Fig. 6.

The Abl N terminus is sufficient to inhibit multiple guidance pathways. (A-C) Stage 17 slit/+ embryos expressing TauMycGFP and the indicated transgenes in ipsilateral apterous neurons under control of ap^Gal4. Five abdominal segments are shown. apterous axons are visualized with anti-GFP (green). FasII-positive ipsilateral axons are in magenta. Anterior is up. (A) slit/+ embryo. Occasional ectopic crossing occurs (arrows). (B) slit/+ embryo expressing Abl^WTGFP. Ectopic crossing (arrows) is significantly enhanced. (C) slit/+ embryo expressing Abl^NGFP. Ectopic crossing (arrows) is enhanced. (D) Quantification of ap ectopic crossing defects. Expression of Abl^WTGFP and Abl^NGFP results in a similarly penetrant phenotype. Error bars indicate s.e.m. Number of segments scored is shown in parentheses. ^*P<0.05, ^***P<0.001. (E-G) Stage 17 embryos expressing the indicated Abl-GFP fusions under control of pan-neural Elav-Gal4. Motor axons are visualized with anti-FasII. Three segments are shown. Anterior is up. Approximate location of muscle clefts and muscle numbers are indicated. (E) Abl^KNGFP has no effect when overexpressed. All three muscle clefts are properly innervated. (F) Abl^WTGFP expression results in full ISNb bypass phenotype. (G) Abl^NGFP expression generates ISNb bypass, although to a lesser degree than Abl^WTGFP.