Regulation of neuronal axon specification by glia-neuron gap junctions in C.elegans

被引：16

作者：

Meng, Lingfeng ^{[1
,2
,3
]}

Zhang, Albert ^{[1
,2
,3
]}

Jin, Yishi ^{[4
,5
]}

Yan, Dong ^{[1
,2
,3
]}

机构：

[1] Duke Univ, Med Ctr, Dept Mol Genet & Microbiol, Durham, NC 27708 USA

[2] Duke Univ, Med Ctr, Dept Neurobiol, Durham, NC 27710 USA

[3] Duke Med Ctr, Duke Inst Brain Sci, Durham, NC 27710 USA

[4] Univ Calif San Diego, Howard Hughes Med Inst, Div Biol Sci, Neurobiol Sect, San Diego, CA 92103 USA

[5] Univ Calif San Diego, Sch Med, Dept Cellular & Mol Med, San Diego, CA 92103 USA

来源：

ELIFE | 2016年 / 5卷

关键词：

ASTROCYTE-SECRETED PROTEINS; CENTRAL-NERVOUS-SYSTEM; ADULT CEREBRAL-CORTEX; CAENORHABDITIS-ELEGANS; C; ELEGANS; SYNAPSE ELIMINATION; MAMMALIAN BRAIN; PRESYNAPTIC COMPONENTS; POLARIZED TRAFFICKING; HIPPOCAMPAL-NEURONS;

D O I：

10.7554/eLife.19510

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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.

引用

页数：20

共 77 条

[1] Astrocyte glypicans 4 and 6 promote formation of excitatory synapses via GluA1 AMPA receptors [J].