Davidson Andrew J, Insall Robert H
The Beatson Institute for Cancer Research; Glasgow, UK.
Commun Integr Biol. 2013 Nov 1;6(6):e27033. doi: 10.4161/cib.27033. Epub 2013 Nov 13.
The SCAR/WAVE complex drives the actin polymerisation that underlies protrusion of the front of the cell and thus drives migration. However, it is not understood how the activity of SCAR/WAVE is regulated to generate the infinite range of cellular shape changes observed during cell motility. What are the relative roles of the subunits of the SCAR/WAVE complex? What signaling molecules do they interact with? And how does the complex integrate all this information in order to control the temporal and spatial polymerisation of actin during protrusion formation? Unfortunately, the interdependence of SCAR complex members has made genetic dissection hard. In our recent paper,(1) we describe stabilization of the Dictyostelium SCAR complex by a small fragment of Abi. Here we summarize the main findings and discuss how this approach can help reveal the inner workings of this impenetrable complex.
SCAR/WAVE复合体驱动肌动蛋白聚合，而肌动蛋白聚合是细胞前端突出的基础，从而推动细胞迁移。然而，目前尚不清楚SCAR/WAVE的活性是如何被调节的，以产生在细胞运动过程中观察到的无限范围的细胞形状变化。SCAR/WAVE复合体的亚基各自发挥着怎样的作用？它们与哪些信号分子相互作用？以及该复合体如何整合所有这些信息，以便在突出形成过程中控制肌动蛋白的时空聚合？不幸的是，SCAR复合体成员之间的相互依赖性使得基因剖析变得困难。在我们最近的论文中，(1)我们描述了通过Abi的一个小片段对盘基网柄菌SCAR复合体的稳定作用。在此，我们总结主要发现，并讨论这种方法如何有助于揭示这个难以理解的复合体的内部运作机制。
