Vibrio cholerae LexA Coordinates CTX Prophage Gene Expression▿
AUTOR(ES)
Kimsey, Harvey H.
FONTE
American Society for Microbiology (ASM)
RESUMO
The filamentous bacteriophage CTXΦ transmits the cholera toxin genes by infecting and lysogenizing its host, Vibrio cholerae. CTXΦ 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 CTXΦ 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 CTXΦ lysogens.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2772474Documentos Relacionados
- Promoter activities in Vibrio cholerae ctx phi prophage.
- Phenotypes of lexA Mutations in Salmonella enterica: Evidence for a Lethal lexA Null Phenotype Due to the Fels-2 Prophage
- LexA protein of Escherichia coli represses expression of the Tn5 transposase gene.
- Mechanism of action of the lexA gene product.
- The lexA gene product represses its own promoter.