Figure 2. Rheb overexpression defects are Tor-dependent.

(A–C) Heterozygosity for a Tor null mutation, Tor^Δ6B, rescued Rheb-directed deficits in phototaxis behavior, axon guidance, and synapse expansion. (A) Neuronally-directed expression of Rheb (elav^C155>UAS-Rheb⁺) caused a substantial drop in phototaxis response compared to controls (UAS-Rheb⁺/+). Heterozygosity for a Tor null allele (elav^C155>UAS-Rheb⁺ Tor^Δ6B/+) almost completely rescued this defect. (B) Measures of axon guidance misrouting showed a significant decrease in severity when Tor function was reduced by 50%. (C) Reduced Tor function rescued synapse overgrowth to nearly wild-type levels in animals with neuronally-directed (elav-Gal4) expression of Rheb (MSA = “Muscle Surface Area”). Asterisks denote p<0.05 using a two-tailed student's t-test. Note that different neuronal-directed Gal4 drivers were used for assessing the influence of Tor function on Rheb-directed axon misrouting and synapse expansion. These two different Gal4 drivers were selected for producing phenotypes at a penetrance and expressivity where Tor-dependence could readily be assessed.