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The Journal of Neuroscience, June 20, 2007, 27(25):6723-6728; doi:10.1523/JNEUROSCI.1517-07.2007

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Brief Communications
Specific Drosophila Dscam Juxtamembrane Variants Control Dendritic Elaboration and Axonal Arborization

Lei Shi, * Hung-Hsiang Yu, * Jacob S. Yang, * and Tzumin Lee

Department of Neurobiology, University of Massachusetts Medical School, Worcester, Massachusetts 01605

Correspondence should be addressed to Tzumin Lee at the above address. Email: tzumin.lee{at}umassmed.edu

Drosophila Dscam isoforms are derived from two alternative transmembrane/juxtamembrane domains (TMs) in addition to thousands of ectodomain variants. Using a microRNA-based RNA interference technology, we selectively knocked down different subsets of Dscams containing either the exon 17.1- or exon 17.2-encoding TM. Eliminating Dscam[TM1] reduced Dscam expression but minimally affected postembryonic axonal morphogenesis. In contrast, depleting Dscam[TM2] blocked axon arborization. Further removal of Dscam[TM1] enhanced the loss-of-Dscam[TM2] axonal phenotypes. However, Dscam[TM1] primarily regulates dendritic development, as evidenced by the observations that removing Dscam[TM1] alone impeded elaboration of dendrites and that transgenic Dscam[TM1], but not Dscam[TM2], effectively rescued Dscam mutant dendritic phenotypes in mosaic organisms. These distinct Dscam functions can be attributed to the juxtamembrane regions of TMs that govern dendritic versus axonal targeting of Dscam as well. Together, we suggest that specific Drosophila Dscam juxtamembrane variants control dendritic elaboration and axonal arborization.

Key words: protein targeting; axon; dendrite; down syndrome; Drosophila; RNA interference

Received Nov. 28, 2006; revised May 8, 2007; accepted May 14, 2007.

Correspondence should be addressed to Tzumin Lee at the above address. Email: tzumin.lee{at}umassmed.edu






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