ArticlePLoS pathogens2018
The Vibrio cholerae RND efflux systems impact virulence factor production and adaptive responses via periplasmic sensor proteins.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- Host Factor Induced Bacterial Extracellular Vesicles Promote Horizontal Gene Transfer in Vibrio cholerae.Journal of extracellular vesicles · 2026Article
- How resistance-nodulation-division (RND) efflux pumps contribute to virulence.PLoS pathogens · 2026Review
- Two-component systems in Vibrio species: Regulation of virulence and implications for therapeutic development.Folia microbiologica · 2026Review
- RND-mediated efflux couples antimicrobial resistance and hypervirulence in contemporary Vibrio cholerae.PLoS pathogens · 2026Article
- The carRS-ompV-virK operon of Vibrio cholerae senses antimicrobial peptides and activates the expression of multiple resistance systems.Scientific reports · 2025Article
- Non-O1/Non-O139Microorganisms · 2024Review
- Prevalence, antibiotic susceptibility, and genomic analysis ofFrontiers in microbiology · 2024Article
- Article
- Article
- Vibrio cholerae RND efflux systems: mediators of stress responses, colonization and pathogenesis.Frontiers in cellular and infection microbiology · 2023Review
- Intestinal colonization againstAIMS microbiology · 2023Review
- Biological and transcriptional studies reveal VmeL is involved in motility, biofilm formation and virulence inFrontiers in microbiology · 2022Article
- Bile Salts Promote ToxR Regulon Activation during Growth under Virulence-Inducing Conditions.Infection and immunity · 2021Article
- Vibrio cholerae TolC Is Required for Expression of the ToxR Regulon.Infection and immunity · 2021Article
- ToxR Mediates the Antivirulence Activity of Phenyl-Arginine-β-Naphthylamide To Attenuate Vibrio cholerae Virulence.Infection and immunity · 2021Article
- The periplasmic domains of Vibriocholerae ToxR and ToxS are forming a strong heterodimeric complex independent on the redox state of ToxR cysteines.Molecular microbiology · 2021Article
- Biosensing in Smart Engineered Probiotics.Biotechnology journal · 2020Review
- Vibrio cholerae OmpR Contributes to Virulence Repression and Fitness at Alkaline pH.Infection and immunity · 2020Article
- Vibrio cholerae OmpR Represses the ToxR Regulon in Response to Membrane Intercalating Agents That Are Prevalent in the Human Gastrointestinal Tract.Infection and immunity · 2020Article
- Virulence Regulation and Innate Host Response in the Pathogenicity ofFrontiers in cellular and infection microbiology · 2020Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Resistance-nodulation-division (RND) efflux systems are ubiquitous transporters in Gram-negative bacteria that are essential for antibiotic resistance. The RND efflux systems also contribute to diverse phenotypes independent of antimicrobial resistance, but the mechanism by which they affect most of these phenotypes is unclear. This is the case in Vibrio cholerae where the RND systems function in antimicrobial resistance and virulence factor production. Herein, we investigated the linkage between RND efflux and V. cholerae virulence. RNA sequencing revealed that the loss of RND efflux affected the activation state of periplasmic sensing systems including the virulence regulator ToxR. Activation of ToxR in an RND null mutant resulted in ToxR-dependent transcription of the LysR-family regulator leuO. Increased leuO transcription resulted in the repression of the ToxR virulence regulon and attenuated virulence factor production. Consistent with this, leuO deletion restored virulence factor production in an RND-null mutant, but not its ability to colonize infant mice; suggesting that RND efflux was epistatic to virulence factor production for colonization. The periplasmic sensing domain of ToxR was required for the induction of leuO transcription in the RND null mutant, suggesting that ToxR responded to metabolites that accumulated in the periplasm. Our results suggest that ToxR represses virulence factor production in response to metabolites that are normally effluxed from the cell by the RND transporters. We propose that impaired RND efflux results in periplasmic metabolite accumulation, which then activates periplasmic sensors including ToxR and two-component regulatory systems to initiate the expression of adaptive responses.
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Registered trials
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.