Shaggy, the homolog of glycogen synthase kinase 3, controls neuromuscular junction growth in Drosophila
Shaggy, the homolog of glycogen synthase kinase 3, controls neuromuscular junction growth in Drosophila
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DOI：
10.1523/jneurosci.1580-04.2004
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发表时间：
2004-07-21
影响因子：
5.3
通讯作者：
Grau, Y
中科院分区：
文献类型：
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作者：
Franco, B;Bogdanik, L;Grau, Y
使用果蝇神经肌肉连接（NMJ）作为模型突触进行蛋白质陷阱筛选，以确定控制突触结构或可塑性的基因。我们发现，与哺乳动物糖原合成酶激酶3 α和β（两种丝氨酸-苏氨酸激酶）同源的果蝇Shaggy （Sgg）集中在这个突触上。利用shaggy突变等位基因的不同组合，我们发现shaggy对NMJ的生长具有负向控制作用。此外，组织特异性表达的显性阴性Sgg表明，这种激酶在运动神经元中是必需的，而不是在肌肉中，控制NMJ的生长。最后，我们发现Sgg控制着运动神经元中的微管细胞骨架动力学，而Futsch，一种微管相关蛋白，是Shaggy在突触生长中的功能所必需的。
A protein-trap screen using the Drosophila neuromuscular junction (NMJ) as a model synapse was performed to identify genes that control synaptic structure or plasticity. We found that Shaggy (Sgg), the Drosophila homolog of the mammalian glycogen synthase kinases 3 alpha and beta, two serine-threonine kinases, was concentrated at this synapse. Using various combinations of mutant alleles of shaggy, we found that Shaggy negatively controlled the NMJ growth. Moreover, tissue-specific expression of a dominant-negative Sgg indicated that this kinase is required in the motoneuron, but not in the muscle, to control NMJ growth. Finally, we show that Sgg controlled the microtubule cytoskeleton dynamics in the motoneuron and that Futsch, a microtubule-associated protein, was required for Shaggy function on synaptic growth.