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Fig. 3 | Acta Neuropathologica Communications

Fig. 3

From: Senataxin helicase, the causal gene defect in ALS4, is a significant modifier of C9orf72 ALS G4C2 and arginine-containing dipeptide repeat toxicity

Fig. 3

SETX co-expression suppresses neuromuscular junction degeneration in a Drosophila model of GR(50) dipeptide toxicit. a We directed expression of GR(50)-GFP or membrane targeted mCD8-GFP, alone or in combination with normal SETX(wt) or mutant SETX(L389S), to motor neurons by crossing transgenic flies with flies expressing the OK6-GAL4 driver. Here we see representative images of the neuromuscular junction (NMJ) of muscle 6/7 at hemi-segment A3 for 3rd instar wandering larvae. Note the reduced length of the NMJ for fly larvae expressing GR(50)-GFP. Scale bar = . b We measured the NMJ length at muscle 6/7 at hemi-segment A3 as shown in ‘a’ for fly larvae of the indicated genotypes (n = 9–13). NMJ length was normalized to the muscle surface area. ANOVA with post-hoc Tukey test; *P < 0.05, ****P < 0.0001. c We counted the number of synaptic boutons from NMJs as shown in (A) for fly larvae of the indicated genotypes (n = 9–13). Bouton number was normalized to the muscle surface area. ANOVA with post-hoc Tukey test; *P < 0.05, ****P < 0.0001. See Additional file 1: Table S1 for all P values. Error bars = s.e.m

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