Patronin knockdown activates DLK/JNK signaling, but only a subset of phenotypes depends on DLK/JNK. (A–D) Quantification of FI of puc-GFP reporter and microtubule dynamics with drug treatments. Numbers on the graph are numbers of neurons quantified. The same neurons were used to measure puc-GFP levels, microtubule dynamics, and polarity. *, P < 0.05; **, P < 0.01; ****, P < 0.0001 with one-way ANOVA followed by Dunnett’s multiple comparison. Statistical tests were performed for each drug treatment group, except for the comparison between control RNAi with vehicle control and Patronin RNAi 1 with GNE-3511 treatment for puc-GFP reporter, which was done by t test. (B) Representative images of puc-GFP reporter coexpressed with EB1-TagRFP-T. Bar, 5 μm. (D) Numbers on the graph are the total comet numbers collected from each group. ****, P < 0.0001 with Fisher’s exact test. (E) Representative kymographs of EB1-TagRFP-T with drug treatments. Turquoise lines mark plus ends. Horizontal bar, 5 μm. Vertical bar, 60 s. (F and G) Quantification of minus end polymerization duration and length with drug treatment. Note that the control RNAi and Patronin RNAi 1 data have been shown in Fig. 3, B and C, and are shown again here for comparison. In the drug treatment group, 135 traces were collected from 18 neurons. Kruskal–Wallis tests followed by Dunnett’s multiple comparisons were performed because of non-Gaussian distribution of these data. ****, P < 0.0001. (H) Schematic diagram showing the effects of Patronin knockdown. Note that short minus end growth phenotype and mixed polarity are not secondary to activated DLK/JNK signaling.