Figure 5.
The cytoplasmic domain of PlexA is dispensable. A, Wild type. B, Overexpression of PlexA under control of GMR-GAL4 caused the formation of thicker axonal bundles. C, Overexpression of PlexAΔcyt driven by GMR-GAL4 caused an identical hyperfasciculation phenotype. D, Western blot analysis using anti-HA antibody showed the expression of HA-tagged full-length and cytoplasmic-domain-truncated PlexA in flies under control of GMR-GAL4. The size of transgenic proteins is consistent with the predicted size. E, An eye-specific PlexA knockdown mutant. F, Expression of PlexAΔcyt largely restored the R1–R6 growth-cone organization pattern in the lamina in PlexA knockdown mutants. Scale bar, 20 μm.