Membrane transformation during malaria parasite release from human red blood cells
Membrane transformation during malaria parasite release from human red blood cells
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DOI：
10.1016/j.cub.2005.07.067
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发表时间：
2005-09-20
期刊：
影响因子：
9.2
通讯作者：
Zimmerberg, J
中科院分区：
文献类型：
--
作者：
Glushakova, S;Yin, D;Zimmerberg, J
疟疾寄生虫从受感染的红细胞中释放有三种相反的途径[1][2，3]：成熟寄生虫周围的两层膜协调破裂[4，5];红细胞和寄生虫空泡膜（PVM）融合[6-8];以及封闭在空泡内的寄生虫从红细胞中释放，随后PVM解体[9]。细胞肿胀引起的破裂应产生红细胞血影;膜融合受到内小叶正内曲率两亲物的抑制[10]，这反过来促进膜破裂;在没有蛋白酶抑制剂的情况下[9]，寄生虫将使红细胞堆积在空泡内。因此，我们可视化红细胞释放恶性疟原虫荧光显微镜的差异标记的膜。释放没有产生红细胞鬼，正曲率两亲物没有抑制释放，但促进它，并释放包装裂殖子被证明是一个文物。相反，两个连续的形态学阶段之前的惊厥性膜破裂和分离裂殖子的快速放射状放电，留下隔离的内部膜片段和质膜囊泡或水泡在寄生虫出口的网站。这些结果，连同通过渗透压应力的释放的调制，表明寄生虫释放的途径，其特征在于在压力驱动的膜破裂后折叠的生化改变的红细胞膜。
Three opposing pathways are proposed for the release of malaria parasites [1] from infected erythrocytes [2, 3]: coordinated rupture of the two membranes surrounding mature parasites [4, 5]; fusion of erythrocyte and parasitophorus vacuolar membranes (PVM) [6-8]; and liberation of parasites enclosed within the vacuole from the erythrocyte followed by PVM disintegration [9]. Rupture by cell swelling should yield erythrocyte ghosts; membrane fusion is inhibited by inner-leaflet amphiphiles of positive intrinsic curvature [10], which contrariwise promote membrane rupture; and without protease inhibitors [9], parasites would leave erythrocytes packed within the vacuole. Therefore, we visualized erythrocytes releasing P falciparum using fluorescent microscopy of differentially labeled membranes. Release did not yield erythrocyte ghosts, positive-curvature amphiphiles did not inhibit release but promoted it, and release of packed merozoites was shown to be an artifact. Instead, two sequential morphological stages preceded a convulsive rupture of membranes and rapid radial discharge of separated merozoites, leaving segregated internal membrane fragments and plasma membrane vesicles or blebs at the sites of parasite egress. These results, together with the modulation of release by osmotic stress, suggest a pathway of parasite release that features a biochemically altered erythrocyte membrane that folds after pressure-driven rupture of membranes.