ArticleProceedings of the National Academy of Sciences of the United States of America2005
Bile acids induce cholera toxin expression in Vibrio cholerae in a ToxT-independent manner.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
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Who cites it
89 citing papers in PubMed, 161 citations in OpenAlex.
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- Effects of Bile on PathogenicBiomolecules · 2025Article
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- A simple mechanism for integration of quorum sensing and cAMP signalling inbioRxiv : the preprint server for biology · 2023Article
- Modulation of Host-Microbe Metabolism by Cholera Toxin.Infection and immunity · 2023Review
- Host-derived O-glycans inhibit toxigenic conversion by a virulence-encoding phage in Vibrio cholerae.The EMBO journal · 2023Article
- Achieving Single-Molecule Tracking of Subcellular Regulation in Bacteria during Real-Time Environmental Perturbations.Analytical chemistry · 2023Article
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- Intestinal colonization againstAIMS microbiology · 2023Review
- Advances in cholera research: from molecular biology to public health initiatives.Frontiers in microbiology · 2023Review
- Chemical proteomic analysis of bile acid-protein targets inRSC chemical biology · 2022Article
- Co-component signal transduction systems: Fast-evolving virulence regulation cassettes discovered in enteric bacteria.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
29 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
The production of cholera toxin (CT) during Vibrio cholerae infection results in the hallmark diarrhea that characterizes the disease cholera. The transmembrane protein ToxR was originally identified as a functional transcriptional activator of ctxAB in a heterologous Escherichia coli system. However, direct ToxR activation of the ctxAB promoter in V. cholerae has not been previously demonstrated. Instead, a regulatory cascade has been defined in which the activators ToxRS and TcpPH modulate ctxAB expression by acting in concert to transcriptionally activate another regulator, ToxT. ToxT, in turn, directly activates ctxAB expression as well as expression of the tcp genes and other virulence-associated genes. In this study, we show that ToxRS directly activates ctxAB in a ToxT-independent manner in a classical biotype V. cholerae, and that this activation requires the presence of bile acids. Although the levels of CT induced by this mechanism are lower than levels induced under other in vitro conditions, the bile-dependent conditions described here are more physiologic, being independent of pH and temperature. We further show that the inability of bile acids to stimulate ToxRS-dependent expression of CT in El Tor biotype strains is related to the differences between classical and El Tor ctxAB promoters, which differ in the number of heptad TTTTGAT repeats in their respective upstream regions. The ability of bile acids to stimulate direct activation of ctxAB by ToxRS depends upon the transmembrane domain of ToxR, which may interact with bile acids in the inner membrane of V. cholerae.
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