Role of type I myosins in receptor-mediated endocytosis in yeast
Role of type I myosins in receptor-mediated endocytosis in yeast
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DOI：
10.1126/science.272.5261.533
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发表时间：
1996-04-26
期刊：
影响因子：
56.9
通讯作者：
Riezman, H
中科院分区：
文献类型：
--
作者：
Geli, MI;Riezman, H
I型肌凝蛋白被认为驱动肌动蛋白依赖的膜运动，但在体内直接证明它们参与特定的细胞过程是困难的。编码酵母I型肌球蛋白的基因MYO3和MYO5的缺失几乎破坏了酵母的生长。与MYO5温度敏感等位基因（MYO5 -1）互补的双缺失突变体在受体介导的内吞作用的内化步骤中表现出强烈缺陷，而分泌途径显然未受影响。因此，肌凝蛋白I的活性是内吞作用中出芽事件所必需的，而不是膜运输的其他几个方面。
Type I myosins are thought to drive actin-dependent membrane motility, but the direct demonstration in vivo of their involvement in specific cellular processes has been difficult. Deletion of the genes MYO3 and MYO5, which encode the yeast type I myosins, almost abolished growth. A double-deleted mutant complemented with a MYO5 temperature-sensitive allele (myo5-1) showed a strong defect in the internalization step of receptor-mediated endocytosis, whereas the secretory pathway remained apparently unaffected. Thus, myosin I activity is required for a budding event in endocytosis but not for several other aspects of membrane traffic.