Microtubule Minus-End Stabilization by Polymerization-Driven CAMSAP Deposition
Microtubule Minus-End Stabilization by Polymerization-Driven CAMSAP Deposition
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DOI：
10.1016/j.devcel.2014.01.001
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发表时间：
2014-02-10
影响因子：
11.8
通讯作者：
Akhmanova, Anna
中科院分区：
文献类型：
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作者：
Jiang, Kai;Hua, Shasha;Akhmanova, Anna
微管是细胞骨架聚合物，具有两个结构和功能不同的末端，即正末端和负末端。在这里，我们专注于微管负末端的调控的机制，由CAMSAP/哪吒/Patronin蛋白家族。我们表明，CAMSAP 2是必要的适当组织和稳定的间期微管和定向细胞迁移。通过结合活细胞成像和体外重建的微管组装从纯化的成分与激光显微手术，我们证明，CAMSAP调节微管负端生长，并专门沉积在由微管负端聚合形成的晶格上。这一过程导致CAMSAP修饰的微管延伸的形成，其从两端稳定并作为非中心体微管生长的位点。延伸的长度由微管切断蛋白katanin调节，该蛋白与CAMSAP相互作用。因此，我们的数据表明，微管负端组装驱动非中心体微管的稳定和katanin调节这一过程。
Microtubules are cytoskeletal polymers with two structurally and functionally distinct ends, the plus- and the minus-end. Here, we focus on the mechanisms underlying the regulation of microtubule minus-ends by the CAMSAP/Nezha/Patronin protein family. We show that CAMSAP2 is required for the proper organization and stabilization of interphase microtubules and directional cell migration. By combining live-cell imaging and in vitro reconstitution of microtubule assembly from purified components with laser microsurgery, we demonstrate that CAMSAPs regulate microtubule minus-end growth and are specifically deposited on the lattice formed by microtubule minus-end polymerization. This process leads to the formation of CAMSAP-decorated microtubule stretches, which are stabilized from both ends and serve as sites of noncentrosomal microtubule outgrowth. The length of the stretches is regulated by the microtubule-severing protein katanin, which interacts with CAMSAPs. Our data thus indicate that microtubule minus-end assembly drives the stabilization of noncentrosomal microtubules and that katanin regulates this process.