ArticleMolecular microbiology2024
Converging Roles of the Metal Transporter SMF11 and the Ferric Reductase FRE1 in Iron Homeostasis of Candida albicans.
Article in Molecular microbiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Role ofJournal of fungi (Basel, Switzerland) · 2026Article
- Ferric reductase related proteins Frp1 and Frp2 mediate reductive heme uptake in the opportunistic pathogen Candida albicans.Journal of inorganic biochemistry · 2026Article
- Manganese homeostasis modulates glucan and chitin unmasking in the opportunistic yeastVirulence · 2025Article
- Article
- An Introduction to the Influence of Nutritional Factors on the Pathogenesis of Opportunist Fungal Pathogens in Humans.Pathogens (Basel, Switzerland) · 2025Review
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Authors and funding
7 authors.
Funding
Abstract
Pathogenic fungi must appropriately sense the host availability of essential metals such as Fe. In Candida albicans and other yeasts, sensing of Fe involves mitochondrial Fe-S clusters. Yeast mutants for Fe-S cluster assembly sense Fe limitation even when Fe is abundant and hyperaccumulate Fe. We observe this same disrupted Fe sensing with C. albicans mutants of SMF11, a NRAMP transporter of divalent metals. Mutants of smf11 hyperaccumulate both Mn and Fe and the elevated Mn is secondary to Fe overload. As with Fe-S biogenesis mutants, smf11∆/∆ mutants show upregulation of ferric reductases that are normally repressed under high Fe, and Fe import is activated. However, unlike Fe-S biogenesis mutants, smf11∆/∆ mutants show no defects in mitochondrial Fe-S enzymes. Intriguingly, this exact condition of disrupted Fe sensing without inhibiting Fe-S clusters occurs with C. albicans fre1∆/∆ mutants encoding a ferric reductase. Mutants of fre1 and smf11 display similar perturbations in the cell wall, in filamentation and in the ROS burst of morphogenesis, a Fe-dependent process. As with FRE1, SMF11 is important for virulence in a mouse model for disseminated candidiasis. We propose a model in which FRE1 and SMF11 operate outside the mitochondrial Fe-S pathway to donate ferrous Fe for Fe sensing.
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