ArticleThe Journal of biological chemistry2012
Activation of cholera toxin production by anaerobic respiration of trimethylamine N-oxide in Vibrio cholerae.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 61 citations in OpenAlex.
- The role of cytochrome oxidases in bacterial virulence.Infection and immunity · 2026Review
- Tracking a misclassified pathogen: genomic and epidemiological features ofMicrobial genomics · 2026Article
- Amine-recognizing domain in diverse receptors from bacteria and archaea evolved from the universal amino acid sensor.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Contribution of Trimethylamine N-Oxide (TMAO) to Chronic Inflammatory and Degenerative Diseases.Biomedicines · 2023Review
- Intestinal colonization againstAIMS microbiology · 2023Review
- Vibrio cholerae requires oxidative respiration through the bd-I and cbb3 oxidases for intestinal proliferation.PLoS pathogens · 2022Article
- Population Analysis of Vibrio cholerae in Aquatic Reservoirs Reveals a Novel Sister Species (Applied and environmental microbiology · 2021Article
- Oxidation of trimethylamine to trimethylamineScience advances · 2021Article
- Pathogenicity and virulence regulation ofVirulence · 2020Review
- The Tat system and its dependent cell division proteins are critical for virulence of extra-intestinal pathogenicVirulence · 2020Article
- Genetic Dissection of the Fermentative and Respiratory Contributions Supporting Vibrio cholerae Hypoxic Growth.Journal of bacteriology · 2020Article
- A Hybrid Extracellular Electron Transfer Pathway Enhances the Survival of Vibrio natriegens.Applied and environmental microbiology · 2020Article
- Aerobic Metabolism in Vibrio cholerae Is Required for Population Expansion during Infection.mBio · 2020Article
- Article
- Cholera Toxin Production inFrontiers in microbiology · 2020Article
- Article
- Adaptation ofFrontiers in microbiology · 2020Review
- Commensal-derived metabolites govern Vibrio cholerae pathogenesis in host intestine.Microbiome · 2019Article
- Ubiquinone Biosynthesis over the Entire OmBio · 2019Article
- Stimulating Respiratory Activity Primes Anaerobically GrownPathogens (Basel, Switzerland) · 2018Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vibrio cholerae is a gram-negative bacterium that causes cholera. Although the pathogenesis caused by this deadly pathogen takes place in the intestine, commonly thought to be anaerobic, anaerobiosis-induced virulence regulations are not fully elucidated. Anerobic growth of the V. cholerae strain, N16961, was promoted when trimethylamine N-oxide (TMAO) was used as an alternative electron acceptor. Strikingly, cholera toxin (CT) production was markedly induced during anaerobic TMAO respiration. N16961 mutants unable to metabolize TMAO were incapable of producing CT, suggesting a mechanistic link between anaerobic TMAO respiration and CT production. TMAO reductase is transported to the periplasm via the twin arginine transport (TAT) system. A similar defect in both anaerobic TMAO respiration and CT production was also observed in a N16961 TAT mutant. In contrast, the abilities to grow on TMAO and to produce CT were not affected in a mutant of the general secretion pathway. This suggests that V. cholerae may utilize the TAT system to secrete CT during TMAO respiration. During anaerobic growth with TMAO, N16961 cells exhibit green fluorescence when stained with 2',7'-dichlorofluorescein diacetate, a specific dye for reactive oxygen species (ROS). Furthermore, CT production was decreased in the presence of an ROS scavenger suggesting a positive role of ROS in regulating CT production. When TMAO was co-administered to infant mice infected with N16961, the mice exhibited more severe pathogenic symptoms. Together, our results reveal a novel anaerobic growth condition that stimulates V. cholerae to produce its major virulence factor.
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