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恶性疟原虫裂殖子表面蛋白MSP1的加工激活血影蛋白结合功能,使疟原虫能够从红细胞中逸出。

Processing of Plasmodium falciparum Merozoite Surface Protein MSP1 Activates a Spectrin-Binding Function Enabling Parasite Egress from RBCs.

作者信息

Das Sujaan, Hertrich Nadine, Perrin Abigail J, Withers-Martinez Chrislaine, Collins Christine R, Jones Matthew L, Watermeyer Jean M, Fobes Elmar T, Martin Stephen R, Saibil Helen R, Wright Gavin J, Treeck Moritz, Epp Christian, Blackman Michael J

机构信息

The Francis Crick Institute, Mill Hill Laboratory, Mill Hill, London, NW7 1AA, UK.

Department für Infektiologie, Parasitologie, Universitätsklinikum Heidelberg, D-69120 Heidelberg, Germany.

出版信息

Cell Host Microbe. 2015 Oct 14;18(4):433-44. doi: 10.1016/j.chom.2015.09.007.

Abstract

The malaria parasite Plasmodium falciparum replicates within erythrocytes, producing progeny merozoites that are released from infected cells via a poorly understood process called egress. The most abundant merozoite surface protein, MSP1, is synthesized as a large precursor that undergoes proteolytic maturation by the parasite protease SUB1 just prior to egress. The function of MSP1 and its processing are unknown. Here we show that SUB1-mediated processing of MSP1 is important for parasite viability. Processing modifies the secondary structure of MSP1 and activates its capacity to bind spectrin, a molecular scaffold protein that is the major component of the host erythrocyte cytoskeleton. Parasites expressing an inefficiently processed MSP1 mutant show delayed egress, and merozoites lacking surface-bound MSP1 display a severe egress defect. Our results indicate that interactions between SUB1-processed merozoite surface MSP1 and the spectrin network of the erythrocyte cytoskeleton facilitate host erythrocyte rupture to enable parasite egress.

摘要

疟原虫恶性疟原虫在红细胞内复制,产生子代裂殖子,这些裂殖子通过一个名为逸出的过程从受感染细胞中释放出来,而该过程目前了解甚少。最丰富的裂殖子表面蛋白MSP1是以一种大的前体形式合成的,在逸出之前,它会被寄生虫蛋白酶SUB1进行蛋白水解成熟。MSP1的功能及其加工过程尚不清楚。在这里,我们表明SUB1介导的MSP1加工对寄生虫的生存能力很重要。加工改变了MSP1的二级结构,并激活了其与血影蛋白结合的能力,血影蛋白是一种分子支架蛋白,是宿主红细胞细胞骨架的主要成分。表达加工效率低下的MSP1突变体的寄生虫显示出逸出延迟,而缺乏表面结合MSP1的裂殖子则表现出严重的逸出缺陷。我们的结果表明,SUB-1加工的裂殖子表面MSP1与红细胞细胞骨架的血影蛋白网络之间的相互作用促进了宿主红细胞破裂,从而使寄生虫得以逸出。

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