QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

First published online November 11, 2004
doi: 10.1242/10.1242/dev.01457

This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lai, T. Articles by Garriga, G. Search for Related Content PubMed PubMed Citation Articles by Lai, T. Articles by Garriga, G. Social Bookmarking                         What's this?

The conserved kinase UNC-51 acts with VAB-8 and UNC-14 to regulate axon outgrowth in C. elegans

Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA

^* Author for correspondence (e-mail: garriga{at}berkeley.edu)

Accepted 22 September 2004

Directional cues guide growth cones. While molecules like UNC-6/netrin direct migrations along the dorsoventral axis of many organisms, it is unclear how anteroposterior guidance is achieved. We describe a physical interaction between VAB-8, a protein both necessary and sufficient for posteriorly directed migrations in C. elegans, and UNC-51, a conserved serine/threonine kinase that functions generally in axon outgrowth. We show that both proteins function in the CAN neurons to direct their axons posteriorly. Expression in the CANs of peptides predicted to interfere with interactions between UNC-51 and both VAB-8 and UNC-14, a second protein that interacts physically with UNC-51, disrupts CAN axon outgrowth. We provide genetic evidence that VAB-8 functions in an UNC-51 pathway for posteriorly directed CAN axon guidance and show that VAB-8 and UNC-14 can be targets of UNC-51 kinase activity. Taken together, our results suggest that VAB-8 and UNC-14 are substrates that mediate the function of UNC-51 in axon outgrowth.

Key words: C. elegans, UNC-14, UNC-51, VAB-8, Axon guidance

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				E. Y. Chan mTORC1 Phosphorylates the ULK1-mAtg13-FIP200 Autophagy Regulatory Complex Sci. Signal., August 18, 2009; 2(84): pe51 - pe51. [Abstract] [Full Text] [PDF]

				H. Toda, H. Mochizuki, R. Flores III, R. Josowitz, T. B. Krasieva, V. J. LaMorte, E. Suzuki, J. G. Gindhart, K. Furukubo-Tokunaga, and T. Tomoda UNC-51/ATG1 kinase regulates axonal transport by mediating motor-cargo assembly Genes & Dev., December 1, 2008; 22(23): 3292 - 3307. [Abstract] [Full Text] [PDF]

				D. J. Solecki, E.-E. Govek, T. Tomoda, and M. E. Hatten Neuronal polarity in CNS development Genes & Dev., October 1, 2006; 20(19): 2639 - 2647. [Abstract] [Full Text] [PDF]

				K.-i. Ogura and Y. Goshima The autophagy-related kinase UNC-51 and its binding partner UNC-14 regulate the subcellular localization of the Netrin receptor UNC-5 in Caenorhabditis elegans Development, September 1, 2006; 133(17): 3441 - 3450. [Abstract] [Full Text] [PDF]

				L. Jia and S. W. Emmons Genes That Control Ray Sensory Neuron Axon Development in the Caenorhabditis elegans Male Genetics, July 1, 2006; 173(3): 1241 - 1258. [Abstract] [Full Text] [PDF]