Fig. 2. Src64B is required for Wnt5/drl-mediated axon repulsion. (A) Ectopic WNT5 expression in the midline glia (SIM-GAL4, UAS-WNT5/+) results in frequent thinning or complete loss (arrow) of the AC. (B) Heterozygosity for Src64B suppresses the thinning/loss of the AC (SIM-GAL4, UAS-WNT5/+; Src64B^Pl/+). (C) EG⁺ neurons crossing in the AC and PC in a Drosophila embryo with one copy of UAS-DRL-MYC and one copy of UAS-NLS-β-Gal visualized by anti-MYC staining (UAS-DRL-MYC/+; UAS-NLS-β-Gal/+; EG-GAL4/+). (D) Overexpression of SRC64B in EG⁺ neurons does not cause the PC axons to switch commissures (UAS-mCD8-GFP/UAS-SRC64B; EG-GAL4/+). (E) Simultaneous expression of DRL-MYC and SRC64B in the EG⁺ axons significantly increases the number of the PC-crossing lineages to switch to the AC (arrow) (UAS-DRL-MYC/+; UAS-SRC64B/+; EG-GAL4/+). Quantitation is presented in Tables 2 and 3. Stage 16 embryos are shown, anterior is up.