Cell shape is controlled by the submembranous cortex, an actomyosin network mainly generated by two actin nucleators: the Arp2/3 complex and the formin mDia1. Changes in relative nucleator activity may alter cortical organization, mechanics and cell shape. Here we investigate how nucleation-promoting factors mediate interactions between nucleators. In vitro, the nucleation-promoting factor SPIN90 promotes formation of unbranched filaments by Arp2/3, a process thought to provide the initial filament for generation of dendritic networks. Paradoxically, in cells, SPIN90 appears to favour a formin-dominated cortex. Our in vitro experiments reveal that this feature stems mainly from two mechanisms: efficient recruitment of mDia1 to SPIN90–Arp2/3 nucleated filaments and formation of a ternary SPIN90–Arp2/3–mDia1 complex that greatly enhances filament nucleation. Both mechanisms yield rapidly elongating filaments with mDia1 at their barbed ends and SPIN90–Arp2/3 at their pointed ends. Thus, in networks, SPIN90 lowers branching densities and increases the proportion of long filaments elongated by mDia1.

细胞形状由膜下皮层控制，这是一种肌动球蛋白网络，主要由两种肌动蛋白成核剂产生：Arp2/3 复合物和formin mDia1。相对成核活性的变化可能会改变皮质组织、力学和细胞形状。在这里，我们研究了成核促进因子如何介导成核剂之间的相互作用。在体外，成核促进因子 SPIN90 促进 Arp2/3 形成未支化的细丝，这一过程被认为为生成树枝状网络提供初始细丝。矛盾的是，在细胞中，SPIN90 似乎偏向于以甲酸为主的皮层。我们的体外实验表明，这一特征主要源于两种机制：有效地将 mDia1 募集到 SPIN90-Arp2/3 有核细丝并形成三元 SPIN90-Arp2/3-mDia1 复合物，大大增强细丝成核。这两种机制都会产生快速伸长的细丝，在它们的倒刺末端具有 mDia1，在它们的尖端具有 SPIN90-Arp2/3。因此，在网络中，SPIN90 降低了分支密度并增加了由 mDia1 拉长的长丝的比例。