ArticleThe EMBO journal2005
The F1-ATP synthase complex in bloodstream stage trypanosomes has an unusual and essential function.
Article in The EMBO journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 131 papers, 1 of them a synthesis that pooled it.
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Who cites it
131 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Novel amidines and analogues as promising agents against intracellular parasites: a systematic review.Parasitology · 2013Pooled it
- A cell surface transporter mediates phenanthridine resistance in African trypanosomes.npj antimicrobials and resistance · 2026Article
- Proteolytic processing of the unique FScientific reports · 2026Article
- Reversal of ATP synthase is a key attribute accompanying cellular differentiation of Trypanosoma brucei insect forms.Communications biology · 2026Article
- TbTim20 facilitates protein import at a low membrane potential in trypanosomes lacking the mitochondrial genome.The FEBS journal · 2026Article
- Genetic origins and proteomic consequences of kinetoplast loss in trypanosomes.PLoS pathogens · 2026Article
- Modular Design of Mitochondrion-Targeted Iron Chelators Allows Highly Selective Antiparasitic Activity against Trypanosomes and Apicomplexan Parasites.ACS infectious diseases · 2026Article
- Assessment of Mitochondrial Membrane Potential in Intact and Detergent-Permeabilized Trypanosoma brucei Insect and Bloodstream Forms.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Article
- The proton motive force maintains mtDNA euploidy by balancing mtDNA replication with cell proliferation.bioRxiv : the preprint server for biology · 2025Article
- Thermo-related degeneration of stumpy forms of Trypanosoma brucei, the pathogen of African sleeping sickness.Advanced biotechnology · 2025Article
- Comparative Quantitative Proteomic Analysis of High and Low Toxin-ProducingMarine drugs · 2025Article
- Comparative mitochondrial genome and transcriptome analyses reveal strain-specific features of RNA editing in Trypanosoma brucei.Nucleic acids research · 2025Article
- Evolutionary divergent kinetoplast genome structure and RNA editing patterns in the trypanosomatidProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Uncovering the Mechanism of Action of Antiprotozoal Agents: A Survey on Photoaffinity Labeling Strategy.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Venturicidin A affects the mitochondrial membrane potential and induces kDNA loss inAntimicrobial agents and chemotherapy · 2024Article
- Mitochondrion of the Trypanosoma brucei long slender bloodstream form is capable of ATP production by substrate-level phosphorylation.PLoS pathogens · 2023Article
- mt-LAF3 is a pseudouridine synthase ortholog required for mitochondrial rRNA and mRNA gene expression in Trypanosoma brucei.International journal for parasitology · 2023Article
- Trypanosome RNA helicase KREH2 differentially controls non-canonical editing and putative repressive structure via a novel proposed 'bifunctional' gRNA in mRNA A6.Nucleic acids research · 2023Article
- How much (ATP) does it cost to build a trypanosome? A theoretical study on the quantity of ATP needed to maintain and duplicate a bloodstream-form Trypanosoma brucei cell.PLoS pathogens · 2023Article
71 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
4 authors.
Funding
Abstract
Survival of bloodstream form Trypanosoma brucei, the agent of African sleeping sickness, normally requires mitochondrial gene expression, despite the absence of oxidative phosphorylation in this stage of the parasite's life cycle. Here we report that silencing expression of the alpha subunit of the mitochondrial F(1)-ATP synthase complex is lethal for bloodstream stage T. brucei as well as for T. evansi, a closely related species that lacks mitochondrial protein coding genes (i.e. is dyskinetoplastic). Our results suggest that the lethal effect is due to collapse of the mitochondrial membrane potential, which is required for mitochondrial function and biogenesis. We also identified a mutation in the gamma subunit of F(1) that is likely to be involved in circumventing the requirement for mitochondrial gene expression in another dyskinetoplastic form. Our data reveal that the mitochondrial ATP synthase complex functions in the bloodstream stage opposite to that in the insect stage and in most other eukaryotes, namely using ATP hydrolysis to generate the mitochondrial membrane potential.
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