Caldesmon Regulates Axon Extension through Interaction with Myosin II
Caldesmon Regulates Axon Extension through Interaction with Myosin II
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DOI：
10.1074/jbc.m111.295618
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发表时间：
2012-01-27
影响因子：
4.8
通讯作者：
Sobue, Kenji
中科院分区：
文献类型：
--
作者：
Morita, Tsuyoshi;Mayanagi, Taira;Sobue, Kenji
为了开始形成神经回路的过程，新的神经元首先建立它们的极性并延伸它们的轴突。轴突延伸是由高度协调的细胞骨架动力学引导和调节的。在这里，我们表明，在海马神经元中，肌动蛋白结合蛋白caldesmon积累在远端轴突，其N-末端与肌球蛋白II的相互作用增强轴突的延伸。在皮质神经前体细胞中，钙调素敲低抑制轴突延伸和神经元极性。这些结果表明，caldesmon是轴突发育的重要调节因子。
To begin the process of forming neural circuits, new neurons first establish their polarity and extend their axon. Axon extension is guided and regulated by highly coordinated cytoskeletal dynamics. Here we demonstrate that in hippocampal neurons, the actin-binding protein caldesmon accumulates in distal axons, and its N-terminal interaction with myosin II enhances axon extension. In cortical neural progenitor cells, caldesmon knockdown suppresses axon extension and neuronal polarity. These results indicate that caldesmon is an important regulator of axon development.