Specific Drosophila Dscam juxtamembrane variants control dendritic elaboration and axonal arborization
Student Authors
Lei Shi; Jacob YangUMass Chan Affiliations
Graduate School of Biomedical Sciences, Neuroscience ProgramLee Lab
Neurobiology
Document Type
Journal ArticlePublication Date
2007-06-22Keywords
Animals; Animals, Genetically Modified; Axons; Dendrites; Drosophila; Drosophila Proteins; Membrane Proteins; Morphogenesis; Neural Cell Adhesion Molecules; Protein Isoforms; Variation (Genetics)Neuroscience and Neurobiology
Metadata
Show full item recordAbstract
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.Source
J Neurosci. 2007 Jun 20;27(25):6723-8. Link to article on publisher's siteDOI
10.1523/JNEUROSCI.1517-07.2007Permanent Link to this Item
http://hdl.handle.net/20.500.14038/33776PubMed ID
17581959Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1523/JNEUROSCI.1517-07.2007