<p>(A-D) Stage 15–16 embryos of the indicated genotype carrying eg-GAL4 and UAS-tauMycGFP transgenes, stained with anti-GFP (grey or green) (A-C) or anti-HRP (magenta) (D) antibodies. Anti-GFP labels cell bodies and axons of the eagle neurons (EG and EW), Anti-HRP reveals all of the CNS axons. Scale bar represents 10μm (A). Arrowheads indicate segments with non-crossing EW axons (A-C) or thin commissures (D). (A) In a FraΔC background the heterozygosity for <i>Apc2</i> enhances the EW crossing defects to 59%. (B) In the embryos double heterozygous for <i>Apc2</i> and <i>brat</i> expressing UAS-FraΔC selectively in eagle neurons, EW axons fail to cross in the posterior commissure in 72% of segments. (C) In <i>Apc2</i> and <i>brat</i> double mutant embryos, EW axons fail to cross in the posterior commissure in 20% of segments and show thinner commissures in some segments (D). (E) Quantification of EW midline crossing defects in the genotypes shown in (A-D). Df (2L) Exel6168 is a chromosomal deficiency containing <i>Apc2</i>. Data are presented as mean ± SEM. 20 embryos were scored for each genotype. Significance was assessed by multiple comparisons using ANOVA (<sup>∗∗∗∗</sup>p< 0.0001). (F) Quantification of EW midline crossing defects in the indicated genotypes. Data are presented as mean ± SEM. 20 embryos were scored for each genotype. Significance was assessed by multiple comparisons using ANOVA (<sup>∗∗∗</sup>p < 0.001).</p
