Geli M I, Riezman H
Department of Biochemistry, Biozentrum, University of Basel, Klingelbergstrasse 70, Basel, Switzerland.
Science. 1996 Apr 26;272(5261):533-5. doi: 10.1126/science.272.5261.533.
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.
I型肌球蛋白被认为驱动肌动蛋白依赖性的膜运动,但在体内直接证明它们参与特定细胞过程一直很困难。编码酵母I型肌球蛋白的基因MYO3和MYO5的缺失几乎消除了生长。用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,肌球蛋白I活性是内吞作用中出芽事件所必需的,但不是膜运输其他几个方面所必需的。