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. Author manuscript; available in PMC: 2012 Dec 8.
Published in final edited form as: Neuron. 2011 Dec 8;72(5):760–775. doi: 10.1016/j.neuron.2011.09.031

Figure 4. Presynaptic Knockdown of Wengen Suppresses ank2-Dependent Degeneration.

Figure 4

(A) Wengen-Venus (green) expressed in motor neurons using OK371-GAL4 shows localization to motoneuron axons that are costained with the neuronal membrane marker HRP (red).

(B) Wengen-Venus (green) driven by OK371-GAL4. Wengen-Venus localizes to the NMJ, albeit at lower levels than in the axons.

(C) Neuronal-specific Wengen knockdown stained with the presynaptic active zone marker Brp (green) and the postsynaptic marker Dlg (red) at NMJ 6/7. Presynaptic expression of wengen-RNAi does not cause any significant synaptic degeneration.

(D) Representative image stained with Brp (green) and Dlg (red) showing suppression of ank2-dependent degeneration by neuronal expression of wengen-RNAi.

(E and F) Quantification of degeneration severity as in Figures 2E and 2F. wt = w1118 (n = 59 NMJs); wgnRNAi = elavC155-GAL4/+; wgnRNAi/+; ank22001/+ (n = 58 NMJs); ank2 = ank22001/ank22001 (n = 52 NMJs); wgnRNAi; ank2 = elavC155-GAL4/+; wgnRNAi/+; ank22001/ank22001 (n = 159 NMJs). ank2 mutants have significantly more synaptic degeneration than either wild-type or wengen-RNAi larva (p < 0.001), whereas wgn-RNAi; ank2 larva have significant suppression of ank2-dependent degeneration (p < 0.001). Error bars represent SEM. p values were determined using one-way ANOVA with post hoc Tukey-Kramer: *p < 0.05; ***p < 0.001. Statistical differences remain when comparisons are made using Student’s t test. n.s., not significant.