ArticleProceedings of the National Academy of Sciences of the United States of America2013
Single point mutations in ATP synthase compensate for mitochondrial genome loss in trypanosomes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 1 of them a synthesis that pooled it.
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Who cites it
101 citing papers in PubMed, 1 synthesis or guideline pooled it, 152 citations in OpenAlex.
- African animal trypanocide resistance: A systematic review and meta-analysis.Frontiers in veterinary science · 2022Pooled it
- A cell surface transporter mediates phenanthridine resistance in African trypanosomes.npj antimicrobials and resistance · 2026Article
- A genome-wide genetic screen identifies a novel kDNA replication protein in trypanosomes.Nucleic acids research · 2026Article
- KREPA6 functions in RNA editing catalytic complex structural organization and gRNA utilization in Trypanosoma brucei.Nucleic acids research · 2026Article
- Genetic origins and proteomic consequences of kinetoplast loss in trypanosomes.PLoS pathogens · 2026Article
- TbTim20 facilitates protein import at a low membrane potential in trypanosomes lacking the mitochondrial genome.The FEBS journal · 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
- Why Euglenozoans.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Sustainable Antiparasitic Agents from an Agro-Industrial Waste: Mitochondria-Targeting Cashew Nutshell Liquid-Derived Phosphonium and Ammonium Salts.Journal of medicinal chemistry · 2025Article
- Interventions for Neglected Diseases Caused by Kinetoplastid Parasites: A One Health Approach to Drug Discovery, Development, and Deployment.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Connecting basal body and mitochondrial DNA: TAC53 and the tubular organization of the tripartite attachment complex.PLoS pathogens · 2025Article
- Assembly of the mitochondrial outer membrane module of the trypanosomal tripartite attachment complex.PLoS pathogens · 2025Article
- Uncovering the Unusual Inhibition Mechanism of a Trypanosome Alternative Oxidase Inhibitor Displaying Broad-Spectrum Activity against African Animal Trypanosomes.Journal of medicinal chemistry · 2025Article
- Antitrypanosomal and Antileishmanial Activities ofMolecules (Basel, Switzerland) · 2025Article
- Mechanisms of life cycle simplification in African trypanosomes.Nature communications · 2024Article
- Molecular characterization of the permanent outer-inner membrane contact site of the mitochondrial genome segregation complex in trypanosomes.PLoS pathogens · 2024Article
- KREH2 helicase represses ND7 mRNA editing in procyclic-stage Trypanosoma brucei by opposite modulation of canonical and 'moonlighting' gRNA utilization creating a proposed mRNA structure.Nucleic acids research · 2024Article
- Pam16 and Pam18 were repurposed during Trypanosoma brucei evolution to regulate the replication of mitochondrial DNA.PLoS biology · 2024Article
- Venturicidin A affects the mitochondrial membrane potential and induces kDNA loss inAntimicrobial agents and chemotherapy · 2024Article
- Multiple domains of the integral KREPA3 protein are critical for the structure and precise functions of RNA editing catalytic complexes inRNA (New York, N.Y.) · 2023Article
41 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Viability of the tsetse fly-transmitted African trypanosome Trypanosoma brucei depends on maintenance and expression of its kinetoplast (kDNA), the mitochondrial genome of this parasite and a putative target for veterinary and human antitrypanosomatid drugs. However, the closely related animal pathogens T. evansi and T. equiperdum are transmitted independently of tsetse flies and survive without a functional kinetoplast for reasons that have remained unclear. Here, we provide definitive evidence that single amino acid changes in the nuclearly encoded F1FO-ATPase subunit γ can compensate for complete physical loss of kDNA in these parasites. Our results provide insight into the molecular mechanism of compensation for kDNA loss by showing FO-independent generation of the mitochondrial membrane potential with increased dependence on the ADP/ATP carrier. Our findings also suggest that, in the pathogenic bloodstream stage of T. brucei, the huge and energetically demanding apparatus required for kDNA maintenance and expression serves the production of a single F1FO-ATPase subunit. These results have important implications for drug discovery and our understanding of the evolution of these parasites.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.