ArticleEukaryotic cell2011
Variation among Plasmodium falciparum strains in their reliance on mitochondrial electron transport chain function.
Article in Eukaryotic cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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43 citing papers in PubMed, 65 citations in OpenAlex.
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- 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
- ATAD3 megadalton complex in Plasmodium falciparum is essential for mitochondrial and cellular viability.PLoS pathogens · 2026Article
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- Direct tests of cytochromeProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Direct Tests of Cytochrome Function in the Electron Transport Chain of Malaria Parasites.bioRxiv : the preprint server for biology · 2023Article
- Transcriptional changes in Plasmodium falciparum upon conditional knock down of mitochondrial ribosomal proteins RSM22 and L23.PloS one · 2022Article
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- Design, synthesis, and biological evaluation of multiple targeting antimalarials.Acta pharmaceutica Sinica. B · 2021Article
- Biochemical Studies of Mitochondrial Malate: Quinone Oxidoreductase fromInternational journal of molecular sciences · 2021Article
- Non-canonical metabolic pathways in the malaria parasite detected by isotope-tracing metabolomics.Molecular systems biology · 2021Article
- Exploring Ubiquinone Biosynthesis Inhibition as a Strategy for Improving Atovaquone Efficacy in Malaria.Antimicrobial agents and chemotherapy · 2021Article
- Atypical Molecular Basis for Drug Resistance to Mitochondrial Function Inhibitors in Plasmodium falciparum.Antimicrobial agents and chemotherapy · 2021Article
- Chemoprotective antimalarials identified through quantitative high-throughput screening of Plasmodium blood and liver stage parasites.Scientific reports · 2021Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies demonstrated that Plasmodium falciparum strain D10 became highly resistant to the mitochondrial electron transport chain (mtETC) inhibitor atovaquone when the mtETC was decoupled from the pyrimidine biosynthesis pathway by expressing the fumarate-dependent (ubiquinone-independent) yeast dihydroorotate dehydrogenase (yDHODH) in parasites. To investigate the requirement for decoupled mtETC activity in P. falciparum with different genetic backgrounds, we integrated a single copy of the yDHODH gene into the genomes of D10attB, 3D7attB, Dd2attB, and HB3attB strains of the parasite. The yDHODH gene was equally expressed in all of the transgenic lines. All four yDHODH transgenic lines showed strong resistance to atovaquone in standard short-term growth inhibition assays. During longer term growth with atovaquone, D10attB-yDHODH and 3D7attB-yDHODH parasites remained fully resistant, but Dd2attB-yDHODH and HB3attB-yDHODH parasites lost their tolerance to the drug after 3 to 4 days of exposure. No differences were found, however, in growth responses among all of these strains to the Plasmodium-specific DHODH inhibitor DSM1 in either short- or long-term exposures. Thus, DSM1 works well as a selective agent in all parasite lines transfected with the yDHODH gene, whereas atovaquone works for some lines. We found that the ubiquinone analog decylubiquinone substantially reversed the atovaquone inhibition of Dd2attB-yDHODH and HB3attB-yDHODH transgenic parasites during extended growth. Thus, we conclude that there are strain-specific differences in the requirement for mtETC activity among P. falciparum strains, suggesting that, in erythrocytic stages of the parasite, ubiquinone-dependent dehydrogenase activities other than those of DHODH are dispensable in some strains but are essential in others.
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