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Fig. 3. Fra is required cell autonomously to guide axons and the P3 motif is critical for mediating Fra attractive function. (A-D) Stage 16 embryos stained with mAb BP102 to visualize all axons, and anti-GFP to highlight the Egl neurons. Indicated genotypes also contain UAS-TauMycGFP and eagleGal4. Anterior is up. (A) EW axons fail to cross the midline in many segments of fra mutants (starred arrows). Also notice the overall thinning of CNS commissural bundles (arrowhead). (B) fra mutant defects can be rescued (arrows) by specifically expressing UAS-Fra-Myc in the Egl neurons. (C) Similar to UAS-Fra-Myc, expression of UAS-FraP1P2-Myc in the Egl neurons results in rescue of the fra guidance defects. (D) A Fra receptor lacking the P3 motif cannot rescue the guidance defects of fra mutants. (B-D, bottom panels) Anti-Myc staining (green) of embryos expressing UAS-Fra-Myc (B), UAS-FraP1P2-Myc (C) or UAS-FraP3-Myc (D) under the control of elavGal4 shows that the transgenes are expressed at comparable levels and are similarly localized to CNS axons. One segment is shown. (E) The rescuing ability of each of the constructs used in this study. Green bars indicate rescue that is comparable to that of wild type; red bars indicate a failure to rescue. Data is presented as the percentage of EW axons that fail to cross the midline. Mutant defects were scored as the complete absence or thinning of EW axons across the midline. Each bar represents an independent transgenic line (see Fig. S1 in the supplementary material; Materials and methods). A total of 60-80 embryos were scored for each genotype (or approximately 15-20 embryos for each line). Error bars indicate s.e.m. For statistical analysis, see Fig. S1 in the supplementary material.

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