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The Journal of Neuroscience, July 21, 2004, 24(29):6573-6577; doi:10.1523/JNEUROSCI.1580-04.2004

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Shaggy, the Homolog of Glycogen Synthase Kinase 3, Controls Neuromuscular Junction Growth in Drosophila

Bénédicte Franco,¹ Laurent Bogdanik,¹ Yves Bobinnec,² Alain Debec,² Joël Bockaert,¹ Marie-Laure Parmentier,¹ and Yves Grau¹

¹Laboratoire de Génomique Fonctionnelle, Unité Propre de Recherche Centre National de la Recherche Scientifique 2580, 34094 Montpellier Cedex 5, France, and ²Biologie du Développement, Unité Mixte de Recherche 7009, Observatoire Océanologique, 06230 Villefranche sur Mer, France

A protein-trap screen using the Drosophila neuromuscular junction (NMJ) as a model synapse was performed to identify genes that control synaptic structure or plasticity. We found that Shaggy (Sgg), the Drosophila homolog of the mammalian glycogen synthase kinases 3 and , two serine-threonine kinases, was concentrated at this synapse. Using various combinations of mutant alleles of shaggy, we found that Shaggy negatively controlled the NMJ growth. Moreover, tissue-specific expression of a dominant-negative Sgg indicated that this kinase is required in the motoneuron, but not in the muscle, to control NMJ growth. Finally, we show that Sgg controlled the microtubule cytoskeleton dynamics in the motoneuron and that Futsch, a microtubule-associated protein, was required for Shaggy function on synaptic growth.

Key words: motoneuron; morphological plasticity; microtubule loop; microtubule-associated protein; glycogen synthase kinase; synaptic plasticity

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Received Nov 12, 2003; revised June 1, 2004; accepted June 1, 2004.

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