Abelson, enabled, and p120catenin exert distinct effects on dendritic morphogenesis in Drosophila
Article first published online: 7 JUL 2005
Copyright © 2005 Wiley-Liss, Inc.
Special Issue: Developmental Neurobiology Special Issue
Volume 234, Issue 3, pages 512–522, November 2005
How to Cite
Li, W., Li, Y. and Gao, F.-B. (2005), Abelson, enabled, and p120catenin exert distinct effects on dendritic morphogenesis in Drosophila. Dev. Dyn., 234: 512–522. doi: 10.1002/dvdy.20496
- Issue published online: 18 OCT 2005
- Article first published online: 7 JUL 2005
- Manuscript Accepted: 16 MAY 2005
- Manuscript Revised: 28 APR 2005
- Manuscript Received: 18 APR 2005
- National Institutes of Health. Grant Numbers: HD044752, NS050117
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. Developmental Dynamics 234:512–522, 2005. © 2005 Wiley-Liss, Inc.