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© Thierry Blisnick & Philippe Bastin, Institut Pasteur
Bloodstream Trypanosoma brucei cell
Publication : Cell

Lysophosphatidylcholine Regulates Sexual Stage Differentiation in the Human Malaria Parasite Plasmodium falciparum.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Cell - 14 Dec 2017

Brancucci NMB, Gerdt JP, Wang C, De Niz M, Philip N, Adapa SR, Zhang M, Hitz E, Niederwieser I, Boltryk SD, Laffitte MC, Clark MA, Grüring C, Ravel D, Blancke Soares A, Demas A, Bopp S, Rubio-Ruiz B, Conejo-Garcia A, Wirth DF, Gendaszewska-Darmach E, Duraisingh MT, Adams JH, Voss TS, Waters AP, Jiang RHY, Clardy J, Marti M,

Link to Pubmed [PMID] – 29129376

Link to DOI – S0092-8674(17)31242-410.1016/j.cell.2017.10.020

Cell 2017 Dec; 171(7): 1532-1544.e15

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.