Fig. 5. PAT-related transporters and InR/TOR signalling components enhance FOXO activity by inhibiting the InR pathway. GMR-GAL4 was used to drive expression of the following transgenes in the differentiating eye: dominant-negative Dp110^D954A (D-F), Rheb^AV4 (G-L), UAS-S6K (M,N), CG1139^GS10666 (O-Q), path^GS13857 (R-T), UAS-path (U,V,Y) and UAS-Tor (W-Y). Flies overexpressing these transgenes together with foxo^GS9928 (E,H,K,N,P,S,V,X,Y), or with foxo^GS9928 and UAS-Akt1 (F,I,L,Q,T) were compared with GMR-GAL4 controls expressing the transgenes alone (D,G,J,M,O,R,U,W), no transgene (A), foxo^GS9928 alone (B) or a combination of foxo^GS9928 and UAS-Akt1 (C). A small eye phenotype and posteroventral reduction (arrow in B) is produced by GMR-GAL4 foxo^GS9928. All eyes except G-I are from adult males, which produced stronger foxo^GS9928 genetic interactions.