ArticlePLoS pathogens2023
A malaria parasite phospholipase facilitates efficient asexual blood stage egress.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- An in vivo fitness gene of Toxoplasma, MIC11, is essential for PLP1-mediated egress from host cells.Nature communications · 2026Article
- Article
- A scaleable inducible knockout system for studying essential gene function in the malaria parasite.Nucleic acids research · 2025Article
- Pivotal roles of Plasmodium falciparum lysophospholipid acyltransferase 1 in cell cycle progression and cytostome internalization.Communications biology · 2025Article
- The malaria parasite PP1 phosphatase controls the initiation of the egress pathway of asexual blood-stages by regulating the rounding-up of the vacuole.PLoS pathogens · 2025Article
- Comparative immunological roles of TEP1 inFrontiers in immunology · 2025Review
- Targeting host-specific metabolic pathways-opportunities and challenges for anti-infective therapy.Frontiers in molecular biosciences · 2024Review
- Phospholipases A and Lysophospholipases in protozoan parasites.Microbial cell (Graz, Austria) · 2023Review
- The patatin-like phospholipaseFrontiers in cellular and infection microbiology · 2023Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Malaria parasite release (egress) from host red blood cells involves parasite-mediated membrane poration and rupture, thought to involve membrane-lytic effector molecules such as perforin-like proteins and/or phospholipases. With the aim of identifying these effectors, we disrupted the expression of two Plasmodium falciparum perforin-like proteins simultaneously and showed that they have no essential roles during blood stage egress. Proteomic profiling of parasite proteins discharged into the parasitophorous vacuole (PV) just prior to egress detected the presence in the PV of a lecithin:cholesterol acyltransferase (LCAT; PF3D7_0629300). Conditional ablation of LCAT resulted in abnormal egress and a reduced replication rate. Lipidomic profiles of LCAT-null parasites showed drastic changes in several phosphatidylserine and acylphosphatidylglycerol species during egress. We thus show that, in addition to its previously demonstrated role in liver stage merozoite egress, LCAT is required to facilitate efficient egress in asexual blood stage malaria parasites.
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Registered trials
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 OpenQuestion graph.