ArticleNature communications2019
Physiologically relevant reconstitution of iron-sulfur cluster biosynthesis uncovers persulfide-processing functions of ferredoxin-2 and frataxin.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
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87 citing papers in PubMed, 191 citations in OpenAlex.
- Chemical modulation of Miro1 alleviates cell-type-specific vulnerabilities in Friedreich's ataxia.Cell chemical biology · 2026Article
- FeSseqdb: a curated sequence-level database and interpretable machine learning framework for identifying iron-sulfur proteins.BMC bioinformatics · 2026Article
- A Dinuclear Iron(II) Persulfide Complex Reacts with OJournal of the American Chemical Society · 2026Article
- Pathological frataxin deficiency in mice causes tissue-specific alterations in iron homeostasis.iScience · 2026Article
- Bioinformatic Analyses of the Ataxin-2 Family Since Algae Emphasize Its Small Isoforms, Large Chimerisms, and the Importance of Human Exon 1B as Target of Therapies to Prevent Neurodegeneration.International journal of molecular sciences · 2026Article
- Promiscuous Metal Site in Hepatitis B Virus X Protein Binds an Fe-S Cluster.bioRxiv : the preprint server for biology · 2026Article
- Nanobodies as tools for studying human frataxin biology.Communications biology · 2026Article
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- A novel mutation in FDX2 provides insights into the pathogenesis of MEOAL mitochondrial neuromuscular disease.Cell death & disease · 2025Article
- Evaluation of Mitochondrial Complex 1 Density with [Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2025Article
- The cytochrome oxidase defect in ISC-depleted yeast is caused by impaired iron-sulfur cluster maturation of the mitoribosome assembly factor Rsm22.FEBS letters · 2025Article
- Oxygen needs sulfur, sulfur needs oxygen: a relationship of interdependence.The EMBO journal · 2025Review
- Salutary Effects of Overexpression of Rsm22, an Assembly Factor for the Mitochondrial Ribosome, on Frataxin/Yfh1 Depletion Phenotypes inBiomolecules · 2025Article
- The ISC machinery assembles [2Fe-2S] clusters by formation and fusion of [1Fe-1S] precursors.Nature chemical biology · 2025Article
- Shedding Light on the Electron Delocalization Pathway at the [FeInorganic chemistry · 2025Article
- A global perspective on research advances and future challenges in Friedreich ataxia.Nature reviews. Neurology · 2025Review
- Identification of a Selective Inhibitor of Human NFS1, a Cysteine Desulfurase Involved in Fe-S Cluster Assembly, via Structure-Based Virtual Screening.International journal of molecular sciences · 2025Article
- Frataxin Traps Low Abundance Quaternary Structure to Stimulate Human Fe-S Cluster Biosynthesis.Biochemistry · 2025Article
- The human zinc-binding cysteine proteome.Cell · 2025Article
27 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Iron-sulfur (Fe-S) clusters are essential protein cofactors whose biosynthetic defects lead to severe diseases among which is Friedreich's ataxia caused by impaired expression of frataxin (FXN). Fe-S clusters are biosynthesized on the scaffold protein ISCU, with cysteine desulfurase NFS1 providing sulfur as persulfide and ferredoxin FDX2 supplying electrons, in a process stimulated by FXN but not clearly understood. Here, we report the breakdown of this process, made possible by removing a zinc ion in ISCU that hinders iron insertion and promotes non-physiological Fe-S cluster synthesis from free sulfide in vitro. By binding zinc-free ISCU, iron drives persulfide uptake from NFS1 and allows persulfide reduction into sulfide by FDX2, thereby coordinating sulfide production with its availability to generate Fe-S clusters. FXN stimulates the whole process by accelerating persulfide transfer. We propose that this reconstitution recapitulates physiological conditions which provides a model for Fe-S cluster biosynthesis, clarifies the roles of FDX2 and FXN and may help develop Friedreich's ataxia therapies.
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