Journal
NEURON
Volume 41, Issue 4, Pages 521-534Publisher
CELL PRESS
DOI: 10.1016/S0896-6273(04)00016-9
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Funding
- NIGMS NIH HHS [5 T32GM08349] Funding Source: Medline
- NINDS NIH HHS [NS43244, NS44722-01, R01 NS043244-03, R01 NS043244, NS15390] Funding Source: Medline
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We describe the isolation and characterization of nwk (nervous wreck), a temperature-sensitive paralytic mutant that causes excessive growth of larval neuromuscular junctions (NMJs), resulting in increased synaptic bouton number and branch formation. Ultrastructurally, mutant boutons have reduced size and fewer active zones, associated with a reduction in synaptic transmission. nwk encodes an FCH and SH3 domain-containing adaptor protein that localizes to the perk active zone of presynaptic terminals and binds to the Drosophila ortholog of Wasp (Wsp), a key regulator of actin polymerization. wsp null mutants display synaptic overgrowth similar to nwk and enhance the nwk morphological phenotype in a dose-dependent manner. Evolutionarily, Nwk belongs to a previously undescribed family of adaptor proteins that includes the human srGAPs, which regulate Rho activity downstream of Robo receptors. We propose that Nwk controls synapse morphology by regulating actin dynamics downstream of growth signals in presynaptic terminals.
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