Cardiovascular Research Institute and Department of Biochemistry, University of California, San Francisco, CA 94158, USA.
J Cell Sci. 2012 Mar 1;125(Pt 5):1165-76. doi: 10.1242/jcs.091157. Epub 2012 Feb 20.
The SCAR/WAVE complex drives lamellipodium formation by enhancing actin nucleation by the Arp2/3 complex. Phosphoinositides and Rac activate the SCAR/WAVE complex, but how SCAR/WAVE and Arp2/3 complexes converge at sites of nucleation is unknown. We analyzed the single-molecule dynamics of WAVE2 and p40 (subunits of the SCAR/WAVE and Arp2/3 complexes, respectively) in XTC cells. We observed lateral diffusion of both proteins and captured the transition of p40 from diffusion to network incorporation. These results suggest that a diffusive 2D search facilitates binding of the Arp2/3 complex to actin filaments necessary for nucleation. After nucleation, the Arp2/3 complex integrates into the actin network and undergoes retrograde flow, which results in its broad distribution throughout the lamellipodium. By contrast, the SCAR/WAVE complex is more restricted to the cell periphery. However, with single-molecule imaging, we also observed WAVE2 molecules undergoing retrograde motion. WAVE2 and p40 have nearly identical speeds, lifetimes and sites of network incorporation. Inhibition of actin retrograde flow does not prevent WAVE2 association and disassociation with the membrane but does inhibit WAVE2 removal from the actin cortex. Our results suggest that membrane binding and diffusion expedites the recruitment of nucleation factors to a nucleation site independent of actin assembly, but after network incorporation, ongoing actin polymerization facilitates recycling of SCAR/WAVE and Arp2/3 complexes.
SCAR/WAVE 复合物通过增强 Arp2/3 复合物的肌动蛋白成核作用来驱动片状伪足的形成。磷酸肌醇和 Rac 激活 SCAR/WAVE 复合物,但 SCAR/WAVE 和 Arp2/3 复合物在成核部位如何收敛尚不清楚。我们在 XTC 细胞中分析了 WAVE2 和 p40(SCAR/WAVE 和 Arp2/3 复合物的亚基)的单分子动力学。我们观察到两种蛋白质的侧向扩散,并捕获了 p40 从扩散到网络结合的转变。这些结果表明,扩散的 2D 搜索有利于 Arp2/3 复合物与肌动蛋白丝的结合,这对于成核是必要的。成核后,Arp2/3 复合物整合到肌动蛋白网络中并发生逆行流动,这导致其在整个片状伪足中广泛分布。相比之下,SCAR/WAVE 复合物更局限于细胞边缘。然而,通过单分子成像,我们也观察到 WAVE2 分子发生逆行运动。WAVE2 和 p40 的速度、寿命和网络结合部位几乎相同。肌动蛋白逆行流动的抑制不会阻止 WAVE2 与膜的结合和解离,但会抑制 WAVE2 从肌动蛋白皮质中的去除。我们的结果表明,膜结合和扩散促进了成核因子在不依赖肌动蛋白组装的情况下向成核部位的募集,但在网络结合后,持续的肌动蛋白聚合有利于 SCAR/WAVE 和 Arp2/3 复合物的循环利用。