Effect on axonal DCV transport of RNAi knockdown of different genes involved in trafficking of DCV membrane proteins or suspected to play a role in motor adaptor recruitment. (A) Representative kymographs showing transport of ILP2-GFP–positive DCVs in motor axons of control larvae and larvae subjected to motor neuron-targeted knockdown of Rab14, dNischarin, or CG6707. Scale bar: 10 µm. (B) Top, directional distributions derived from A, averaged from the following number of larvae: control 13, Rab14-KD 7, dNischarin-KD 8, CG6707(KK)-KD 7, and CG6707(VAL10)-KD 6. Bottom, the retrograde peak amplitude (ANOVA, P = 0.917), anterograde peak amplitude (ANOVA, P = 0.150), logarithmic ratio of retrograde to anterograde peak amplitude (ANOVA, P = 0.738), and relative static peak amplitude (ANOVA, P = 0.089) for the directional distributions at the top. In A and B, KK and VAL20 refer to the use of UAS-RNAi lines from the KK collection and the VALIUM10 vector-based collection, respectively. For simplicity, only KK line data are illustrated in A. (C) Representative kymographs showing transport of ILP2-GFP–positive DCVs in motor axons of control larvae and larvae subjected to motor neuron-targeted knockdown of Rab4, ruby, or Vps35. Scale bar: 10 µm. (D) Top, directional distributions derived from C, averaged from the following number of larvae: control 9, Rab4-KD 9, ruby-KD 8, and Vps35-KD 9. Bottom, the retrograde peak amplitude (ANOVA, P = 0.431), anterograde peak amplitude (ANOVA, P = 0.298), logarithmic ratio of retrograde to anterograde peak amplitude (ANOVA, P = 0.415), and relative static peak amplitude (ANOVA, P <0.005, followed by Dunnett’s test obtaining the indicated P values). Data in all panels are from third instar larvae. Bar graphs in B and D represent mean + SEM. N.s., not significant.