ArticleCell reports2015
Genetic investigation of tricarboxylic acid metabolism during the Plasmodium falciparum life cycle.
Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.
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Who cites it
101 citing papers in PubMed.
- The Plasmodium heme detoxification protein functions in mitochondrial protein synthesis.Nature communications · 2026Article
- A prokaryotic-like cardiolipin synthase is essential to maintain mitochondrial function, lipid homeostasis, and survival of the blood stage malaria parasite Plasmodium falciparum.The Journal of biological chemistry · 2026Article
- Differential expression of mitochondria-associated genes in clinical samples of Plasmodium falciparum showing severe manifestations.BMC genomics · 2026Article
- Mechanisms of PfDNMT2 inhibition and PfATP6-mediated resistance to the antimalarial candidate SC83288 in Plasmodium falciparum.Nature communications · 2026Article
- A metabolism-chromatin axis promotes differential ribosomal RNA transcription in the human malaria parasite.Nature communications · 2025Article
- Disruption of mitochondrial function in blood and sexual stages of Plasmodium falciparum by ferulenol.Parasites & vectors · 2025Article
- Shared host, distinct invaders: metabolomic footprints of plasmodium and babesia in host red cells.Current opinion in hematology · 2025Review
- Targeting Mitochondrial Function inInternational journal of molecular sciences · 2025Review
- Photo Quiz: Unexpected pathogens in the Gram staining of a blood culture smear.Journal of clinical microbiology · 2025Article
- Altered Fibroblast Glutamine Metabolism Is Linked to the Severity of Cardiac Dysfunction in DCMA, a Mitochondrial Cardiomyopathy.Journal of inherited metabolic disease · 2025Article
- Mutational analysis of an antimalarial drug target,Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The dynamin-related protein PfDyn2 is essential for both apicoplast and mitochondrial fission inmBio · 2025Article
- The apicoplast localized isocitrate dehydrogenase is needed forFrontiers in cellular and infection microbiology · 2025Article
- Exploration and characterization of the antimalarial activity of cyclopropyl carboxamides that target the mitochondrial protein, cytochrome b.European journal of medicinal chemistry · 2024Article
- Identification and characterization of thiamine analogs with antiplasmodial activity.Antimicrobial agents and chemotherapy · 2024Article
- Detailing organelle division and segregation in Plasmodium falciparum.The Journal of cell biology · 2024Article
- Mitochondrial ATP synthesis is essential for efficient gametogenesis in Plasmodium falciparum.Communications biology · 2024Article
- Malate dehydrogenase in parasitic protozoans: roles in metabolism and potential therapeutic applications.Essays in biochemistry · 2024Review
- Understanding the significance of oxygen tension on the biology of Plasmodium falciparum blood stages: From the human body to the laboratory.PLoS pathogens · 2024Review
- Transmission-Blocking Strategies for Malaria Eradication: Recent Advances in Small-Molecule Drug Development.Pharmaceuticals (Basel, Switzerland) · 2024Review
41 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors.
Funding
Abstract
New antimalarial drugs are urgently needed to control drug-resistant forms of the malaria parasite Plasmodium falciparum. Mitochondrial electron transport is the target of both existing and new antimalarials. Herein, we describe 11 genetic knockout (KO) lines that delete six of the eight mitochondrial tricarboxylic acid (TCA) cycle enzymes. Although all TCA KOs grew normally in asexual blood stages, these metabolic deficiencies halted life-cycle progression in later stages. Specifically, aconitase KO parasites arrested as late gametocytes, whereas α-ketoglutarate-dehydrogenase-deficient parasites failed to develop oocysts in the mosquitoes. Mass spectrometry analysis of (13)C-isotope-labeled TCA mutant parasites showed that P. falciparum has significant flexibility in TCA metabolism. This flexibility manifested itself through changes in pathway fluxes and through altered exchange of substrates between cytosolic and mitochondrial pools. Our findings suggest that mitochondrial metabolic plasticity is essential for parasite development.
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