ArticleMolecular microbiology2016
Thiol-based switch mechanism of virulence regulator AphB modulates oxidative stress response in Vibrio cholerae.
Article in Molecular microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed.
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- Vibrio cholerae virulence is blocked by chitosan oligosaccharide-mediated inhibition of ChsR activity.Nature microbiology · 2024Article
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- Magnetic chitin beads (MCB) coated withGut microbes · 2023Article
- Dps-dependent in vivo mutation enhances long-term host adaptation in Vibrio cholerae.PLoS pathogens · 2023Article
- DegS protease regulates antioxidant capacity and adaptability to oxidative stress environment inFrontiers in cellular and infection microbiology · 2023Article
- PAS Domain-Containing Chemoreceptors Influence the Signal Sensing and Intestinal Colonization ofGenes · 2022Article
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- S-Nitrosylation of the virulence regulator AphB promotes Vibrio cholerae pathogenesis.PLoS pathogens · 2022Article
- ToxT Regulon Is Nonessential for Vibrio cholerae Colonization in Adult Mice.Applied and environmental microbiology · 2022Article
- Thiol-based functional mimicry of phosphorylation of the two-component system response regulator ArcA promotes pathogenesis in enteric pathogens.Cell reports · 2021Article
- CBS-derived H2S facilitates host colonization of Vibrio cholerae by promoting the iron-dependent catalase activity of KatB.PLoS pathogens · 2021Article
- Identification of the Type IX Secretion System Component, PorV (CHU_3238), Involved in Secretion and Localization of Proteins inFrontiers in microbiology · 2021Article
- On or Off: Life-Changing Decisions Made byInfectious microbes & diseases · 2020Review
- Pathogenicity and virulence regulation ofVirulence · 2020Review
- Siderophore piracy enhancesMicrobiology (Reading, England) · 2020Article
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7 authors.
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Abstract
Bacterial pathogens display versatile gene expression to adapt to changing surroundings. For example, Vibrio cholerae, the causative agent of cholera, utilizes distinct genetic programs to combat reactive oxygen species (ROS) in aquatic environments or during host infection. We previously reported that the virulence activator AphB in V. cholerae is involved in ROS resistance. Here by performing a genetic screen, we show that AphB represses ROS resistance gene ohrA, which is also repressed by another regulator, OhrR. Reduced forms of both AphB and OhrR directly bind to the ohrA promoter and repress its expression, whereas organic hydroperoxides such as cumene hydroperoxide (CHP) deactivate AphB and OhrR. OhrA is critical for V. cholerae adult mouse colonization but is dispensable when the mice are treated with antioxidants. Furthermore, similar to our previous finding that AphB and OhrR exhibit different reduction rates during the shift from oxic to anoxic environments, we found that AphB is also oxidized more slowly than OhrR under peroxide stress or exposure to oxygen. This differential regulation optimizes the expression of ohrA and contributes to V. cholerae's ability to survive in a variety of environmental niches that contain different levels of ROS.
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