Epidermis-Derived Semaphorin Promotes Dendrite Self-Avoidance by Regulating Dendrite-Substrate Adhesion in Drosophila Sensory Neurons.
Epidermis-Derived Semaphorin Promotes Dendrite Self-Avoidance by Regulating Dendrite-Substrate Adhesion in Drosophila Sensory Neurons.
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DOI：
10.1016/j.neuron.2016.01.020
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发表时间：
2016-02-17
期刊：
影响因子：
16.2
通讯作者：
Jan YN
中科院分区：
文献类型：
--
作者：
Meltzer S;Yadav S;Lee J;Soba P;Younger SH;Jin P;Zhang W;Parrish J;Jan LY;Jan YN
树突轴的精确图案对于神经回路的布线和功能至关重要。树突-细胞外基质（ECM）粘附确保果蝇树突分枝（da）感觉神经元的树突被适当地限制在二维空间中，从而促进接触介导的树突自我回避和平铺。然而，体内调节树突-ECM粘附的机制尚不清楚。在这里，我们发现，由于树突-ECM 粘附缺陷，信号蛋白配体 sema-2b 的突变导致树突自交叉急剧增加，从而导致无法将树突限制在 2D 平面上。此外，我们发现 Sema-2b 由表皮分泌，并通过邻近神经元中的 Plexin B 受体发出信号。重要的是，我们发现 Sema-2b/PlexB 在遗传和物理上与 TORC2 复合物、三角 (Trc) 激酶和整合素相互作用。这些结果揭示了信号蛋白在树突图案化中的新作用，并说明了表皮衍生的信号如何调节神经回路组装。梅尔策等人。证明需要来自表皮的信号蛋白配体将树突限制在二维空间中，从而促进自我回避。他们进一步表明，Trc/Fry 和整合素信号传导途径是 Sema-2b/PlexB 信号传导的组成部分。
Precise patterning of dendritic arbors is critical for the wiring and function of neural circuits. Dendrite-extracellular matrix (ECM) adhesion ensures that the dendrites of Drosophila dendritic arborization (da) sensory neurons are properly restricted in a 2D space, and thereby facilitates contact-mediated dendritic self-avoidance and tiling. However, the mechanisms regulating dendrite-ECM adhesion in vivo are poorly understood. Here, we show that mutations in the semaphorin ligand sema-2b lead to a dramatic increase in self-crossing of dendrites due to defects in dendrite-ECM adhesion, resulting in a failure to confine dendrites to a 2D plane. Furthermore, we find that Sema-2b is secreted from the epidermis and signals through the Plexin B receptor in neighboring neurons. Importantly, we find that Sema-2b/PlexB genetically and physically interacts with TORC2 complex, Tricornered (Trc) kinase and integrins. These results reveal a novel role for semaphorins in dendrite patterning and illustrate how epidermal-derived cues regulate neural circuit assembly. Meltzer et al. demonstrate that semaphorin ligand derived from epidermis is required to restrict dendrites into a 2D space, thereby facilitating self-avoidance. They further show that Trc/Fry and integrin signaling pathways are components of Sema-2b/PlexB signaling.