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Figure 4 | Molecular Neurodegeneration

Figure 4

From: Motor neuron apoptosis and neuromuscular junction perturbation are prominent features in a Drosophila model of Fus-mediated ALS

Figure 4

The overexpression of Fus/Caz causes morphological and functional defects in NMJs. (A) A representative confocal image (projection over the Z axis) of muscle 6/7 NMJs in the abdominal segment A2 of a third instar larva expressing mGFP by OK371-Gal4. The anti-HRP antibody staining labels the neuronal membrane and the anti-Dlg antibody staining marks the subsynaptic reticulum surrounding each bouton. (B-E) NMJs in the abdominal segment A2 from larvae coexpressing mGFP with Fus, FusR521G, FusΔ32, or Caz by OK371-Gal4 were stained for Dlg, HRP, and Myc or HA with the appropriate antibodies. Branches and the number of large boutons revealed by Dlg staining were dramatically reduced by Fus, FusR521G, and Caz, but not by FusΔ32 expression. (F) Quantification analysis of the large boutons in the NMJs from ventral longitudinal muscles 6 and 7 of segment A2 (mean ± s.d.; n ≥ 20). OK371-Gal4 alone served as control. (G-H) Representative images of axon branches and small boutons, as visualized by both mGFP and HRP staining, at muscle 6/7 NMJs in the abdominal segment A2. (I) Quantification of the small boutons in the NMJs from ventral segment A2 (mean ± s.d.; n ≥ 20). OK371-Gal4 alone served as control.

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