期刊
JOURNAL OF BACTERIOLOGY
卷 191, 期 22, 页码 6788-6795出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JB.00682-09
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- Howard Hughes Medical Institute
- NIH [AI-42347]
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.
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