Grinnell F, Tobleman M Q, Hackenbrock C R
J Cell Biol. 1975 Sep;66(3):470-9. doi: 10.1083/jcb.66.3.470.
The distribution and mobility of anionic sites on the surfaces of baby hamster kidney cells were studied by utilizing the multivalent ligand, polycationic ferritin, as a visual probe. Our observations revealed that anionic sites are distributed over the entire cell surface, with the highest density of sites being located on cell surface microextensions. Following the initial binding of polycationic ferritin to the surface of unfixed cells, the ligand-bound anionic sites redistributed by migrating from the surface of microextensions to the surface of the cell body. In 20 min, this migration resulted in a total clearing of anionic sites from the surface of microextensions concomitant with the formation of patches of anionic sites on the surface of the cell body. Polycationic ferritin-induced migration and patch formation of anionic sites was not prevented by 2,4-dinitrophenol, N-ethylmaleimide, colchicine, or cytochalasin B. However, the ligand-induced redistribution of cell surface anionic sites was prevented by prefixation of cells with glutaraldehyde.
利用多价配体聚阳离子铁蛋白作为可视化探针,研究了幼仓鼠肾细胞表面阴离子位点的分布和流动性。我们的观察结果显示,阴离子位点分布在整个细胞表面,位点密度最高的区域位于细胞表面微突起上。在聚阳离子铁蛋白与未固定细胞表面最初结合后,结合配体的阴离子位点通过从微突起表面迁移到细胞体表面而重新分布。在20分钟内,这种迁移导致微突起表面的阴离子位点完全清除,同时在细胞体表面形成阴离子位点斑块。聚阳离子铁蛋白诱导的阴离子位点迁移和斑块形成不受2,4-二硝基苯酚、N-乙基马来酰亚胺、秋水仙碱或细胞松弛素B的影响。然而,细胞用戊二醛预固定可阻止配体诱导的细胞表面阴离子位点重新分布。