Fig. 7. The dfer gain-of-function mutant disrupts axon guidance at the ventral midline of the CNS. (A,B) Fillets of stage 16 embryos immunostained on the same slide show significantly higher levels of DFer protein in the CNS of dfer^gof mutants (B) than in wild type (A). (C) DFer protein is not expressed in the CNS of dfer^ex1 mutant embryos. (D) In wild-type embryos, Fasciclin 2 (brown) is expressed on longitudinal axons. (E,F) In dfer^gof mutants, axons cross the midline aberrantly (E, arrowhead), a phenotype that is enhanced when the levels of DFerRB are increased (F, arrowheads; UAS-DFerRB/+;+;dfer^gof). (G) Expression of the JNK inhibitor Puc rescues the midline phenotype of dfer^gof mutants (UAS-Puc,dfer^gof/dfer^gof).