Magowan C, Coppel R L, Lau A O, Moronne M M, Tchernia G, Mohandas N
Life Sciences Division, Lawrence Berkeley Laboratory, Berkeley, CA, USA.
Blood. 1995 Oct 15;86(8):3196-204.
During intraerythrocytic growth of Plasmodium falciparum, several parasite proteins are transported from the parasite to the erythrocyte membrane, where they bind to membrane skeletal proteins. Mature-parasite-infected erythrocyte surface antigen (MESA) has previously been shown to associate with host erythrocyte membrane skeletal protein 4.1. Using a spontaneous mutant of P falciparum that has lost the ability to synthesize MESA and 4.1-deficient erythrocytes, we examined growth of MESA(+) and MESA(-) parasites in normal and 4.1-deficient erythrocytes. Viability of MESA(+) parasites was reduced in 4.1-deficient erythrocytes as compared with that for normal erythrocytes, but MESA(-) parasites grew equally well in 4.1-deficient and normal erythrocytes. Cytoadherence of MESA(+)- and MESA (-)-parasitized normal and 4.1-deficient erythrocytes to C32 melanoma cells was similar, indicating that neither protein 4.1 nor MESA plays a major role in cytoadherence of infected erythrocytes. Localization of MESA in normal and 4.1-deficient erythrocytes was examined by confocal microscopy. MESA was diffusely distributed in the cytosol of 4.1-deficient erythrocytes but was membrane-associated in normal erythrocytes. These findings suggest that MESA binding to protein 4.1 plays a major role in intraerythrocytic parasite viability.
在恶性疟原虫的红细胞内生长过程中，几种寄生虫蛋白从寄生虫转运至红细胞膜，在那里它们与膜骨架蛋白结合。成熟寄生虫感染的红细胞表面抗原（MESA）先前已被证明与宿主红细胞膜骨架蛋白4.1相关。利用一个已丧失合成MESA能力的恶性疟原虫自发突变体以及缺乏4.1的红细胞，我们检测了MESA（+）和MESA（-）寄生虫在正常和缺乏4.1的红细胞中的生长情况。与正常红细胞相比，MESA（+）寄生虫在缺乏4.1的红细胞中的活力降低，但MESA（-）寄生虫在缺乏4.1的红细胞和正常红细胞中的生长情况相同。MESA（+）和MESA（-）寄生的正常和缺乏4.1的红细胞对C32黑色素瘤细胞的细胞黏附情况相似，表明蛋白4.1和MESA在感染红细胞的细胞黏附中均不发挥主要作用。通过共聚焦显微镜检查了MESA在正常和缺乏4.1的红细胞中的定位。MESA在缺乏4.1的红细胞的胞质溶胶中呈弥散分布，但在正常红细胞中与膜相关。这些发现表明MESA与蛋白4.1的结合在红细胞内寄生虫的活力中起主要作用。
