Figure 4.

The cytoplasmic domain of Sema1a is required for its function in R-cell axon guidance. A, Overexpression of wild-type Sema1a under control of GMR-GAL4 caused the hyper-fasciculation of R-cell axons. B, Overexpression of sema1a^Δcyt driven by GMR-GAL4 did not induce the formation of thicker bundles, but instead disrupted the organization of R1–R6 growth cones in the lamina plexus, which was indistinguishable from that in sema1a^P1 mutants (Fig. 2B). C, Neuronal-specific expression of wild-type Sema1a under control of elav-GAL4 in a sema1a^P1 hemizygote (i.e., sema1a^P1/Df(2)N22–5) restored the normal R-cell projection pattern in 14 of 22 mutant hemispheres. The remaining eight mutant hemispheres displayed the axonal hyper-fasciculation phenotype (data not shown), likely caused by an above threshold expression level of the sema1a transgene in these individuals. D, No rescue was observed when the sema1a^Δcyt transgene was expressed in a sema1a^P1 hemizygote. Note the discontinuous lamina plexus and the aberrant projections of some R-cell axons (arrow) at the bottom of lamina. Scale bar: (in A) 20 μm.