Regulation of retrograde signaling at neuromuscular junctions by the novel C2 domain protein AEX-1
Regulation of retrograde signaling at neuromuscular junctions by the novel C2 domain protein AEX-1
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DOI：
10.1016/s0896-6273(01)00587-6
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发表时间：
2002-01-17
期刊：
影响因子：
16.2
通讯作者：
Iwasaki, K
中科院分区：
文献类型：
--
作者：
Doi, M;Iwasaki, K
从突触后细胞到突触前神经元的逆行信号对于调节突触的发育、维持和可塑性是必不可少的。在这里，我们报告了新的蛋白AEX-1控制逆行信号在神经肌肉接头在C。优雅的。aex-1突变体显示神经缺陷，包括突触前活性降低和突触囊泡融合蛋白aex-13的异常定位。肌肉特异性AEX-1表达挽救了这些缺陷，但神经元特异性表达不能。AEX-1有一个β-13同源结构域，似乎可以调节肌肉中的胞吐作用。这种逆行信号需要肌肉中的脯氨酸转化酶功能，这表明肽是逆行信号。该信号通过突触前末端的EGL-30 Gq α蛋白调节突触囊泡释放。
Retrograde signaling from postsynaptic cells to presynaptic neurons Is essential for regulation of synaptic development, maintenance, and plasticity. Here we report that the novel protein AEX-1 controls retrograde signaling at neuromuscular junctions in C. elegans. aex-1 mutants show neural defects including reduced presynaptic activity and abnormal localization of the synaptic vesicle fusion protein UNC-13. Muscle-specific AEX-1 expression rescues these defects but neuron-specific expression does not. AEX-1 has an UNC-13 homologous domain and appears to regulate exocytosis in muscles. This retrograde signaling requires prohormone-convertase function in muscles, suggesting that a peptide is the retrograde signal. This signal regulates synaptic vesicle release via the EGL-30 Gqalpha protein at presynaptic terminals.