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Originally published as MBC in Press, 10.1091/mbc.E06-09-0818 on August 1, 2007

Vol. 18, Issue 10, 3883-3893, October 2007

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CDK-5 Regulates the Abundance of GLR-1 Glutamate Receptors in the Ventral Cord of Caenorhabditis elegans

Peter Juo*,{dagger}, Tom Harbaugh{ddagger}, Gian Garriga{ddagger}, and Joshua M. Kaplan*

*Department of Molecular Biology, Massachusetts General Hospital, and Department of Genetics, Harvard Medical School, Boston, MA 02114; {ddagger}Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720; and {dagger}Department of Physiology, Tufts University School of Medicine, Boston, MA 02111

Submitted September 14, 2006; Revised June 21, 2007; Accepted July 20, 2007
Monitoring Editor: Francis Barr

The proline-directed kinase Cdk5 plays a role in several aspects of neuronal development. Here, we show that CDK-5 activity regulates the abundance of the glutamate receptor GLR-1 in the ventral cord of Caenorhabditis elegans and that it produces corresponding changes in GLR-1–dependent behaviors. Loss of CDK-5 activity results in decreased abundance of GLR-1 in the ventral cord, accompanied by accumulation of GLR-1 in neuronal cell bodies. Genetic analysis of cdk-5 and the clathrin adaptin unc-11 AP180 suggests that CDK-5 functions prior to endocytosis at the synapse. The scaffolding protein LIN-10/Mint-1 also regulates GLR-1 abundance in the nerve cord. CDK-5 phosphorylates LIN-10/Mint-1 in vitro and bidirectionally regulates the abundance of LIN-10/Mint-1 in the ventral cord. We propose that CDK-5 promotes the anterograde trafficking of GLR-1 and that phosphorylation of LIN-10 may play a role in this process.

This was published online ahead of print in MBC in Press (http://www.molbiolcell.org/cgi/doi/10.1091/mbc.E06-09-0818) on August 1, 2007.

Address correspondence to: Peter Juo (peter.juo{at}tufts.edu)




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