Fig. 7. Synergistic interaction between elevated PVR levels and excess apical PVF1. As PVR overexpression leads to pupal lethality, we were able to induce lower levels of PVR by using an unusual insertion of the UAS-Pvr-RNAi construct. Although most Pvr-RNAi constructs lead to a reduced level of PVR (A, arrow), this insertion (termed RNAi-GOF) gave rise to elevated PVR levels (B, arrow). This elevation is also reflected in defects in actin microfilament organization at the basal side of the epithelium (C, arrow). As RNAi-GOF flies were viable, it was possible to examine their pupal wings. We noted that whereas the organization of apical F-actin was unaltered (D,E), a dramatic misorganization was induced at the basal domain (F,G). Expression of adult wing phenotype. Females carrying two copies of MS1096-Gal4 had normal wings (H). Minor defects could be observed with a single dose of MS1096-Gal4 and UAS-RNAi-GOF (I). This phenotype was enhanced when having two copies of the Gal4 driver (J). Overexpression of Pvf1, which accumulates at the extracellular apical side, does not lead to defects in the wing (K). Flies containing a single dose of the driver and UAS-RNAi-GOF and UAS-Pvf1 show a dramatic enhancement of the phenotype (L). This demonstrates that the phenotypes observed following PVR overexpression represent activation of the endogenous pathway by its ligands.