Transmission represents a population bottleneck in the Plasmodium life cycle and a key intervention target of ongoing efforts to eradicate malaria. Sexual differentiation is essential for this process, as only sexual parasites, called gametocytes, are infective to the mosquito vector. Gametocyte production rates vary depending on environmental conditions, but external stimuli remain obscure. Here, we show that the host-derived lipid lysophosphatidylcholine (LysoPC) controls P. falciparum cell fate by repressing parasite sexual differentiation. We demonstrate that exogenous LysoPC drives biosynthesis of the essential membrane component phosphatidylcholine. LysoPC restriction induces a compensatory response, linking parasite metabolism to the activation of sexual-stage-specific transcription and gametocyte formation. Our results reveal that malaria parasites can sense and process host-derived physiological signals to regulate differentiation. These data close a critical knowledge gap in parasite biology and introduce a major component of the sexual differentiation pathway in Plasmodium that may provide new approaches for blocking malaria transmission.
Pubmed ID: 29129376 RIS Download
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Functional genomic database for malaria parasites. Database for Plasmodium spp. Provides resource for data analysis and visualization in gene-by-gene or genome-wide scale. PlasmoDB 5.5 contains annotated genomes, evidence of transcription, proteomics evidence, protein function evidence, population biology and evolution data. Data can be queried by selecting from query grid or drop down menus. Results can be combined with each other on query history page. Search results can be downloaded with associated functional data and registered users can store their query history for future retrieval or analysis.Key community database for malaria researchers, intersecting many types of laboratory and computational data, aggregated by gene.
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