ArticleJournal of bacteriology2013
Characterization of BreR interaction with the bile response promoters breAB and breR in Vibrio cholerae.
Article in Journal of bacteriology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Vibrio cholerae RND efflux systems: mediators of stress responses, colonization and pathogenesis.Frontiers in cellular and infection microbiology · 2023Review
- Genetic circuit design automation for the gut resident species Bacteroides thetaiotaomicron.Nature biotechnology · 2020Article
- Survival of the Fittest: How Bacterial Pathogens Utilize Bile To Enhance Infection.Clinical microbiology reviews · 2016Review
- Biofilm Formation and Detachment in Gram-Negative Pathogens Is Modulated by Select Bile Acids.PloS one · 2016Article
- Intestinal GPS: bile and bicarbonate control cyclic di-GMP to provide Vibrio cholerae spatial cues within the small intestine.Gut microbes · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The Vibrio cholerae BreR protein is a transcriptional repressor of the breAB efflux system operon, which encodes proteins involved in bile resistance. In a previous study (F. A. Cerda-Maira, C. S. Ringelberg, and R. K. Taylor, J. Bacteriol. 190:7441-7452, 2008), we used gel mobility shift assays to determine that BreR binds at two independent binding sites at the breAB promoter and a single site at its own promoter. Here it is shown, by DNase I footprinting and site-directed mutagenesis, that BreR is able to bind at a distal and a proximal site in the breAB promoter. However, only one of these sites, the proximal 29-bp site, is necessary for BreR-mediated transcriptional repression of breAB expression. In addition, it was determined that BreR represses its own expression by recognizing a 28-bp site at the breR promoter. These sites comprise regions of dyad symmetry within which residues critical for BreR function could be identified. The BreR consensus sequence AANGTANAC-N(6)-GTNTACNTT overlaps the -35 region at both promoters, implying that the repression of gene expression is achieved by interfering with RNA polymerase binding at these promoters.
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Registered trials
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