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

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.

间隙连接广泛存在于从线虫到哺乳类的脊椎动物与无脊椎动物体内。尽管间隙连接的重要性已在诸多生物学过程中得到证实，但其动力学相关的分子机制仍未明确。本研究以秀丽隐杆线虫（C. elegans）的PLM神经元为实验模型，发现UNC-44/锚蛋白（ankyrin）在调控潜在驱动蛋白VAB-8的通路中，位于UNC-33/CRMP的上游，以此控制间隙连接的动力学过程；而UNC-44/UNC-33/VAB-8信号通路的功能缺失会抑制间隙连接通道的周转。综上，本研究首次揭示了一条包含锚蛋白、CRMP与驱动蛋白的信号通路，可调控间隙连接的功能。