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Regulation of Gap Junction Dynamics by UNC-44/ankyrin and UNC-33/CRMP through VAB-8 in C. elegans Neurons.

PLoS Genet.2016 Mar 25;12(3):e1005948. eCollection 2016 Mar
Lingfeng Meng 1 , Chia-hui Chen 2 , Dong Yan 2
Lingfeng Meng 1 , Chia-hui Chen 2 , Dong Yan 2

[No authors listed]

Author information
  • 1 Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina, United States of America.
  • 2 Department of Neurobiology and Duke Institute for Brain Sciences, Duke University Medical Center, Durham, North Carolina, United States of America.

摘要

Gap junctions are present in both vertebrates and invertebrates from nematodes to mammals. Although the importance of gap junctions has been documented in many biological processes, the molecular mechanisms underlying gap junction dynamics remain unclear. Here, using the C. elegans PLM neurons as a model, we show that UNC-44/ankyrin acts upstream of UNC-33/CRMP in regulation of a potential kinesin VAB-8 to control gap junction dynamics, and loss-of-function in the UNC-44/UNC-33/VAB-8 pathway suppresses the turnover of gap junction channels. Therefore, we first show a signal pathway including ankyrin, CRMP, and kinesin in regulating gap junctions.

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