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首页> 外文期刊>Molecular and Cellular Biology >Insulin Stimulates Membrane Fusion and GLUT4 Accumulation in Clathrin Coats on Adipocyte Plasma Membranes
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Insulin Stimulates Membrane Fusion and GLUT4 Accumulation in Clathrin Coats on Adipocyte Plasma Membranes

机译：胰岛素刺激脂肪细胞血浆膜上网格蛋白外套的膜融合和GLUT4积累。

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Total internal reflection fluorescence (TIRF) microscopy reveals highly mobile structures containing enhanced green fluorescent protein-tagged glucose transporter 4 (GLUT4) within a zone about 100 nm beneath the plasma membrane of 3T3-L1 adipocytes. We developed a computer program (Fusion Assistant) that enables direct analysis of the docking/fusion kinetics of hundreds of exocytic fusion events. Insulin stimulation increases the fusion frequency of exocytic GLUT4 vesicles by ～4-fold, increasing GLUT4 content in the plasma membrane. Remarkably, insulin signaling modulates the kinetics of the fusion process, decreasing the vesicle tethering/docking duration prior to membrane fusion. In contrast, the kinetics of GLUT4 molecules spreading out in the plasma membrane from exocytic fusion sites is unchanged by insulin. As GLUT4 accumulates in the plasma membrane, it is also immobilized in punctate structures on the cell surface. A previous report suggested these structures are exocytic fusion sites (Lizunov et al., J. Cell Biol. 169:481-489, 2005). However, two-color TIRF microscopy using fluorescent proteins fused to clathrin light chain or GLUT4 reveals these structures are clathrin-coated patches. Taken together, these data show that insulin signaling accelerates the transition from docking of GLUT4-containing vesicles to their fusion with the plasma membrane and promotes GLUT4 accumulation in clathrin-based endocytic structures on the plasma membrane.
机译：全内反射荧光（TIRF）显微镜显示在3T3-L1脂肪细胞质膜下方约100 nm区域内包含增强的绿色荧光蛋白标签葡萄糖转运蛋白4（GLUT4）的高度活动的结构。我们开发了一个计算机程序（Fusion Assistant），可以直接分析数百种胞外融合事件的对接/融合动力学。胰岛素刺激使胞外GLUT4囊泡的融合频率增加约4倍，从而增加了质膜中GLUT4的含量。值得注意的是，胰岛素信号传导调节融合过程的动力学，从而减少了膜融合之前的囊泡束缚/对接持续时间。相反，胰岛素从细胞外融合部位在质膜中扩散的GLUT4分子的动力学没有改变。当GLUT4积聚在质膜中时，它也被固定在细胞表面的点状结构中。先前的报道表明这些结构是胞外融合位点（Lizunov等人，J.Cell Biol.169：481-489，2005）。但是，使用融合到网格蛋白轻链或GLUT4上的荧光蛋白的双色TIRF显微镜检查显示这些结构是网格蛋白包被的斑块。综上所述，这些数据表明胰岛素信号传导加速了从含GLUT4的囊泡对接过渡到它们与质膜融合的过程，并促进了GLUT4在质膜上基于网格蛋白的内吞结构中的积累。

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