ArticleScientific reports2016
Selective inhibition of apicoplast tryptophanyl-tRNA synthetase causes delayed death in Plasmodium falciparum.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 43 citations in OpenAlex.
- An essential adaptor for apicoplast fission and inheritance in malaria parasites.Nature communications · 2025Article
- The organization principles of P. falciparum translation initiation features and their potential as drug targets.Nucleic acids research · 2025Article
- An Essential Adaptor for Apicoplast Fission and Inheritance in Malaria Parasites.bioRxiv : the preprint server for biology · 2025Article
- Dissecting apicoplast functions through continuous cultivation of Toxoplasma gondii devoid of the organelle.Nature communications · 2025Article
- The dynamin-related protein PfDyn2 is essential for both apicoplast and mitochondrial fission inmBio · 2025Article
- Apicoplast-derived isoprenoids are essential for biosynthesis of GPI protein anchors, and consequently for egress and invasion in Plasmodium falciparum.PLoS pathogens · 2024Article
- Aminoacyl tRNA Synthetases: Implications of Structural Biology in Drug Development against Trypanosomatid Parasites.ACS omega · 2023Review
- Cytoplasmic isoleucyl tRNA synthetase as an attractive multistage antimalarial drug target.Science translational medicine · 2023Article
- New insights into apicoplast metabolism in blood-stage malaria parasites.Current opinion in microbiology · 2023Review
- PMRT1, amBio · 2022Article
- Dephospho-CoA kinase, a nuclear-encoded apicoplast protein, remains active and essential after Plasmodium falciparum apicoplast disruption.The EMBO journal · 2021Article
- An engineered biosynthetic-synthetic platform for production of halogenated indolmycin antibiotics.Chemical science · 2021Article
- MalDA, Accelerating Malaria Drug Discovery.Trends in parasitology · 2021Review
- Melatonin action in Plasmodium infection: Searching for molecules that modulate the asexual cycle as a strategy to impair the parasite cycle.Journal of pineal research · 2021Review
- Resistance to Some But Not Other Dimeric Lindenane Sesquiterpenoid Esters Is Mediated by Mutations in aACS infectious diseases · 2020Article
- The Plasmodium falciparum eIK1 kinase (PfeIK1) is central for melatonin synchronization in the human malaria parasite. Melatotosil blocks melatonin action on parasite cell cycle.Journal of pineal research · 2020Article
- Article
- Role of Melatonin in the Synchronization of Asexual Forms in the ParasiteBiomolecules · 2020Review
- A mevalonate bypass system facilitates elucidation of plastid biology in malaria parasites.PLoS pathogens · 2020Article
- Antimalarial Properties of Isoquinoline Derivative fromBioMed research international · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The malaria parasite Plasmodium falciparum relies on efficient protein translation. An essential component of translation is the tryptophanyl-tRNA synthetase (TrpRS) that charges tRNA(trp). Here we characterise two isoforms of TrpRS in Plasmodium; one eukaryotic type localises to the cytosol and a bacterial type localises to the remnant plastid (apicoplast). We show that the apicoplast TrpRS aminoacylates bacterial tRNA(trp) while the cytosolic TrpRS charges eukaryotic tRNA(trp). An inhibitor of bacterial TrpRSs, indolmycin, specifically inhibits aminoacylation by the apicoplast TrpRS in vitro, and inhibits ex vivo Plasmodium parasite growth, killing parasites with a delayed death effect characteristic of apicoplast inhibitors. Indolmycin treatment ablates apicoplast inheritance and is rescuable by addition of the apicoplast metabolite isopentenyl pyrophosphate (IPP). These data establish that inhibition of an apicoplast housekeeping enzyme leads to loss of the apicoplast and this is sufficient for delayed death. Apicoplast TrpRS is essential for protein translation and is a promising, specific antimalarial target.
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