Development and host cell modifications of Plasmodium falciparum blood stages in four dimensions

Grüring C, et al. 2011. Nat. commun. 2(165), doi: 10.1038/ncomms1169.

Speaker: Yu-Cheng Lin (林祐丞)                                  Time: 14:00~15:00, March 2, 2011

Commentator: Chih-Li Lilian Hsu (胥直利老師)        Place: Room 601

Abstract:

Plasmodium falciparum is the most severe form of malaria, and infects more than 300 million people annually, of whom more than 2 million die as a result of the disease1. The life cycle of the parasite is very complex in mosquitoes and humans. The continuous asexual development in human erythrocytes, the blood stages of the parasite life cycle, mainly causes the symptoms of malaria. Therefore, many people would like to study about the development and pathogenesis between the parasite and human erythrocytes in the blood stages. Some studies visualized the blood stages of the parasite in erythrocytes by diverse systems2. However, the complete progression of the parasite through this complex part of the life cycle has never been visualized. The authors used 3D microscopy over time (4D imaging) to show for the first time the development and host cell modifications in the erythrocyte cycle of the parasite. In this study, the ~48h asexual development in erythrocytes with the three successive morphological stages could be visualized clearly. Moreover, the host cell modifications also were visualized completely, and the Maurer’s clefts, a kind of the host cell modification, would be analyzed in detail. The data showed that Maurer’s clefts were formed in very early ring stage, and the total number remains constant until shortly before egress. Thus the export of proteins is independent of cleft formation, and this model challenged the other model that protein export in P. falciparum is linked to the biogenesis of Maurer’s clefts³. These results provide a novel view of the blood-stage development, Maurer’s clefts development, and the links between protein export and Maurer’s clefts in malaria parasites. The authors also open the door to study dynamic processes, drug effects and the phenotype of mutants in malaria parasites.

References:

1.      Show RW et al. 2005. The global distribution of clinical episodes of Plasmodium falciparum malaria. Nature. 434, 214-217.

2.      Gilson PR & Crabb BS. 2009. Morphology and kinetics of the three distinct phases of erythrocyte invasion by Plasmodium falciparum merozoites. Int. J. Parasitol. 39, 91-96.

3.      Tilley L, et al. 2008. The twists and turns of Maurer's cleft trafficking in P. falciparum-infected erythrocytes. Traffic. 9(2):187-97.