ArticlePLoS pathogens2013
The suf iron-sulfur cluster synthesis pathway is required for apicoplast maintenance in malaria parasites.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 136 citations in OpenAlex.
- Article
- The spatial proteome of the Plasmodium falciparum schizont illuminates the composition and evolutionary trajectories of its organelles.Nature communications · 2026Article
- Fifty shades of iron: Unorthodox mechanisms of iron acquisition and utilization in blood-stage Plasmodium parasites.PLoS pathogens · 2026Review
- An apicoplast-localized GTPase is essential formSphere · 2026Article
- Monothiol glutaredoxins in microbial iron metabolism: From iron-sulfur cluster trafficking to iron-dependent regulation.Advances in microbial physiology · 2026Review
- An essential adaptor for apicoplast fission and inheritance in malaria parasites.Nature communications · 2025Article
- An Essential Adaptor for Apicoplast Fission and Inheritance in Malaria Parasites.bioRxiv : the preprint server for biology · 2025Article
- Decoding the Minimal Translation System of the Plasmodium falciparum Apicoplast: Essential tRNA-modifying Enzymes and Their Roles in Organelle Maintenance.Journal of molecular biology · 2025Article
- The dynamin-related protein PfDyn2 is essential for both apicoplast and mitochondrial fission inmBio · 2025Article
- tRNA modifying enzymes MnmE and MnmG are essential forbioRxiv : the preprint server for biology · 2025Article
- Targeting Malaria's Achilles' Heels: A Review of Plasmodium Life Cycle Vulnerabilities for Drug Discovery.Current topics in medicinal chemistry · 2025Review
- Identification of a divalent metal transporter required for cellular iron metabolism in malaria parasites.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- ATM1, an essential conserved transporter in Apicomplexa, bridges mitochondrial and cytosolic [Fe-S] biogenesis.PLoS pathogens · 2024Article
- Identification of a divalent metal transporter required for cellular iron metabolism in malaria parasites.bioRxiv : the preprint server for biology · 2024Article
- Apicoplast-Resident Processes: Exploiting the Chink in the Armour ofAdvances in pharmacological and pharmaceutical sciences · 2024Review
- Coordination of apicoplast transcription in a malaria parasite by internal and host cues.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Article
- TheeLife · 2023Article
- Regulation of Mitochondrial Energy Metabolism by Glutaredoxin 5 in the Apicomplexan Parasite Neospora caninum.Microbiology spectrum · 2023Article
- New insights into apicoplast metabolism in blood-stage malaria parasites.Current opinion in microbiology · 2023Review
6 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The apicoplast organelle of the malaria parasite Plasmodium falciparum contains metabolic pathways critical for liver-stage and blood-stage development. During the blood stages, parasites lacking an apicoplast can grow in the presence of isopentenyl pyrophosphate (IPP), demonstrating that isoprenoids are the only metabolites produced in the apicoplast which are needed outside of the organelle. Two of the isoprenoid biosynthesis enzymes are predicted to rely on iron-sulfur (FeS) cluster cofactors, however, little is known about FeS cluster synthesis in the parasite or the roles that FeS cluster proteins play in parasite biology. We investigated two putative FeS cluster synthesis pathways (Isc and Suf) focusing on the initial step of sulfur acquisition. In other eukaryotes, these proteins can be located in multiple subcellular compartments, raising the possibility of cross-talk between the pathways or redundant functions. In P. falciparum, SufS and its partner SufE were found exclusively the apicoplast and SufS was shown to have cysteine desulfurase activity in a complementation assay. IscS and its effector Isd11 were solely mitochondrial, suggesting that the Isc pathway cannot contribute to apicoplast FeS cluster synthesis. The Suf pathway was disrupted with a dominant negative mutant resulting in parasites that were only viable when supplemented with IPP. These parasites lacked the apicoplast organelle and its organellar genome--a phenotype not observed when isoprenoid biosynthesis was specifically inhibited with fosmidomycin. Taken together, these results demonstrate that the Suf pathway is essential for parasite survival and has a fundamental role in maintaining the apicoplast organelle in addition to any role in isoprenoid biosynthesis.
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