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. 2013 Jul 1;140(13):2724–2733. doi: 10.1242/dev.093831

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© 2013. Published by The Company of Biologists Ltd

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Fig. 2. — The pro-crossing function of Abl relies partly on its kinase activity. (A,B) Quantification of EW axon crossing defects in Abl mutants. (A) fra^hypo embryos. Expression of kinase-inactive Abl (Abl^KN) in EW neurons rescues the dominant interaction between fra and Abl. Data from two independent transgenic UAS-Abl^KN lines are shown. (B) Embryos expressing a weak DN-Fra transgene, which causes no defects in WT embryos (data not shown). Abl^WTGFP rescues midline-crossing defects in Abl² homozygous mutants, though Abl^KNGFP does not. ^*P<0.05, ^**P<0.01, ^***P<0.001. n.s., not significant. Error bars indicate s.e.m. Number of segments scored is shown in parentheses. Genotypes are as follows: (A) fra^hypo denotes fra³,[UAS-TauMycGFP]/fra⁶; [eg-Gal4]/+; Abl⁴/+ denotes fra³,[UAS-TauMycGFP]/fra⁶; Abl⁴,[eg-Gal4]/+; these two are a repetition of data shown in Fig. 1. +Abl^KN denotes fra³,[UAS-TauMycGFP]/fra⁶, [UAS-Abl^KN]2; Abl⁴,[eg-Gal4]/+; and +Abl^KNGFP denotes fra³,[UAS-TauMycGFP]/fra⁶; Abl⁴,[eg-Gal4]/[UAS-Abl^KNGFP]. (B) abl²/+ denotes [UAS-DN-Fra]#8/[UAS-TauMycGFP]; Abl², [eg-Gal4] / +. On the right, all are [UAS-DN-Fra]#8/[UAS-TauMycGFP]; Abl², [eg-Gal4]/Abl², [UAS-Abl^XGFP].