科研之友
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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 (DNIg1) regulates synaptic structure and function through WAVE regulatory complex (WRC)-mediated postsynaptic actin reorganization. The disruption of DNIg1, DNIg2, or their presynaptic partner neurexin (DNrx) led to a dramatic decrease in the amount of F-actin. Further study showed that DNIg1, but not DNIg2 or DNIg3, 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 DNIg1 and the WRC is essential for DNIg1 to rescue the morphological and electrophysiological defects in dnlgl mutants. Our results reveal a novel mechanism by which the DNrx-DNIg1 trans-synaptic interaction coordinates structural and functional properties at the neuromuscular junction.
