Abelson, enabled, and P120catenin exert distinct effects on dendritic morphogenesis in Drosophila
Abelson, enabled, and P120catenin exert distinct effects on dendritic morphogenesis in Drosophila
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DOI：
10.1002/dvdy.20496
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发表时间：
2005-11-01
影响因子：
2.5
通讯作者：
Gao, FB
中科院分区：
文献类型：
--
作者：
Li, WJ;Li, Y;Gao, FB
神经元表现出不同的树突分支模式，这对它们的功能很重要。然而，控制不同树突结构形成的信号通路在很大程度上仍然未知。为了在体内解决这个问题，我们使用果蝇的周围神经系统（PNS）作为模型系统。通过体内功能丧失和功能获得分析，我们发现非受体酪氨酸激酶Abelson （Abl）是细胞骨架动力学的重要调节因子，可以抑制果蝇树突树突（DA）感觉神经元的树突分支。Enabled （Ena）是Abl的底物，促进DA神经元树突分支和富含肌动蛋白的棘状突起的形成，与Abl的作用相反。相反，p120catenin （p120ctn）主要促进棘样突起的发展。这些结果表明，Ena是树突分支的关键调节剂，不同的肌动蛋白细胞骨架调节剂对树突形态发生的影响不同。
Neurons exhibit diverse dendritic branching patterns that are important for their function. However, the signaling pathways that control the formation of different dendritic structures remain largely unknown. To address this issue in vivo, we use the peripheral nervous system (PNS) of Drosophila as a model system. Through both loss-of-function and gain-of-function analyses in vivo, we show here that the nonreceptor tyrosine kinase Abelson (Abl), an important regulator of cytoskeleton dynamics, inhibits dendritic branching of dendritic arborization (DA) sensory neurons in Drosophila. Enabled (Ena), a substrate for Abl, promotes the formation of both dendritic branches and actin-rich spine-like protrusions of DA neurons, an effect opposite to that of Abl. In contrast, p120catenin (p120ctn) primarily enhances the development of spine-like protrusions. These results suggest that Ena is a key regulator of dendritic branching and that different regulators of the actin cytoskeleton exert distinct effects on dendritic morphogenesis.