Kappe S, Bruderer T, Gantt S, Fujioka H, Nussenzweig V, Ménard R
Department of Pathology, Kaplan Cancer Center, New York University School of Medicine, New York, New York 10016, USA.
J Cell Biol. 1999 Nov 29;147(5):937-44. doi: 10.1083/jcb.147.5.937.
Most Apicomplexan parasites, including the human pathogens Plasmodium, Toxoplasma, and Cryptosporidium, actively invade host cells and display gliding motility, both actions powered by parasite microfilaments. In Plasmodium sporozoites, thrombospondin-related anonymous protein (TRAP), a member of a group of Apicomplexan transmembrane proteins that have common adhesion domains, is necessary for gliding motility and infection of the vertebrate host. Here, we provide genetic evidence that TRAP is directly involved in a capping process that drives both sporozoite gliding and cell invasion. We also demonstrate that TRAP-related proteins in other Apicomplexa fulfill the same function and that their cytoplasmic tails interact with homologous partners in the respective parasite. Therefore, a mechanism of surface redistribution of TRAP-related proteins driving gliding locomotion and cell invasion is conserved among Apicomplexan parasites.
大多数顶复门寄生虫,包括人类病原体疟原虫、弓形虫和隐孢子虫,都会主动侵入宿主细胞并表现出滑行运动,这两种行为均由寄生虫微丝提供动力。在疟原虫子孢子中,血小板反应蛋白相关无名蛋白(TRAP)是一组具有共同粘附结构域的顶复门跨膜蛋白中的一员,它对于滑行运动和感染脊椎动物宿主是必需的。在此,我们提供了遗传学证据,表明TRAP直接参与了一个驱动子孢子滑行和细胞入侵的封帽过程。我们还证明,其他顶复门中的TRAP相关蛋白具有相同的功能,并且它们的细胞质尾巴与各自寄生虫中的同源伴侣相互作用。因此,驱动滑行运动和细胞入侵的TRAP相关蛋白的表面重新分布机制在顶复门寄生虫中是保守的。