Presynaptic local signaling by a canonical wingless pathway regulates development of the Drosophila neuromuscular junction.
Presynaptic local signaling by a canonical wingless pathway regulates development of the Drosophila neuromuscular junction.
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DOI：
10.1523/jneurosci.0164-08.2008
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发表时间：
2008-10-22
期刊：
影响因子：
--
通讯作者：
Schwarz TL
中科院分区：
文献类型：
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作者：
Miech C;Pauer HU;He X;Schwarz TL
Wnt/wingless信号有助于神经元突触的发育，包括果蝇神经肌肉接头。失去无翼（wg）功能改变了这个模型突触的扣结的数量和结构。检查Wnt/wingless信号机制，我们发现，一个独特的途径运作突触前的运动神经元，可以解释许多wingless在这个突触的影响。该通路包括典型元件arrow/LRP（disevelled）和糖原合成酶激酶shaggy（GSK 3），并调节突触结内微管环的形成以及突触结的数量。然而，该途径似乎不依赖于β-连环蛋白信号传导和最常见的这些组分下游的转录调节。相反，对shaggy的抑制可能是局部作用。因此，这条途径提供了一个平行的机制，卷曲受体的突触后激活，并表明，突触发育的结果从双向影响的无翅通过不同的细胞内途径对突触前和突触后结构。
Wnt/wingless signaling contributes to the development of neuronal synapses, including the Drosophila neuromuscular junction. Loss of wingless (wg) function alters the number and structure of boutons at this model synapse. Examining Wnt/wingless signaling mechanisms, we find that a distinct pathway operates presynaptically in the motoneuron and can account for many of the effects of wingless at this synapse. This pathway includes the canonical elements arrow/LRP, dishevelled, and the glycogen synthase kinase shaggy (GSK3) and regulates the formation of microtubule loops within synaptic boutons as well as the number of synaptic boutons. This pathway, however, appears to be independent of β-catenin signaling and the transcriptional regulation that is most frequently downstream of these components. Instead, inhibition of shaggy is likely to act locally. This pathway thus provides a parallel mechanism to the postsynaptic activation of frizzled receptors and indicates that synaptic development results from the bidirectional influence of wingless on both pre- and postsynaptic structures via distinct intracellular pathways.