Altankov G, Grinnell F
Department of Cell Biology and Neuroscience, University of Texas Southwestern Medical Center, Dallas 75235.
Exp Cell Res. 1995 Feb;216(2):299-309. doi: 10.1006/excr.1995.1038.
Potassium-depleted fibroblasts are unable to develop polarized morphology and lack coated pits. Experiments were carried out to measure internalization of fibronectin receptors (FNR) in potassium-depleted cells and possible association of FNR with AP-2 complexes after adding potassium back to the cells, which restores cell polarization. AP-2 complexes are the cell surface component of coated pits that contain both clathrin and membrane receptor binding domains. Potassium-depleted fibroblasts endocytosed antibody-tagged FNR and also internalized fluorescent fibronectin that previously had been adsorbed to the substratum. During cell polarization, antibody-tagged FNR reorganized into fibrillar structures along stress fibers beginning from nucleation sites at cell margins. Plasma membrane AP-2 complexes, which were undetectable in potassium-depleted cells, reappeared at the cell surface above the nucleus and then spread toward the cell margins. The results show that endocytosis of FNR can occur at least partially by a coated pit-independent mechanism.
低钾的成纤维细胞无法形成极化形态且缺乏被膜小窝。开展了实验来测量低钾细胞中纤连蛋白受体（FNR）的内化情况，以及在细胞重新添加钾后FNR与AP - 2复合物的可能关联，钾的添加可恢复细胞极化。AP - 2复合物是被膜小窝的细胞表面成分，包含网格蛋白和膜受体结合结构域。低钾的成纤维细胞内吞抗体标记的FNR，并且也内化了先前吸附在基质上的荧光纤连蛋白。在细胞极化过程中，抗体标记的FNR从细胞边缘的成核位点开始沿着应力纤维重新组织成纤维状结构。质膜AP - 2复合物在低钾细胞中无法检测到，重新出现在细胞核上方的细胞表面，然后向细胞边缘扩散。结果表明，FNR的内吞作用至少部分可以通过一种不依赖被膜小窝的机制发生。
