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首页> 外文期刊>eLife journal >Neurexin–Neuroligin 1 regulates synaptic morphology and functions via the WAVE regulatory complex in Drosophila neuromuscular junction
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Neurexin–Neuroligin 1 regulates synaptic morphology and functions via the WAVE regulatory complex in Drosophila neuromuscular junction

机译:Neurexin–Neuroligin 1通过果蝇神经肌肉接头中的WAVE调节复合物调节突触形态和功能

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摘要

Neuroligins are postsynaptic adhesion molecules that are essential for postsynaptic specialization and synaptic function. But the underlying molecular mechanisms of neuroligin functions remain unclear. We found that Drosophila Neuroligin 1 (DNlg1) regulates synaptic structure and function through WAVE regulatory complex (WRC)-mediated postsynaptic actin reorganization. The disruption of DNlg1, DNlg2, or their presynaptic partner neurexin (DNrx) led to a dramatic decrease in the amount of F-actin. Further study showed that DNlg1, but not DNlg2 or DNlg3, directly interacts with the WRC via its C-terminal interacting receptor sequence. That interaction is required to recruit WRC to the postsynaptic membrane to promote F-actin assembly. Furthermore, the interaction between DNlg1 and the WRC is essential for DNlg1 to rescue the morphological and electrophysiological defects in dnlg1 mutants. Our results reveal a novel mechanism by which the DNrx-DNlg1 trans-synaptic interaction coordinates structural and functional properties at the neuromuscular junction.
机译:神经胶蛋白是突触后粘附分子,对于突触后的特化和突触功能至关重要。但是神经胶蛋白功能的潜在分子机制仍不清楚。我们发现果蝇Neuroligin 1(DNlg1)通过WAVE调节复合体(WRC)介导的突触后肌动蛋白重组来调节突触的结构和功能。 DNlg1,DNlg2或其突触前伴侣神经毒素(DNrx)的破坏导致F-肌动蛋白的量急剧减少。进一步的研究表明,DNlg1,而不是DNlg2或DNlg3,不是通过其C末端相互作用受体序列与WRC直接相互作用。需要这种相互作用才能将WRC募集到突触后膜以促进F-肌动蛋白装配。此外,DNlg1与WRC之间的相互作用对于DNlg1挽救dnlg1突变体的形态和电生理缺陷至关重要。我们的结果揭示了一种新的机制,通过该机制,DNrx-DNlg1反突触相互作用可协调神经肌肉接头处的结构和功能特性。

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