Helgeson Luke A, Nolen Brad J
Institute of Molecular Biology , University of Oregon , Eugene , United States ; Department of Chemistry and Biochemistry , University of Oregon , Eugene , United States.
Elife. 2013 Sep 3;2:e00884. doi: 10.7554/eLife.00884.
Nucleation promoting factors (NPFs) initiate branched actin network assembly by activating Arp2/3 complex, a branched actin filament nucleator. Cellular actin networks contain multiple NPFs, but how they coordinately regulate Arp2/3 complex is unclear. Cortactin is an NPF that activates Arp2/3 complex weakly on its own, but with WASP/N-WASP, another class of NPFs, potently activates. We dissect the mechanism of synergy and propose a model in which cortactin displaces N-WASP from nascent branches as a prerequisite for nucleation. Single-molecule imaging revealed that unlike WASP/N-WASP, cortactin remains bound to junctions during nucleation, and specifically targets junctions with a ∼160-fold increased on rate over filament sides. N-WASP must be dimerized for potent synergy, and targeted mutations indicate release of dimeric N-WASP from nascent branches limits nucleation. Mathematical modeling shows cortactin-mediated displacement but not N-WASP recycling or filament recruitment models can explain synergy. Our results provide a molecular basis for coordinate Arp2/3 complex regulation. DOI:http://dx.doi.org/10.7554/eLife.00884.001.
成核促进因子(NPFs)通过激活Arp2/3复合体(一种分支肌动蛋白丝成核剂)来启动分支肌动蛋白网络组装。细胞肌动蛋白网络包含多种NPFs,但它们如何协同调节Arp2/3复合体尚不清楚。Cortactin是一种NPF,其自身对Arp2/3复合体的激活作用较弱,但与另一类NPF即WASP/N-WASP一起时,则能有效激活。我们剖析了协同作用机制并提出了一个模型,其中Cortactin从新生分支上取代N-WASP是成核的前提条件。单分子成像显示,与WASP/N-WASP不同,Cortactin在成核过程中仍与分支点结合,并且特异性靶向分支点,其结合速率比丝状体侧面高约160倍。N-WASP必须二聚化才能产生有效的协同作用,靶向突变表明二聚体N-WASP从新生分支上的释放限制了成核。数学建模表明,Cortactin介导的取代作用而非N-WASP循环利用或丝状体招募模型能够解释协同作用。我们的结果为Arp2/3复合体的协同调节提供了分子基础。DOI:http://dx.doi.org/10.7554/eLife.00884.001。