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双肌动蛋白结合蛋白是一种非持续性解聚酶,它与formin协同作用,可显著加速肌动蛋白丝去封端过程达300倍。

Twinfilin is a nonprocessive depolymerase which synergizes with formin to dramatically accelerate actin filament uncapping by 300-fold.

作者信息

Reddy Vishal, Arya Ankita, Shekhar Shashank

机构信息

Departments of Physics, Cell Biology and Biochemistry, Emory University, Atlanta, GA 30322.

出版信息

Proc Natl Acad Sci U S A. 2025 May 6;122(18):e2501078122. doi: 10.1073/pnas.2501078122. Epub 2025 Apr 28.

Abstract

For over four decades, our understanding of cellular actin dynamics has been guided by the concept of treadmilling. However, this paradigm has been challenged by the evidence that twinfilin can uncap and promote depolymerization of filament barbed ends, though its precise mechanism remains debated. Using single-molecule microscopy and microfluidics-assisted TIRF imaging, we demonstrate that twinfilin transiently associates with barbed ends for ~0.2 to 0.5 s, acting as a nonprocessive depolymerase that likely removes one or both terminal actin subunits. Furthermore, we show that twinfilin's barbed-end residence time and its ability to uncap CP-capped filaments (both alone and with formin mDia1) are significantly influenced by filament age. The synergistic enhancement in uncapping by twinfilin and mDia1 ranges from 11-fold for newly assembled to ~318-fold for aged actin filaments. These represent the fastest uncapping rates measured in vitro and approach CP turnover rates in vivo. Our study thus reinforces twinfilin's central role as a multifunctional barbed-end regulator which nonprocessively depolymerizes actin filaments, transiently caps barbed ends, and synergizes with formin to destabilize CP, thereby facilitating rapid actin turnover that depends on filament age.

摘要

四十多年来,我们对细胞肌动蛋白动力学的理解一直受踏车行为概念的指引。然而,这一范式受到了如下证据的挑战:双肌动蛋白丝结合蛋白(twinfilin)能够解开肌动蛋白丝的帽并促进其末端解聚,尽管其确切机制仍存在争议。通过单分子显微镜和微流控辅助的全内反射荧光(TIRF)成像,我们证明双肌动蛋白丝结合蛋白与肌动蛋白丝末端短暂结合约0.2至0.5秒,作为一种非连续性解聚酶,可能移除一个或两个末端肌动蛋白亚基。此外,我们表明双肌动蛋白丝结合蛋白在肌动蛋白丝末端的停留时间以及它解开由帽蛋白(CP)封端的肌动蛋白丝(单独或与formin mDia1一起)的能力,都受到肌动蛋白丝老化程度的显著影响。双肌动蛋白丝结合蛋白和formin mDia1协同解帽作用的增强倍数,从新组装的肌动蛋白丝的11倍到老化肌动蛋白丝的约318倍不等。这些代表了体外测量到的最快解帽速率,并且接近体内帽蛋白的周转速率。因此,我们的研究强化了双肌动蛋白丝结合蛋白作为多功能肌动蛋白丝末端调节剂的核心作用,它以非连续性方式使肌动蛋白丝解聚,短暂封端肌动蛋白丝末端,并与formin协同作用使帽蛋白失稳,从而促进依赖于肌动蛋白丝老化程度的快速肌动蛋白周转。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51f9/12067289/346413ed6e3e/pnas.2501078122fig01.jpg

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