Fig. 4

Only ubiquitous and neuronal downregulation of Eip63E leads to embryonic axon defects. Ventral views of stage 14 whole-mount embryos stained with BP102 shown head to the left. A UAS-Gal4 approach was used to drive Eip63E downregulation in specific tissues during embryonic development. Embryos negative for GFP (present in balancers for both the Gal4 and the UAS lines) were considered experimental embryos vs the GFP positive of the same progeny. A A representative GFP + embryo is shown. B Ubiquitous downregulation led to a replica of the germline deficiency lines, with regards to CNS defective phenotype and developmental lethality (see text for details). C Neuronal-specific downregulation led to a robust and highly penetrant axonal phenotype. D–G Downregulation of Eip63E in other tested tissue (indicated in red) did not cause any detectable axonal defects. The number of embryos per genotype and the percentage of embryos per group showing axonal defects is summarized in H. Scale bar 50 μm