A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Reference Report

Reference
Citation Xiong, X., Wang, X., Ewanek, R., Bhat, P., Diantonio, A., Collins, C.A. (2010). Protein turnover of the Wallenda/DLK kinase regulates a retrograde response to axonal injury.  J. Cell Biol. 191(1): 211--223. (Export to RIS)
FlyBase ID FBrf0211939
Publication Type Research paper
PubMed ID 20921142
PubMed Abstract Regenerative responses to axonal injury involve changes in gene expression; however, little is known about how such changes can be induced from a distant site of injury. In this study, we describe a nerve crush assay in Drosophila melanogaster to study injury signaling and regeneration mechanisms. We find that Wallenda (Wnd), a conserved mitogen-activated protein kinase (MAPK) kinase kinase homologous to dual leucine zipper kinase, functions as an upstream mediator of a cell-autonomous injury signaling cascade that involves the c-Jun NH(2)-terminal kinase MAPK and Fos transcription factor. Wnd is physically transported in axons, and axonal transport is required for the injury signaling mechanism. Wnd is regulated by a conserved E3 ubiquitin ligase, named Highwire (Hiw) in Drosophila. Injury induces a rapid increase in Wnd protein concomitantly with a decrease in Hiw protein. In hiw mutants, injury signaling is constitutively active, and neurons initiate a faster regenerative response. Our data suggest that the regulation of Wnd protein turnover by Hiw can function as a damage surveillance mechanism for responding to axonal injury.
DOI 10.1083/jcb.201006039
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Language of Publication English
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Publication Type Journal
Abbreviation J. Cell Biol.
Title Journal of Cell Biology
Publication Year 1966-
ISBN/ISSN 0021-9525
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