ArticleInfection and immunity2005
Iron and fur regulation in Vibrio cholerae and the role of fur in virulence.
Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.
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Who cites it
115 citing papers in PubMed, 198 citations in OpenAlex.
- H-NOX and NosP Regulate Flagellar Protein and Virulence Factor Production in Vibrio Cholerae.Molecular & cellular proteomics : MCP · 2026Article
- Phosphate Limitation Modulates Vibrio Cholerae Outer Membrane Vesicle Formation, Composition and Toxicity.Journal of extracellular biology · 2026Article
- Genomic and phenotypic characterization of Vibrio cholerae strain SU109: a genomic investigation of a shrimp-associated strain from Bangladesh.BMC genomics · 2026Article
- Molecular Adaptations of Ferric Uptake Regulator (Fur) Proteins Drive Iron Homeostasis and Pathogenesis in Vibrio Spp.Current microbiology · 2026Review
- Mobile-CRISPRi as a tool for genetic manipulation in the intracellular pathogenApplied and environmental microbiology · 2026Article
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- Computational and experimental mapping of the allosteric network of two manganese ABC transporters.Protein science : a publication of the Protein Society · 2025Article
- Characterization of the ferric uptake regulatorApplied and environmental microbiology · 2024Article
- Structural Perspectives on Metal Dependent Roles of Ferric Uptake Regulator (Fur).Biomolecules · 2024Review
- The dual role of TonB genes in turnerbactin uptake and carbohydrate utilization in the shipworm symbiontApplied and environmental microbiology · 2023Article
- Increased iron utilization and oxidative stress tolerance in aApplied and environmental microbiology · 2023Article
- The Pleiotropic Phenotypes Caused by anMicroorganisms · 2023Article
- Genomics ofPathogens (Basel, Switzerland) · 2023Article
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- Systemic, Mucosal, and Memory Immune Responses following Cholera.Tropical medicine and infectious disease · 2021Review
- Sleeping ribosomes: Bacterial signaling triggers RaiA mediated persistence to aminoglycosides.iScience · 2021Article
- CBS-derived H2S facilitates host colonization of Vibrio cholerae by promoting the iron-dependent catalase activity of KatB.PLoS pathogens · 2021Article
- Iron Reshapes the Gut Microbiome and Host Metabolism.Journal of lipid and atherosclerosis · 2021Review
- Zur: Zinc-Sensing Transcriptional Regulator in a Diverse Set of Bacterial Species.Pathogens (Basel, Switzerland) · 2021Review
- Searching for putative virulence factors in the genomes of Shewanella indica and Shewanella algae.Archives of microbiology · 2021Article
55 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Regulation of iron uptake and utilization is critical for bacterial growth and for prevention of iron toxicity. In many bacterial species, this regulation depends on the iron-responsive master regulator Fur. In this study we report the effects of iron and Fur on gene expression in Vibrio cholerae. We show that Fur has both positive and negative regulatory functions, and we demonstrate Fur-independent regulation of gene expression by iron. Nearly all of the known iron acquisition genes were repressed by Fur under iron-replete conditions. In addition, genes for two newly identified iron transport systems, Feo and Fbp, were found to be negatively regulated by iron and Fur. Other genes identified in this study as being induced in low iron and in the fur mutant include those encoding superoxide dismutase (sodA), fumarate dehydratase (fumC), bacterioferritin (bfr), bacterioferritin-associated ferredoxin (bfd), and multiple genes of unknown function. Several genes encoding iron-containing proteins were repressed in low iron and in the fur mutant, possibly reflecting the need to reserve available iron for the most critical functions. Also repressed in the fur mutant, but independently of iron, were genes located in the V. cholerae pathogenicity island, encoding the toxin-coregulated pilus (TCP), and genes within the V. cholerae mega-integron. The fur mutant exhibited very weak autoagglutination, indicating a possible defect in expression or assembly of the TCP, a major virulence factor of V. cholerae. Consistent with this observation, the fur mutant competed poorly with its wild-type parental strain for colonization of the infant mouse gut.
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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.