Department of Neuroscience and Physiology, State University of New York Upstate Medical University, Syracuse, NY 13210, USA
Department of Physiology, Howard Hughes Medical Institute, University of California San Francisco, San Francisco, CA 20251, USA.
Development. 2019 Apr 17;146(8):dev163592. doi: 10.1242/dev.163592.
Developmental pruning of axons and dendrites is crucial for the formation of precise neuronal connections, but the mechanisms underlying developmental pruning are not fully understood. Here, we have investigated the function of JNK signaling in dendrite pruning using class IV dendritic arborization (c4da) neurons as a model. We find that loss of JNK or its canonical downstream effectors Jun or Fos led to dendrite-pruning defects in c4da neurons. Interestingly, our data show that JNK activity in c4da neurons remains constant from larval to pupal stages but the expression of Fos is specifically activated by ecdysone receptor B1 (EcRB1) at early pupal stages, suggesting that ecdysone signaling provides temporal control of the regulation of dendrite pruning by JNK signaling. Thus, our work not only identifies a novel pathway involved in dendrite pruning and a new downstream target of EcRB1 in c4da neurons, but also reveals that JNK and Ecdysone signaling coordinate to promote dendrite pruning.
轴突和树突的发育修剪对于形成精确的神经元连接至关重要，但发育修剪的机制尚不完全清楚。在这里，我们使用第四类树突分支（c4da）神经元作为模型，研究了 JNK 信号在树突修剪中的作用。我们发现 JNK 或其经典下游效应物 Jun 或 Fos 的缺失导致 c4da 神经元的树突修剪缺陷。有趣的是，我们的数据表明，c4da 神经元中的 JNK 活性从幼虫到蛹期保持不变，但 Fos 的表达仅在早期蛹期被 EcRB1 特异性激活，这表明蜕皮激素信号提供了对 JNK 信号调控树突修剪的时间控制。因此，我们的工作不仅鉴定了一个参与树突修剪的新途径和 c4da 神经元中 EcRB1 的一个新下游靶标，而且还揭示了 JNK 和蜕皮激素信号协调促进树突修剪。
