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首页> 外文期刊>Neuron >Nervous wreck interacts with thickveins and the endocytic machinery to attenuate retrograde BMP signaling during synaptic growth.
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Nervous wreck interacts with thickveins and the endocytic machinery to attenuate retrograde BMP signaling during synaptic growth.

机译：神经残骸与厚静脉和内吞机制相互作用，以减弱突触生长过程中逆行的BMP信号传导。

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摘要

Regulation of synaptic growth is fundamental to the formation and plasticity of neural circuits. Here, we demonstrate that Nervous wreck (Nwk), a negative regulator of synaptic growth at Drosophila NMJs, interacts functionally and physically with components of the endocytic machinery, including dynamin and Dap160/intersectin, and negatively regulates retrograde BMP growth signaling through a direct interaction with the BMP receptor, thickveins. Synaptic overgrowth in nwk is sensitive to BMP signaling levels, and loss of Nwk facilitates BMP-induced overgrowth. Conversely, Nwk overexpression suppresses BMP-induced synaptic overgrowth. We observe analogous genetic interactions between dap160 and the BMP pathway, confirming that endocytosis regulates BMP signaling at NMJs. Finally, we demonstrate a correlation between synaptic growth and pMAD levels and show that Nwk regulates these levels. We propose that Nwk functions at the interface of endocytosis and BMP signaling to ensure proper synaptic growth by negatively regulating Tkv to set limits on this positive growth signal.
机译：突触生长的调节是神经回路形成和可塑性的基础。在这里，我们证明了神经残骸（Nwk），果蝇NMJs突触生长的负调节剂，在功能上和物理上与内吞机器的成分（包括动力蛋白和Dap160 / intersectin）相互作用，并且通过直接相互作用对逆行的BMP生长信号进行负调节。与BMP受体，厚静脉。 nwk中的突触过度生长对BMP信号传导水平敏感，Nwk的丧失促进BMP诱导的过度生长。相反，Nwk过表达抑制BMP诱导的突触过度生长。我们观察到dap160和BMP途径之间的类似的遗传相互作用，证实内吞作用调节NMJs的BMP信号传导。最后，我们证明了突触生长与pMAD水平之间的相关性，并表明Nwk调节这些水平。我们建议Nwk在内吞作用和BMP信号的接口处起作用，以通过负调节Tkv来设置对这一正向生长信号的限制，从而确保适当的突触生长。

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