Fig. 1. SFKs play redundant roles during formation of the embryonic CNS commissures. Stage 16 Drosophila embryos of the indicated genotypes were stained with mAb BP102 to label all central axons. Anterior is up. (A) Wild type, (B) Wnt5⁴⁰⁰, (C) Src42A^E1, (D) Src64B^KO, (E) Src42A^E1/+; Src64B^KO/+, (F) Src42A^E1; Src64B^KO/+, (G) Src42A^E1/+; Src64B^KO, (H) Src42A^E1; Src64B^KO, (I) ELAV-GAL4/UAS-RNAi-Src64B and (J) Src42A^E1; ELAV-GAL4/UAS-RNAi-Src64B are shown. Defects similar to those seen in Wnt5⁴⁰⁰, namely `fuzzy' commissures and breaks in the longitudinal pathways, are observed in individuals homozygous for one of the SFK mutants and heterozygous for the other and also in individuals of a Src42A mutant background when Src64B expression is reduced in the nervous system by RNA interference. The commissures are completely fused (white arrow in H) in the double homozygotes. See Table 1 for quantitation. AC, anterior commissure; PC, posterior commissure.