期刊
CELL HOST & MICROBE
卷 16, 期 6, 页码 778-786出版社
CELL PRESS
DOI: 10.1016/j.chom.2014.11.006
关键词
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资金
- European Research Council under the EUs Seventh Framework Programme ERC [311502]
- Fundacao para a Ciencia e Tecnologia (FCT) [EXCL/IMI-MIC/0056/ 2012, PTDC/IMI-MIC/1568/2012]
- FP7-Marie Curie Actions Initial Training Networks-Interventions strategies against malaria'' InterMal Training fellowship [PITN-GA-2008-215281]
- Chica and Heinz Schaller Foundation EVIMalaR
- Marie Curie [PIEF-GA-2009-235864]
- FCT [SFRH/BPD/74151/2010, SFRH/BPD/68709/2010, BPD-81953-2011]
- EMBO [ALTF 949-2008, ALTF 357-2009]
- Fundação para a Ciência e a Tecnologia [SFRH/BPD/74151/2010, PTDC/IMI-MIC/1568/2012, SFRH/BPD/68709/2010] Funding Source: FCT
- European Research Council (ERC) [311502] Funding Source: European Research Council (ERC)
During invasion, Plasmodium, the causative agent of malaria, wraps itself in a parasitophorous vacuole membrane (PVM), which constitutes a critical interface between the parasite and its host cell. Within hepatocytes, each Plasmodium sporozoite generates thousands of new parasites, creating high demand for lipids to support this replication and enlarge the PVM. Here, a global analysis of the total lipid repertoire of Plasmodium-infected hepatocytes reveals an enrichment of neutral lipids and the major membrane phospholipid, phosphatidylcholine (PC). While infection is unaffected in mice deficient in key enzymes involved in neutral lipid synthesis and lipolysis, ablation of rate-limiting enzymes in hepatic PC biosynthetic pathways significantly decreases parasite numbers. Host PC is taken up by both P. berghei and P. falciparum and is necessary for correct localization of parasite proteins to the PVM, which is essential for parasite survival. Thus, Plasmodium relies on the abundance of these lipids within hepatocytes to support infection.
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