ArticleMicrobiology (Reading, England)2012
Manganese transporters Yfe and MntH are Fur-regulated and important for the virulence of Yersinia pestis.
Article in Microbiology (Reading, England), 2012. 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, 49 citations in OpenAlex.
- The Mutation of the DNA-Binding Domain of Fur Protein Enhances the Pathogenicity ofMicroorganisms · 2023Article
- Droplet Tn-Seq identifies the primary secretion mechanism for yersiniabactin in Yersinia pestis.EMBO reports · 2023Article
- Consequences of Disturbing Manganese Homeostasis.International journal of molecular sciences · 2023Review
- The Gonococcal Genetic Island defines distinct sub-populations ofMicrobial genomics · 2023Article
- Live and inactivatedFrontiers in immunology · 2023Article
- Ins and Outs: Recent Advancements in Membrane Protein-Mediated Prokaryotic Ferrous Iron Transport.Biochemistry · 2021Review
- Yersiniabactin contributes to overcoming zinc restriction duringProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Molecular Mechanism of Nramp-Family Transition Metal Transport.Journal of molecular biology · 2021Review
- Intracellular Metal Speciation inACS infectious diseases · 2020Article
- Synergy between Nutritional Immunity and Independent Host Defenses Contributes to the Importance of the MntABC Manganese Transporter duringInfection and immunity · 2019Article
- MntC-Dependent Manganese Transport Is Essential formSphere · 2018Article
- The crystal structure of the Yersinia pestis iron chaperone YiuA reveals a basic triad binding motif for the chelated metal.Acta crystallographica. Section D, Structural biology · 2017Article
- The Metallophore Staphylopine EnablesmBio · 2017Article
- Crystal structure of Yersinia pestis virulence factor YfeA reveals two polyspecific metal-binding sites.Acta crystallographica. Section D, Structural biology · 2017Article
- Zinc transporters YbtX and ZnuABC are required for the virulence of Yersinia pestis in bubonic and pneumonic plague in mice.Metallomics : integrated biometal science · 2017Article
- Manganese scavenging and oxidative stress response mediated by type VI secretion system inProceedings of the National Academy of Sciences of the United States of America · 2017Article
- A Superoxide Dismutase Capable of Functioning with Iron or Manganese Promotes the Resistance of Staphylococcus aureus to Calprotectin and Nutritional Immunity.PLoS pathogens · 2017Article
- Transition Metals and Virulence in Bacteria.Annual review of genetics · 2016Review
- Environmental Regulation of Yersinia Pathophysiology.Frontiers in cellular and infection microbiology · 2016Review
- Discrete Responses to Limitation for Iron and Manganese in Agrobacterium tumefaciens: Influence on Attachment and Biofilm Formation.Journal of bacteriology · 2015Article
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8 authors at 1 institution in 1 country.
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Abstract
Yersinia pestis has a flea-mammal-flea transmission cycle, and is a zoonotic pathogen that causes the systemic diseases bubonic and septicaemic plague in rodents and humans, as well as pneumonic plague in humans and non-human primates. Bubonic and pneumonic plague are quite different diseases that result from different routes of infection. Manganese (Mn) acquisition is critical for the growth and pathogenesis of a number of bacteria. The Yfe/Sit and/or MntH systems are the two prominent Mn transporters in Gram-negative bacteria. Previously we showed that the Y. pestis Yfe system transports Fe and Mn. Here we demonstrate that a mutation in yfe or mntH did not significantly affect in vitro aerobic growth under Mn-deficient conditions. A yfe mntH double mutant did exhibit a moderate growth defect which was alleviated by supplementation with Mn. No short-term energy-dependent uptake of (54)Mn was observed in this double mutant. Like the yfeA promoter, the mntH promoter was repressed by both Mn and Fe via Fur. Sequences upstream of the Fur binding sequence in the yfeA promoter converted an iron-repressible promoter to one that is also repressed by Mn and Fe. To our knowledge, this is the first report identifying cis promoter elements needed to alter cation specificities involved in transcriptional repression. Finally, the Y. pestis yfe mntH double mutant had an ~133-fold loss of virulence in a mouse model of bubonic plague but no virulence loss in the pneumonic plague model. This suggests that Mn availability, bacterial Mn requirements or Mn transporters used by Y. pestis are different in the lungs (pneumonic plague) compared with systemic disease.
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