Eitzen Gary
Department of Cell Biology, MSB 5-14, University of Alberta, Edmonton, Alberta, Canada T6G 2H7.
Biochim Biophys Acta. 2003 Aug 18;1641(2-3):175-81. doi: 10.1016/s0167-4889(03)00087-9.
Actin and its associated proteins participate in several intracellular trafficking mechanisms. This review assesses recent work that shows how actin participates in the terminal trafficking event of membrane bilayer fusion. A recent flurry of reports defines a role for Rho proteins in membrane fusion and also demonstrates that this role is distinct from any vesicle transport mechanism. Rho proteins are well known to govern actin remodeling, which implicates this process as a condition of membrane fusion. A small but significant body of work examines actin-regulated events of intracellular membrane fusion, exocytosis and endocytosis. In general, actin has been shown to act as a negative regulator of exocytosis. Cortical actin filaments act as a barrier that requires transient removal to allow vesicles to undergo docking at the plasma membrane. However, once docked, F-actin synthesis may act as a positive regulator to give the final stimulus to drive membrane fusion. F-actin synthesis is clearly needed for endocytosis and intracellular membrane fusion events. What may seem like dissimilar results are perhaps snapshots of a single mechanism of membranous actin remodeling (i.e. dynamic disassembly and reassembly) that is universally needed for all membrane fusion events.
肌动蛋白及其相关蛋白参与多种细胞内运输机制。本综述评估了近期的研究工作，这些研究表明肌动蛋白如何参与膜双层融合的终末运输事件。最近一系列报告确定了Rho蛋白在膜融合中的作用，同时也证明该作用与任何囊泡运输机制不同。众所周知，Rho蛋白调控肌动蛋白重塑，这意味着该过程是膜融合的一个条件。一小部分但意义重大的研究工作探讨了肌动蛋白调节的细胞内膜融合、胞吐作用和胞吞作用事件。一般来说，肌动蛋白已被证明是胞吐作用的负调节因子。皮质肌动蛋白丝充当一种屏障，需要短暂去除以允许囊泡在质膜处对接。然而，一旦对接，F-肌动蛋白的合成可能作为正调节因子，给予驱动膜融合的最终刺激。F-肌动蛋白的合成显然是胞吞作用和细胞内膜融合事件所必需的。看似不同的结果可能是膜性肌动蛋白重塑单一机制（即动态拆卸和重新组装）的不同阶段，而所有膜融合事件都普遍需要这种机制。
