Remodeling of organelle-bound actin is required for yeast vacuole fusion.

Remodeling of organelle-bound actin is required for yeast vacuole fusion.
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DOI:
10.1083/jcb.200204089
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发表时间:
2002-08-19
期刊:
The Journal of cell biology
影响因子:
--
通讯作者:
Wickner W
Wickner W
中科院分区:
其他
文献类型:
--
作者:
Eitzen G;Wang L;Thorngren N;Wickner W

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肌动蛋白参与多种细胞内运输途径。我们现在发现,肌动蛋白在没有细胞质或细胞骨架的情况下结合在纯化的酵母液泡表面,调节同型液泡融合的最后一个室混合阶段。Cdc42p GTPase是液泡融合所必需的。我们现在发现Cdc42p调节的肌动蛋白重塑级联(Cdc42p→Cla4p→Las17p/Vrp1p→Arp2/3复合物→肌动蛋白)的蛋白质在分离的液泡上富集。液泡结合的肌动蛋白受到扰动后,液泡融合会发生显著改变,包括ACT1基因突变、加入特定的肌动蛋白配体(如latrunculin B或jasplakinolide)、针对肌动蛋白调节蛋白Las17p(酵母Wiskott-Aldrich综合征蛋白)或Arp2/3的抗体,或删除肌动蛋白调节基因。在停靠的液泡上,肌动蛋白富集于融合发生的“顶点环”膜微域,这是导致膜融合的最终步骤所必需的。actin的这种作用可能扩展到其他贩运系统。
Actin participates in several intracellular trafficking pathways. We now find that actin, bound to the surface of purified yeast vacuoles in the absence of cytosol or cytoskeleton, regulates the last compartment mixing stage of homotypic vacuole fusion. The Cdc42p GTPase is known to be required for vacuole fusion. We now show that proteins of the Cdc42p-regulated actin remodeling cascade (Cdc42p → Cla4p → Las17p/Vrp1p → Arp2/3 complex → actin) are enriched on isolated vacuoles. Vacuole fusion is dramatically altered by perturbation of the vacuole-bound actin, either by mutation of the ACT1 gene, addition of specific actin ligands such as latrunculin B or jasplakinolide, antibody to the actin regulatory proteins Las17p (yeast Wiskott-Aldrich syndrome protein) or Arp2/3, or deletion of actin regulatory genes. On docked vacuoles, actin is enriched at the “vertex ring” membrane microdomain where fusion occurs and is required for the terminal steps leading to membrane fusion. This role for actin may extend to other trafficking systems.