Cofilin is an actin filament severing protein necessary for fast actin turnover dynamics. Coronin and Aip1 promote cofilin-mediated actin filament disassembly, but the mechanism is somewhat controversial. An early model proposed that the combination of cofilin, coronin, and Aip1 disassembled filaments in bursts. A subsequent study only reported severing. Here, we used EM to show that actin filaments convert directly into globular material. A monomer trap assay also shows that the combination of all three factors produces actin monomers faster than any two factors alone. We show that coronin accelerates the release of Pi from actin filaments and promotes highly cooperative cofilin binding to actin to create long stretches of polymer with a hypertwisted morphology. Aip1 attacks these hypertwisted regions along their sides, disintegrating them into monomers or short oligomers. The results are consistent with a catastrophic mode of disassembly, not enhanced severing alone.

中文翻译：

---

cofilin、Aip1 和 coronin 导致的灾难性肌动蛋白丝破裂。

Cofilin 是一种肌动蛋白丝切断蛋白，是快速肌动蛋白周转动态所必需的。Coronin 和 Aip1 促进 cofilin 介导的肌动蛋白丝分解，但其机制有些争议。一个早期的模型提出 cofilin、coronin 和 Aip1 的组合以爆发方式分解细丝。随后的一项研究仅报告了切断。在这里，我们使用 EM 来显示肌动蛋白丝直接转化为球状材料。单体陷阱分析还表明，所有三个因素的组合比单独的任何两个因素更快地产生肌动蛋白单体。我们表明，coronin 加速了肌动蛋白丝中 Pi 的释放，并促进了高度协同的 cofilin 与肌动蛋白的结合，从而产生了具有超扭曲形态的聚合物长链。Aip1沿着它们的侧面攻击这些超扭曲的区域，将它们分解成单体或短的低聚物。结果与灾难性的拆卸模式一致，而不是单独增强切割。