Figure 6.

KBP interaction with Kif1B is essential for SCG10 growth cone localization and axon extension. A–C, SCG10 is absent in both kbp^st23 and kif1b^st43 mutant pLL axon growth cones during axon extension. A′–C′ show SCG10 immunofluorescence alone. Arrows point to growth cones. D, F, Quantification of SCG10 mean fluorescence intensity in kbp^st23 (D) and kif1b^st43 (F) mutants compared with wild-type siblings shows a dramatic reduction (background subtracted) in SCG10 protein levels in mutant growth cones (ANOVA). E, Whereas expression of full-length KBP in kbp^st23 mutants rescues SCG10 mean fluorescence intensity, a version of KBP lacking the Kif1B binding domain (kbpΔkif1b) fails to do so (ANOVA). G, Expression of full-length KBP but not KBPΔKif1B rescues axon length in kbp^st23 mutants. Zygotes were injected with mRNA encoding either KBP or KBPΔKif1B and larvae were scored at 3 dpf as either having truncated or full-length pLL nerves. The percentage of larvae with truncated (black bar) or full-length (gray bar) nerves in each experimental group is depicted. Twenty-five percent of larvae are expected to show axon truncation from a heterozygous cross, as observed in the uninjected controls (χ²; ***p < 0.0001, **p < 0.005, NS, not significant). Error bars represent standard error of the mean.