stathmin disruption results in loss of Futsch at the axon terminal. A, Images of muscle 4 NMJs in segment 4 from WT (+/+), the stathmin mutant (stai^B200/stai^B200), and the stathmin mutant with rescue expression of tub::stai (stai^B200/stai ^B200; tub::stai/tub::stai) immunostained with α-Futsch (red), α-DVGLUT (green), and α-HRP (blue). B, Images of muscle 4 NMJs in segment 4 from WT (GeneSwitchELAV/+) and following neuronal expression of stathmin RNAi (UAS-stai RNAi/+; +/+; GeneSwitchELAV/+) immunostained with α-Futsch (red), α-DVGLUT (green), and α-HRP (blue). C, Histogram showing the quantification of the average intensity of Futsch NMJ in the genotypes shown in A. WT, n = 11; stathmin mutant, n = 10; stathmin mutant with rescue, n = 13; RNAi control, n = 14; stathmin RNAi, n = 10. *p < 0.001 for the comparisons wild type versus rescue and RNAi control versus stathmin RNAi. Scale bars: 10 μm.