ArticleJournal of bacteriology2009
Vibrio cholerae LexA coordinates CTX prophage gene expression.
Article in Journal of bacteriology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- A 3'UTR-derived small RNA modulates the life cycle of the cholera toxin-encoding filamentous phage, CTXϕ.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Whole-genome comparison using complete genomes fromFrontiers in microbiology · 2024Article
- The transcriptional regulator CtrA controls gene expression in Alphaproteobacteria phages: Evidence for a lytic deferment pathway.Frontiers in microbiology · 2022Article
- ThemSphere · 2021Article
- Replication Region Analysis Reveals Non-lambdoid Shiga Toxin Converting Bacteriophages.Frontiers in microbiology · 2021Article
- Molecular insights into the genome dynamics and interactions between core and acquired genomes ofProceedings of the National Academy of Sciences of the United States of America · 2020Article
- The SOS Response Mediates Sustained Colonization of the Mammalian Gut.Infection and immunity · 2019Article
- Lytic gene expression in the temperate bacteriophage GIL01 is activated by a phage-encoded LexA homologue.Nucleic acids research · 2018Article
- Expansion of the SOS regulon of Vibrio cholerae through extensive transcriptome analysis and experimental validation.BMC genomics · 2018Article
- Effect of LexA on Chromosomal Integration of CTXϕ in Vibrio cholerae.Journal of bacteriology · 2016Article
- Bacteriophage GIL01 gp7 interacts with host LexA repressor to enhance DNA binding and inhibit RecA-mediated auto-cleavage.Nucleic acids research · 2015Article
- Survival and proliferation of the lysogenic bacteriophage CTXΦ in Vibrio cholerae.Virologica Sinica · 2015Review
- RS1 satellite phage promotes diversity of toxigenic Vibrio cholerae by driving CTX prophage loss and elimination of lysogenic immunity.Infection and immunity · 2014Article
- Coevolution of bacteria and their viruses.Folia microbiologica · 2013Review
- Analysis of the SOS response of Vibrio and other bacteria with multiple chromosomes.BMC genomics · 2012Article
- Phage-borne factors and host LexA regulate the lytic switch in phage GIL01.Journal of bacteriology · 2011Article
- Bacteriophage crosstalk: coordination of prophage induction by trans-acting antirepressors.PLoS genetics · 2011Article
- The complete genome sequence of 'Candidatus Liberibacter solanacearum', the bacterium associated with potato zebra chip disease.PloS one · 2011Article
- A new twist on a classic paradigm: illumination of a genetic switch in Vibrio cholerae phage CTX Phi.Journal of bacteriology · 2009Article
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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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.