Figure 9. Rheb-mediated synapse overgrowth was not rescued by knockdown of TorC1 signaling, however it was rescued by loss of the TorC2 components sin1 and rictor.

(A) Anti-CSP staining of third-instar larval NMJs shows considerable overgrowth of motoneuron boutons in Rheb-overexpressing animals. (B–D) RNAi knockdown of either the TorC1 component raptor or the TorC1 downstream mediator S6K failed to decrease the severity of synapse overgrowth defects when Rheb was overexpressed. Reducing S6K function actually worsened the severity of this phenotype. (E–J) In contrast, homozygous loss of the TorC2 components sin1 and rictor significantly rescued synaptic overgrowth in Rheb-overexpressing animals, indicating that this is a TorC2-dependent event. Asterisks denote a two-tailed Student's t-test statistic of p<0.05 compared to elav-Gal4>UAS-Rheb⁺(*) or to elav-Gal4/+ (**) controls. Scale bars are 50 microns.