Regulation of neuronal axon specification by glia-neuron gap junctions in C.elegans
Regulation of neuronal axon specification by glia-neuron gap junctions in C.elegans
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DOI：
10.7554/elife.19510
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发表时间：
2016-10-21
期刊：
影响因子：
7.7
通讯作者：
Yan, Dong
中科院分区：
文献类型：
--
作者：
Meng, Lingfeng;Zhang, Albert;Yan, Dong
轴突规范是神经元发育的关键步骤，神经胶质细胞在此过程中的功能尚不完全清楚。在这里，我们发现秀丽隐杆线虫 GLR 神经胶质细胞通过 GLR-RME 间隙连接调节其附近 GABA 能 RME 神经元的轴突规范。 GLR-RME间隙连接的破坏导致RME神经元的非轴突神经突中轴突标记物的错误积累，并将这些神经突中的微管转化为轴突样组件。我们进一步发现 GLR-RME 间隙连接通过以钙依赖性方式激活 CDK-5 途径（涉及钙蛋白酶 clp-4）来调节 RME 轴突规范。因此，我们的研究揭示了神经胶质细胞-神经元间隙连接在神经元轴突规范中的功能，并表明源自神经胶质细胞的钙可以通过间隙连接调节神经元细胞内通路。
Axon specification is a critical step in neuronal development, and the function of glial cells in this process is not fully understood. Here, we show that C. elegans GLR glial cells regulate axon specification of their nearby GABAergic RME neurons through GLR-RME gap junctions. Disruption of GLR-RME gap junctions causes misaccumulation of axonal markers in non-axonal neurites of RME neurons and converts microtubules in those neurites to form an axon-like assembly. We further uncover that GLR-RME gap junctions regulate RME axon specification through activation of the CDK-5 pathway in a calcium-dependent manner, involving a calpain clp-4. Therefore, our study reveals the function of glia-neuron gap junctions in neuronal axon specification and shows that calcium originated from glial cells can regulate neuronal intracellular pathways through gap junctions.