ArticleMolecular microbiology2015
Nfu facilitates the maturation of iron-sulfur proteins and participates in virulence in Staphylococcus aureus.
Article in Molecular microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 77 citations in OpenAlex.
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- The Staphylococcus aureus non-coding RNA IsrR regulates TCA cycle activity and virulence.Nucleic acids research · 2025Article
- Development of a Spectrophotometric Assay for the Cysteine Desulfurase fromAntibiotics (Basel, Switzerland) · 2025Article
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- Copper ions inhibit pentose phosphate pathway function in Staphylococcus aureus.PLoS pathogens · 2023Article
- CysB Is a Key Regulator of the Antifungal Activity ofInternational journal of molecular sciences · 2023Article
- A Resourceful Race: Bacterial Scavenging of Host Sulfur Metabolism during Colonization.Infection and immunity · 2022Review
- Mycobacterium tuberculosis requires SufT for Fe-S cluster maturation, metabolism, and survival in vivo.PLoS pathogens · 2022Article
- Identification of Methicillin-ResistantAntibiotics (Basel, Switzerland) · 2022Article
- Adaptive Metabolism ofJournal of proteome research · 2022Article
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
The acquisition and metabolism of iron (Fe) by the human pathogen Staphylococcus aureus is critical for disease progression. S. aureus requires Fe to synthesize inorganic cofactors called iron-sulfur (Fe-S) clusters, which are required for functional Fe-S proteins. In this study we investigated the mechanisms utilized by S. aureus to metabolize Fe-S clusters. We identified that S. aureus utilizes the Suf biosynthetic system to synthesize Fe-S clusters and we provide genetic evidence suggesting that the sufU and sufB gene products are essential. Additional biochemical and genetic analyses identified Nfu as an Fe-S cluster carrier, which aids in the maturation of Fe-S proteins. We find that deletion of the nfu gene negatively impacts staphylococcal physiology and pathogenicity. A nfu mutant accumulates both increased intracellular non-incorporated Fe and endogenous reactive oxygen species (ROS) resulting in DNA damage. In addition, a strain lacking Nfu is sensitive to exogenously supplied ROS and reactive nitrogen species. Congruous with ex vivo findings, a nfu mutant strain is more susceptible to oxidative killing by human polymorphonuclear leukocytes and displays decreased tissue colonization in a murine model of infection. We conclude that Nfu is necessary for staphylococcal pathogenesis and establish Fe-S cluster metabolism as an attractive antimicrobial target.
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