Department of Biology, Brandeis University, Waltham, Massachusetts 02454, USA.
J Biol Chem. 2010 Mar 12;285(11):8481-91. doi: 10.1074/jbc.M109.054957. Epub 2010 Jan 12.
The Arp2/3 complex is a conserved seven-subunit actin-nucleating machine activated by WASp (Wiskott Aldrich syndrome protein). Despite its central importance in a broad range of cellular processes, many critical aspects of the mechanism of the Arp2/3 complex have yet to be resolved. In particular, some of the individual subunits in the complex have not been assigned clear functional roles, including p40/ARPC1. Here, we dissected the structure and function of Saccharomyces cerevisiae p40/ARPC1, which is encoded by the essential ARC40 gene, by analyzing 39 integrated alleles that target its conserved surfaces. We identified three distinct sites on p40/ARPC1 required for function in vivo: one site contacts p19/ARPC4, one contacts p15/ARPC5, and one site resides in an extended structural "arm" of p40/ARPC1. Using a novel strategy, we purified the corresponding lethal mutant Arp2/3 complexes from yeast and compared their actin nucleation activities. Lethal mutations at the contact with p19/ARPC4 specifically impaired WASp-induced nucleation. In contrast, lethal mutations at the contact with p15/ARPC5 led to unregulated ("leaky") nucleation in the absence of WASp. Lethal mutations in the extended arm drastically reduced nucleation, and the same mutations disrupted the ability of the purified p40/ARPC1 arm domain to bind the VCA domain of WASp. Together, these data indicate that p40/ARPC1 performs at least three distinct, essential functions in regulating Arp2/3 complex-mediated actin assembly: 1) suppression of spontaneous nucleation by the Arp2/3 complex, which requires proper contacts with p15/ARPC5; 2) propagation of WASp activation signals via contacts with p19/ARPC2; and 3) direct facilitation of actin nucleation through interactions of the extended arm with the VCA domain of WASp.
Arp2/3 复合物是一种保守的七亚基肌动蛋白成核机器,由 WASp(Wiskott Aldrich 综合征蛋白)激活。尽管它在广泛的细胞过程中具有核心重要性,但该复合物的机制仍有许多关键方面尚未解决。特别是,复合物中的一些个别亚基尚未被赋予明确的功能角色,包括 p40/ARPC1。在这里,我们通过分析靶向其保守表面的 39 个整合等位基因,剖析了酿酒酵母 p40/ARPC1 的结构和功能,该基因由必需的 ARC40 基因编码。我们确定了 p40/ARPC1 上三个不同的功能位点:一个位点与 p19/ARPC4 相互作用,一个位点与 p15/ARPC5 相互作用,一个位点位于 p40/ARPC1 的扩展结构“臂”上。我们使用一种新的策略,从酵母中纯化了相应的致死突变体 Arp2/3 复合物,并比较了它们的肌动蛋白成核活性。与 p19/ARPC4 相互作用位点的致死突变特异性地损害了 WASp 诱导的成核。相比之下,与 p15/ARPC5 相互作用位点的致死突变导致在没有 WASp 的情况下无调控(“渗漏”)成核。位于扩展臂上的致死突变极大地降低了成核活性,并且相同的突变破坏了纯化的 p40/ARPC1 臂结构域与 WASp 的 VCA 结构域的结合能力。这些数据表明,p40/ARPC1 在调节 Arp2/3 复合物介导的肌动蛋白组装中至少执行三个不同的、必需的功能:1)通过与 p15/ARPC5 的适当相互作用抑制 Arp2/3 复合物的自发成核;2)通过与 p19/ARPC2 的相互作用传递 WASp 激活信号;3)通过与 WASp 的 VCA 结构域的扩展臂相互作用直接促进肌动蛋白成核。