Vesicle trafficking and cell surface membrane patchiness.
Vesicle trafficking and cell surface membrane patchiness.
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DOI：
10.1016/s0006-3495(01)75691-3
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发表时间：
2001-07
影响因子：
3.4
通讯作者：
Q. Tang;M. Edidin
中科院分区：
文献类型：
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作者：
Q. Tang;M. Edidin
膜蛋白和脂质通常呈斑块状分布在细胞表面。这些斑块通常被认为是膜结构域，由特定的分子结合产生。然而，计算机模拟（Gheber和Edidin， 1999）表明，膜斑块可能是由囊泡运输和横向移动的动态障碍共同造成的。模拟预测，如果囊泡运输受到抑制，在细胞表面看到的蛋白质和脂质的稳态斑块将会衰减。为了验证这一预测，我们比较了I类HLA分子（整体膜蛋白）在抑制细胞表面内吞囊泡运输之前和之后的表观大小和强度，无论是通过高渗培养基孵育还是通过显性阴性突变动力蛋白的表达。正如模拟预测的那样，在胞吞作用和囊泡运输被抑制后，HLA斑块的表观大小增加，而其强度降低。
Membrane proteins and lipids often appear to be distributed in patches on the cell surface. These patches are often assumed to be membrane domains, arising from specific molecular associations. However, a computer simulation (Gheber and Edidin, 1999) shows that membrane patchiness may result from a combination of vesicle trafficking and dynamic barriers to lateral mobility. The simulation predicts that the steady-state patches of proteins and lipids seen on the cell surface will decay if vesicle trafficking is inhibited. To test this prediction, we compared the apparent sizes and intensities of patches of class I HLA molecules, integral membrane proteins, before and after inhibiting endocytic vesicle traffic from the cell surface, either by incubation in hypertonic medium or by expression of a dominant-negative mutant dynamin. As predicted by the simulation, the apparent sizes of HLA patches increased, whereas their intensities decreased after endocytosis and vesicle trafficking were inhibited.