Fig. 7. The FraC misexpression phenotype depends on Netrin but not Slit-Robo or Unc-5 signaling. (A,B,E-J) Stage 16 embryos stained with mAb BP102 to display all axons and anti-HA to reveal FraC-HA expression. Anterior is up. (A) Netrin mutants contain many segments with absent or thin commissures suggesting a decrease in midline attraction (arrowheads). (B) Expression of FraC cannot enhance the Netrin phenotype suggesting that the receptor depends on Netrin to generate an overexpression phenotype (compare this phenotype to the one in Fig. 5E). (C,D) Late stage 16 embryos stained with anti-FasII (1D4) to display three ipsilateral bundles of axons and anti-HA to reveal FraC-HA expression. Anterior is up. (C) Medial FasII-positive bundles frequently cross and re-cross the midline in robo mutants. (D) Fewer FasII-positive axons cross the midline when FraC is overexpressed. (E) fra, robo double mutants have many extra axons crossing the midline, though the defects are slightly less severe than robo single mutants. (F) Expression of FraC in all neurons in fra, robo double mutants causes a dramatic defect in commissure formation, although some commissures still do form relatively normally. (G) In fra, slit double mutants almost all axons collapse at the midline. (H) Expression of FraC is able to push axons laterally in a fra, slit mutant background. (I,J) The FraC misexpression phenotype is not dependent on the presence of the Unc-5 repulsive Netrin receptor.