Open Access Research article

DFsn collaborates with Highwire to down-regulate the Wallenda/DLK kinase and restrain synaptic terminal growth

Chunlai Wu, Richard W Daniels and Aaron DiAntonio*

Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110, USA

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Neural Development 2007, 2:16 doi:10.1186/1749-8104-2-16

Published: 15 August 2007

Additional files

Additional file 1:

Expression of a DFsn transgene in motoneurons rescues the morphological phenotype of DFsn mutants. (a) Representative confocal images of muscle 6/7 and muscle 4 synapses co-stained with DVGLUT (green) and FasII (red), in wild-type (WT), DFsn mutant [P(f06595)/Df(2R)7872] and DFsn motoneuron rescue (DFsn-MN Res) [P(f06595)/Df(2R)7872;UAS-GFP-DFsn/D42-Gal4] third instar larvae. (b) Quantification of bouton number of muscle 4 synapses in WT, DFsn and DFsn motoneuron rescue (DFsn-MN Res) third instar larvae (n = 22, 22 and 27 cells, respectively). The morphological defects in the DFsn mutant are rescued by the expression of GFP-DFsn in motoneurons (p < 0.001 for DFsn-MN Res versus DFsn; p > 0.9 for DFsn-MN Res versus WT).

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