Kinesin-1 controls the polarized localization of RIC-7. (A) Schematic representation of cell-specific knockdown of kinesin-1. (B) Representative images of control and kinesin-1/unc-116 knockdown conditions in the dendrite (left) and in the axon (right). Note the accumulation of mitochondria at the distal tip of the dendrite under auxin treatment, indicating kinesin-1 has been efficiently degraded. Arrowheads point to unpolarized RIC-7::7xSplitGFP puncta, while arrows indicate the polarized ones. (C) Linescans of individual mitochondria in the axons are shown in B. Green traces represent the intensity of RIC-7::7xSplitGFP whereas magenta traces represent that of mito::TagRFP. Arrows indicate the polarized localization of RIC-7::7xSplitGFP. (D) The number of axonal mitochondria does not change after 5 h of auxin treatment. Error bars represent SEM. Each data point represents one animal. Data are pooled from three independent experiments. Number of animals: 17 (ctrl) and 14 (auxin). (E) Quantification of the percentage of mitochondria based on RIC-7::7xSplitGFP’s polarization status. The scoring criteria is the same as Fig. 4 F except that the previous “Non-polarized” and “Proximal” categories are now combined as “Non-distal.” Number of mitochondria counted are indicated at the top of each bar. Error bars represent 95% confidence intervals. Same datasets as in D. ***P < 0.001, ****P < 0.0001 (Fisher’s exact test).