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MBC in Press, published online ahead of print August 1, 2007
Mol. Biol. Cell 10.1091/mbc.E06-09-0818

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Submitted on September 14, 2006
Revised on June 21, 2007
Accepted on July 20, 2007

CDK-5 Regulates the Abundance of GLR-1 Glutamate Receptors in the Ventral Cord of C. 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; {dagger}Department of Physiology, Tufts University School of Medicine, Boston, MA 02111

Monitoring Editor: Francis Barr

The proline-directed kinase CDK-5 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 C. elegans and 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 before 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.

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




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[Abstract] [Full Text] [PDF]


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