GSBS Student Publications

Student Author(s)

Lei Shi; Jacob Yang

GSBS Program

Neuroscience

UMMS Affiliation

Department of Neurobiology; Tzumin Lee Lab; Graduate School of Biomedical Sciences, Neuroscience Program

Date

6-22-2007

Document Type

Article

Medical Subject Headings

Animals; Animals, Genetically Modified; Axons; Dendrites; Drosophila; Drosophila Proteins; Membrane Proteins; Morphogenesis; Neural Cell Adhesion Molecules; Protein Isoforms; Variation (Genetics)

Disciplines

Neuroscience and Neurobiology

Abstract

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.

Rights and Permissions

Citation: J Neurosci. 2007 Jun 20;27(25):6723-8. Link to article on publisher's site

Related Resources

Link to Article in PubMed

Journal Title

The Journal of neuroscience : the official journal of the Society for Neuroscience

PubMed ID

17581959

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