Figure 5

MEC-17 and ATAT-2 function independently from MEC-12/α-tubulin acetylation in maintaining synaptic branch stability. (a) The proportion of animals displaying intact synaptic branches in mec-12(tm5083), mec-12[K40Q], mec-12[K40R] mutants compared to wild-type. For each independent experiment n ≥ 27 (total n ≥ 87). (b) Quantification of animals with intact synaptic branches in mec-17(ok2109) and mec-12(tm5083) single and double mutant animals. For each independent experiment, n ≥ 29 (total n ≥ 89). (c) Quantification of animals with intact synaptic branches in atat-2(ok2415) and mec-12(tm5083) single and double mutant animals. For each independent experiment, n ≥ 23 (total n ≥ 80). (d) The percentage of intact synaptic branches in animals carrying the atat-2(ok2415) mutant alone, or in combination with the mec-12[K40Q] or mec-12[K40Q] mutations. For each independent experiment n ≥ 29 (total n ≥ 89). (e) Quantification of animals with intact synaptic branches in mec-17(ok2109) and mec-7(ok2152) single and double mutant animals. For each independent experiment, n ≥ 30 (total n ≥ 90). Bars show mean ± SE; P values * < 0.05, ** < 0.01, *** < 0.001, **** < 0.0001 from one-way ANOVA with Tukey’s post-hoc test. (f) The percentage of wild-type, mec-17(ok2109) and atat-2(ok2415) animals (transgenic) with intact synaptic branches when treated with 1% DMSO (control, white bars), 0.5 mM colchicine (dark blue bars), or 10 μM paclitaxel (purple bars). For three independent experiments n ≥ 20 (total n ≥ 62). Bars show mean ± SE; P values ** < 0.01, *** < 0.001 from one-way ANOVA with Tukey’s post-hoc test.