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.

中文翻译：

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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

Neuroligins 是突触后粘附分子，对突触后特化和突触功能至关重要。但神经素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 调节复合物 (WRC) 介导的突触后肌动蛋白重组调节突触结构和功能。DNlg1、DNlg2 或其突触前伙伴神经蛋白 (DNrx) 的破坏导致 F-肌动蛋白的数量急剧减少。进一步的研究表明，DNlg1，但不是 DNlg2 或 DNlg3，通过其 C 端相互作用受体序列直接与 WRC 相互作用。这种相互作用是将 WRC 募集到突触后膜以促进 F-肌动蛋白组装所必需的。此外，DNlg1 和 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。我们的研究结果揭示了一种新的机制，通过该机制，DNrx-DNlg1 跨突触相互作用协调神经肌肉接头处的结构和功能特性。