Zheng Ting, Long Keyao, Wang Su, Rui Menglong
School of Life Science and Technology, The Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing, China.
Cell Mol Life Sci. 2025 Jan 21;82(1):47. doi: 10.1007/s00018-024-05560-1.
The selective elimination of inappropriate projections is essential for sculpting neural circuits during development. The class IV dendritic arborization (C4da) sensory neurons of Drosophila remodel the dendritic branches during metamorphosis. Glial cells in the central nervous system (CNS), are required for programmed axonal pruning of mushroom body (MB) γ neurons during metamorphosis in Drosophila. However, it is entirely unknown whether the glial cells are involved in controlling the neurite pruning of C4da sensory neurons. Here, we show that glial deletion of Eiger (Egr), orthologous to mammalian tumor necrosis factor TNF superfamily ligand, results in dendrite remodeling deficiency of Drosophila C4da sensory neurons. Moreover, the attenuation of neuronal Wengen (Wgn) and Grindelwald (Grnd), the receptors for TNF ligands, is also examined for defects in dendrite remodeling. We further discover that Wgn and Grnd facilitate dendrite elimination through the JNK Signaling. Overall, our findings demonstrate that glial-derived Egr signal links to the neuronal receptor Wgn/Grnd, activating the JNK signaling pathway and promoting developmental neuronal remodeling. Remarkably, our findings reveal a crucial role of peripheral glia in dendritic pruning of C4da neurons.
在发育过程中，选择性消除不适当的投射对于构建神经回路至关重要。果蝇的IV类树突状分支（C4da）感觉神经元在变态过程中会重塑树突分支。中枢神经系统（CNS）中的神经胶质细胞是果蝇变态过程中蘑菇体（MB）γ神经元程序性轴突修剪所必需的。然而，神经胶质细胞是否参与控制C4da感觉神经元的神经突修剪完全未知。在这里，我们表明，与哺乳动物肿瘤坏死因子TNF超家族配体同源的Eiger（Egr）在神经胶质细胞中的缺失会导致果蝇C4da感觉神经元的树突重塑缺陷。此外，还检测了神经元Wengen（Wgn）和Grindelwald（Grnd）（TNF配体的受体）的减弱是否存在树突重塑缺陷。我们进一步发现，Wgn和Grnd通过JNK信号促进树突消除。总体而言，我们的研究结果表明，神经胶质细胞衍生的Egr信号与神经元受体Wgn/Grnd相关联，激活JNK信号通路并促进发育过程中的神经元重塑。值得注意的是，我们的研究结果揭示了外周神经胶质细胞在C4da神经元树突修剪中的关键作用。
