Gandhi Meghal, Goode Bruce L
Department of Biology, Rosenstiel Basic Medical Science Research Center, Brandeis University, 415 South Street, Waltham, MA 02454, USA.
Subcell Biochem. 2008;48:72-87. doi: 10.1007/978-0-387-09595-0_7.
Coronin is a conserved actin binding protein that promotes cellular processes that rely on rapid remodeling of the actin cytoskeleton, including endocytosis and cell motility. However, the exact mechanism by which coronin contributes to actin dynamics has remained elusive for many years. Here, we integrate observations from many groups and propose a unified model to explain how coronin controls actin dynamics through coordinated effects on Arp2/3 complex and cofilin. At the front end of actin networks, coronin protects new (ATP-rich) filaments from premature disassembly by cofilin and recruits Arp2/3 complex to filament sides, leading to nucleation, branching and network expansion. At the rear of networks, coronin has strikingly different activities, synergizing with cofilin to dismantle old (ADP-rich) filaments. Thus, coronin spatially targets Arp2/3 complex and cofilin to opposite ends of actin networks. The net effect of coronin's activities is acceleration of polarized actin subunit flux through filamentous arrays. This increases actin network plasticity and replenishes the actin monomer pool required for new filament growth.
冠蛋白是一种保守的肌动蛋白结合蛋白，可促进依赖肌动蛋白细胞骨架快速重塑的细胞过程，包括内吞作用和细胞运动。然而，多年来，冠蛋白促进肌动蛋白动态变化的确切机制一直难以捉摸。在这里，我们整合了多个研究小组的观察结果，提出了一个统一的模型，以解释冠蛋白如何通过对Arp2/3复合体和丝切蛋白的协同作用来控制肌动蛋白动态变化。在肌动蛋白网络的前端，冠蛋白保护新的（富含ATP的）细丝不被丝切蛋白过早解聚，并将Arp2/3复合体招募到细丝侧面，导致成核、分支和网络扩展。在网络的后端，冠蛋白具有截然不同的活性，与丝切蛋白协同作用以拆解旧的（富含ADP的）细丝。因此，冠蛋白在空间上将Arp2/3复合体和丝切蛋白靶向到肌动蛋白网络的相对两端。冠蛋白活性的净效应是加速极化的肌动蛋白亚基通过丝状阵列的流动。这增加了肌动蛋白网络的可塑性，并补充了新细丝生长所需的肌动蛋白单体库。
