Reddy Vishal, Arya Ankita, Shekhar Shashank
bioRxiv. 2024 Jul 19:2024.07.19.604324. doi: 10.1101/2024.07.19.604324.
Cellular actin networks assemble by actin filament elongation at barbed ends and are thought to disassemble primarily by depolymerization at filament pointed ends. Contrary to this conventional understanding of actin dynamics, twinfilin was recently shown to promote barbed-end depolymerization. Twinfilin has additionally been suggested to sequester monomers and cap as well as uncap filament barbed ends. As a result, the exact mechanisms by which twinfilin affects barbed-end dynamics remain controversial. Using multicolor single-molecule microscopy, we show that both mouse and yeast twinfilin are non-processive depolymerases that interact only transiently with barbed ends (~0.2-0.5 s). Each twinfilin binding event, on average, results in the removal of one or two actin subunits. At CP-capped barbed ends, twinfilin synergizes with formin to accelerate uncapping by up to ~320-fold. We find that uncapping by twinfilin, alone and together with formin, depends on the nucleotide state of the filament, with the two proteins causing a much more modest enhancement of uncapping of newly assembled filaments. Our study thus establishes twinfilin as a multifunctional barbed-end binding protein capable of non-processively depolymerizing, transiently capping, and synergizing with formin to rapidly uncap actin filament barbed ends.
细胞肌动蛋白网络通过肌动蛋白丝在其带刺末端的延伸而组装,并且通常被认为主要通过在丝的尖端末端去聚合而解聚。与这种对肌动蛋白动力学的传统理解相反,双肌动蛋白结合蛋白(twinfilin)最近被证明可促进带刺末端的解聚。此外,双肌动蛋白结合蛋白还被认为可以隔离单体、封端以及解封肌动蛋白丝的带刺末端。因此,双肌动蛋白结合蛋白影响带刺末端动力学的确切机制仍存在争议。使用多色单分子显微镜,我们发现小鼠和酵母双肌动蛋白结合蛋白都是非持续性解聚酶,它们仅与带刺末端短暂相互作用(约0.2 - 0.5秒)。平均而言,每次双肌动蛋白结合蛋白的结合事件会导致去除一两个肌动蛋白亚基。在CP封端的带刺末端,双肌动蛋白结合蛋白与formin协同作用,使解封速度加快约320倍。我们发现,双肌动蛋白结合蛋白单独以及与formin一起进行的解封作用取决于肌动蛋白丝的核苷酸状态,这两种蛋白质对新组装丝的解封增强作用要小得多。因此,我们的研究确定双肌动蛋白结合蛋白是一种多功能带刺末端结合蛋白,能够非持续性地解聚、短暂封端,并与formin协同作用以快速解封肌动蛋白丝的带刺末端。