for virion production initiate transcription from the strong PA 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, PR, and show that RstR both positively and negatively autoregulates its own expression from this promoter. LexA is absolutely required for RstR-mediated activation of PR 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 PR spacer region. Our results indicate that LexA, when bound to its single site in the CTX
prophage, both represses transcription from PA and coactivates transcription from the divergent PR. We propose that LexA coordinates PA and PR prophage transcription in a gene regulatory circuit. This circuit is predicted to display transient switch behavior upon induction of CTX
lysogens.
Published ahead of print on 7 August 2009.
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