Regulation of neuronal axon specification by glia-neuron gap junctions in <i>C. elegans</i>.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 27767956.
- Also identified by DOI 10.7554/eLife.19510 and PMC identifier 5083064.
- Licence recorded as CC0.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
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 <i>C. elegans</i> 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 <i>clp-4</i>. 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.
Medical subject headings
- Caenorhabditis elegans
- Cell Differentiation
- Gap Junctions
- Neuroglia
- Neurons