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

Author:

Meng Lingfeng123,Zhang Albert123,Jin Yishi45ORCID,Yan Dong123ORCID

Affiliation:

1. Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, United States

2. Department of Neurobiology, Duke University Medical Center, Durham, United States

3. Duke Institute for Brain Sciences, Duke Medical Center, Durham, United States

4. Neurobiology Section, Division of Biological Sciences, Howard Hughes Medical Institute, University of California, San Diego, United States

5. Department of Cellular and Molecular Medicine, School of Medicine, 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.

Funder

National Institute of Neurological Disorders and Stroke

Duke University School of Medicine

Publisher

eLife Sciences Publications, Ltd

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine,General Neuroscience

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