Regulation of Neuronal Axon Specification by Glia-Neuron Gap Junctions in C. elegans
- Duke Institute for Brain Sciences, United States
- University of California, San Diego, United States
Abstract
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.
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Funding
National Institute of Neurological Disorders and Stroke (NS094171(R01))
- Dong Yan
Duke University School of Medicine (faculty startup)
- Dong Yan
National Institute of Neurological Disorders and Stroke (NS076646 (R00))
- Dong Yan
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
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This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.
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Regulation of Neuronal Axon Specification by Glia-Neuron Gap Junctions in C. elegans
eLife 5:e19510.
https://doi.org/10.7554/eLife.19510
