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利用粗粒度分子动力学研究Arp2/3复合物形成肌动蛋白丝分支的步骤。

Steps of actin filament branch formation by Arp2/3 complex investigated with coarse-grained molecular dynamics.

作者信息

Zhang Shuting, Vavylonis Dimitrios

机构信息

Department of Physics, Lehigh University, Bethlehem, PA, United States.

Center for Computational Biology, Flatiron Institute, New York, NY, United States.

出版信息

Front Cell Dev Biol. 2023 Jan 17;11:1071977. doi: 10.3389/fcell.2023.1071977. eCollection 2023.

Abstract

The nucleation of actin filament branches by the Arp2/3 complex involves activation through nucleation promotion factors (NPFs), recruitment of actin monomers, and binding of the complex to the side of actin filaments. Because of the large system size and processes that involve flexible regions and diffuse components, simulations of branch formation using all-atom molecular dynamics are challenging. We applied a coarse-grained model that retains amino-acid level information and allows molecular dynamics simulations in implicit solvent, with globular domains represented as rigid bodies and flexible regions allowed to fluctuate. We used recent electron microscopy structures of the inactive Arp2/3 complex bound to NPF domains and to mother actin filament for the activated Arp2/3 complex. We studied interactions of Arp2/3 complex with the activating VCA domain of the NPF Wiskott-Aldrich syndrome protein, actin monomers, and actin filament. We found stable configurations with one or two actin monomers bound along the branch filament direction and with CA domain of VCA associated to the strong and weak binding sites of the Arp2/3 complex, supporting prior structural studies and validating our approach. We reproduced delivery of actin monomers and CA to the Arp2/3 complex under different conditions, providing insight into mechanisms proposed in previous studies. Simulations of active Arp2/3 complex bound to a mother actin filament indicate the contribution of each subunit to the binding. Addition of the C-terminal tail of Arp2/3 complex subunit ArpC2, which is missing in the cryo-EM structure, increased binding affinity, indicating a possible stabilizing role of this tail.

摘要

肌动蛋白丝分支由Arp2/3复合物成核涉及通过成核促进因子(NPFs)激活、肌动蛋白单体的募集以及该复合物与肌动蛋白丝侧面的结合。由于系统规模较大且过程涉及柔性区域和扩散成分,使用全原子分子动力学模拟分支形成具有挑战性。我们应用了一种粗粒度模型,该模型保留氨基酸水平信息,并允许在隐式溶剂中进行分子动力学模拟,其中球状结构域表示为刚体,柔性区域允许波动。我们使用了与NPF结构域和母肌动蛋白丝结合的无活性Arp2/3复合物的最新电子显微镜结构来构建活化的Arp2/3复合物。我们研究了Arp2/3复合物与NPF维斯科特-奥尔德里奇综合征蛋白的活化VCA结构域、肌动蛋白单体和肌动蛋白丝的相互作用。我们发现了稳定的构型,其中一个或两个肌动蛋白单体沿分支丝方向结合,并且VCA的CA结构域与Arp2/3复合物的强结合位点和弱结合位点相关联,这支持了先前的结构研究并验证了我们的方法。我们在不同条件下重现了肌动蛋白单体和CA向Arp2/3复合物的递送,深入了解了先前研究中提出的机制。与母肌动蛋白丝结合的活性Arp2/3复合物的模拟表明每个亚基对结合的贡献。添加Arp2/3复合物亚基ArpC2的C末端尾巴(在冷冻电镜结构中缺失)增加了结合亲和力,表明该尾巴可能具有稳定作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcb1/9887124/2ff280adbb4c/fcell-11-1071977-g001.jpg

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