Regulation of synapse structure and function by the Drosophila tumor suppressor gene dlg
Regulation of synapse structure and function by the Drosophila tumor suppressor gene dlg
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DOI：
10.1016/s0896-6273(00)80196-8
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发表时间：
1996-10-01
期刊：
影响因子：
16.2
通讯作者：
Gorczyca, M
中科院分区：
文献类型：
--
作者：
Budnik, V;Koh, YH;Gorczyca, M
肿瘤抑制基因disc -large （dlg）突变导致突触后结构缺陷。在这里，我们报告了dig的突变也导致果蝇神经肌肉连接处更大的突触电流。通过使用Gal-4增强子诱捕系选择性地将DLG蛋白靶向肌肉或运动神经元，我们能够在突变体中大量地恢复突触后结构的减少。生理缺陷的修复是通过突触前靶向完成的，而不是突触后靶向，这与我们的发现一致，即微型兴奋性连接电流在dig突变体中没有改变。这些结果表明，DLG在调节神经递质释放和突触后结构中起作用。我们认为DLG是神经递质释放和突触结构变化在发育和可塑性过程中完成的机制的组成部分。
Mutations of the tumor suppressor gene discs-large (dlg) lead to postsynaptic structural defects. Here, we report that mutations in dig also result in larger synaptic currents at fly neuromuscular junctions. By selectively targeting DLG protein to either muscles or motorneurons using Gal-4 enhancer trap lines, we were able to rescue substantially the reduced postsynaptic structure in mutants. Rescue of the physiological defect was accomplished by presynaptic, but not postsynaptic targeting, consistent with our finding that miniature excitatory junctional currents were not changed in dig mutants. These results suggest that DLG functions in the regulation of neurotransmitter release and postsynaptic structure. We propose that DLG is an integral part of a mechanism by which changes in both neurotransmitter release and synapse structure are accomplished during development and plasticity.