(A–H) Wing discs expressing one copy of crCi-WT or crCi-ΔCORD as the only source of Ci, showing (A, C, E, F) Ci-155 (gray-scale), (B, D, G, H, A’–H’) ptc-lacZ (red) or (B, D, G, H, B”, D”, G”, H”) En (green) and AP compartment boundary (yellow line). Reduced En induction by Ci-ΔCORD was (B, D) not restored to normal by loss of Su(fu). (E–H) Loss of Fu kinase activity in fumH63 wing discs produced (E, F) similarly strong, broad Ci-155 at the AP border and (E’, F’) drastic reduction of ptc-lacZ for Ci-WT and Ci-ΔCORD, while (G, H) additional loss of Su(fu) restored ptc-lacZ without anterior En in both cases. (I–L) induction of ptc-lacZ (red) in smo mutant clones (green, arrows) expressing GAP-Fu was similar for Ci-WT and Ci-ΔCORD encoded by either (I, J) gCi transgenes or (K, L) crCi alleles and was much lower than at the AP border (arrowheads) in all cases, as presented graphically in (N). (M, M’) Much higher ptc-lacZ (red), matching AP border levels (arrowheads) were observed in GAP-Fu clones (green, arrows) expressing processing-resistant Ci-S849AΔCORD, accompanied by (M”) significant Ci-155 (gray-scale) proteolysis. (N) Average intensity of ptc-lacZ in clones as a fraction of AP border levels. Significant differences between values for a given genotype compared to those for crCi-WT, calculated by paired t-tests, are indicated for p<0.001 (*). There was no significant difference (p<0.05) for gCi-ΔCORD versus gCi-WT. Scale bars are (A, C, E, F) 100 μm and (D, G, H, I–M) 40 μm.