Shaggy, the Homolog of Glycogen Synthase Kinase 3, Controls Neuromuscular Junction Growth inDrosophila
Open Access
- 21 July 2004
- journal article
- Published by Society for Neuroscience in Journal of Neuroscience
- Vol. 24 (29) , 6573-6577
- https://doi.org/10.1523/jneurosci.1580-04.2004
Abstract
A protein-trap screen using theDrosophilaneuromuscular junction (NMJ) as a model synapse was performed to identify genes that control synaptic structure or plasticity. We found that Shaggy (Sgg), theDrosophilahomolog of the mammalian glycogen synthase kinases 3 α and β, two serine-threonine kinases, was concentrated at this synapse. Using various combinations of mutant alleles ofshaggy, 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.Keywords
This publication has 19 references indexed in Scilit:
- GSK-3β inhibition reverses axonal transport defects and behavioural phenotypes in DrosophilaMolecular Psychiatry, 2004
- The Drosophila Wnt, Wingless, Provides an Essential Signal for Pre- and Postsynaptic DifferentiationCell, 2002
- LTP, Memory and Structural PlasticityCurrent Molecular Medicine, 2002
- Targeted increase in shaggy activity levels blocks wingless signalingGenesis, 2002
- A protein trap strategy to detect GFP-tagged proteins expressed from their endogenous loci in DrosophilaProceedings of the National Academy of Sciences, 2001
- The renaissance of GSK3Nature Reviews Molecular Cell Biology, 2001
- Identified motor terminals inDrosophila larvae show distinct differences in morphology and physiologyJournal of Neurobiology, 2000
- WNT-7a Induces Axonal Remodeling and Increases Synapsin I Levels in Cerebellar NeuronsDevelopmental Biology, 1997
- Genetic Dissection of Structural and Functional Components of Synaptic Plasticity. II. Fasciclin II Controls Presynaptic Structural PlasticityNeuron, 1996
- Genetic Dissection of Structural and Functional Components of Synaptic Plasticity. I. Fasciclin II Controls Synaptic Stabilization and GrowthNeuron, 1996