Atkinson C T, Aikawa M, Perry G, Fujino T, Bennett V, Davidson E A, Howard R J
Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106.
Eur J Cell Biol. 1988 Feb;45(2):192-9.
The distributions of ankyrin, spectrin, band 3, and glycophorin A were examined in Plasmodium falciparum-infected erythrocytes by immunoelectron microscopy to determine whether movement of parasite proteins and membrane vesicles between the parasitophorous vacuole membrane and erythrocyte surface membrane involves internalization of host membrane skeleton proteins. Monospecific rabbit antisera to spectrin, band 3 and ankyrin and a mouse monoclonal antibody to glycophorin A reacted with these erythrocyte proteins in infected and uninfected human erythrocytes by immunoblotting. Cross-reacting malarial proteins were not detected. The rabbit sera also failed to immunoprecipitate [3H]isoleucine labeled malarial proteins from Triton X-100 and sodium dodecyl sulfate (SDS) extracts of infected erythrocytes. These three antibodies as well as the monoclonal antibody to glycophorin A bound to the membrane skeleton of infected and uninfected erythrocytes. The parasitophorous vacuole membrane was devoid of bound antibody, a result indicating that this membrane contains little, if any, of these host membrane proteins. With ring-, trophozoite- and schizont-infected erythrocytes, spectrin, band 3 and glycophorin A were absent from intracellular membranes including Maurer's clefts and other vesicles in the erythrocyte cytoplasm. In contrast, Maurer's clefts were specifically labeled by anti-ankyrin antibody. There was a slight, corresponding decrease in labeling of the membrane skeleton of infected erythrocytes. A second, morphologically distinct population of circular, vesicle-like membranes in the erythrocyte cytoplasm was not labeled with anti-ankyrin antibody. We conclude that membrane movement between the host erythrocyte surface membrane and parasitophorous vacuole membrane involves preferential sorting of ankyrin into a subpopulation of cytoplasmic membranes.
通过免疫电子显微镜检查恶性疟原虫感染的红细胞中锚蛋白、血影蛋白、带3蛋白和血型糖蛋白A的分布,以确定寄生虫蛋白和膜泡在寄生泡膜与红细胞表面膜之间的移动是否涉及宿主膜骨架蛋白的内化。抗血影蛋白、带3蛋白和锚蛋白的单特异性兔抗血清以及抗血型糖蛋白A的小鼠单克隆抗体,通过免疫印迹法与感染和未感染的人类红细胞中的这些红细胞蛋白发生反应。未检测到交叉反应的疟原虫蛋白。兔血清也未能从感染红细胞的Triton X-100和十二烷基硫酸钠(SDS)提取物中免疫沉淀[3H]异亮氨酸标记的疟原虫蛋白。这三种抗体以及抗血型糖蛋白A的单克隆抗体与感染和未感染红细胞的膜骨架结合。寄生泡膜上没有结合的抗体,这一结果表明该膜中几乎不含有这些宿主膜蛋白(如果有的话)。对于环状体、滋养体和裂殖体感染的红细胞,包括毛氏小体和红细胞胞质中的其他小泡在内的细胞内膜中不存在血影蛋白、带3蛋白和血型糖蛋白A。相比之下,毛氏小体被抗锚蛋白抗体特异性标记。感染红细胞的膜骨架的标记略有相应减少。红细胞胞质中第二种形态上不同的圆形、囊泡样膜群体未被抗锚蛋白抗体标记。我们得出结论,宿主红细胞表面膜与寄生泡膜之间的膜移动涉及锚蛋白优先分选到细胞质膜的一个亚群中。