Cell autonomous action of EJC members and Srp54 on Hh pathway activity. (A) Homozygous Y14Δ28 darkN28 clones (arrows) in a Minute background, marked by loss of GFP (green), had lower Ci-155 levels [white, (A’)] but no cell death or rearrangement evident from nuclear Hoechst staining [blue, (A”)]. (B–C) Expression of UAS-Srp54 RNAi with ptc-GAL4 driver reduced ptc-lacZ (red) and anterior En (green) expression relative to UAS-Diap1 controls. (D–G) Ectopic ptc-lacZ (red) was induced in anterior smo clones expressing UAS-GapFu (marked by GFP, green, arrows) but induction was reduced (E) greatly by UAS-mago RNAi and (G) slightly by UAS-Srp54 RNAi. (D”–G”) Changes in Ci-155 levels (white) were small. (H–K) Ectopic ptc-lacZ (red) was induced in anterior pka clones (marked by GFP, green, arrows) but induction was reduced (I) slightly by UAS-mago RNAi and (K) greatly by UAS-Srp54 RNAi. (H”–K”) The increase of Ci-155 (white) was clearly reduced by Srp54 RNAi in some pka clones. (L–O) ptc-lacZ intensity relative to controls within (L and M) smo GapFu clones or (N and O) pka clones, showing mean, SEM, and significant differences calculated by Student’s t-test (** P < 0.001, *** P < 0.0001), using (L) n = 4 control and n = 8 experimental clones, (M) n = 13 control and n = 21 experimental clones, (N) n = 21 control and n = 18 experimental clones, and (O) n = 15 control and n = 16 experimental clones. EJC, exon junction complex; En, engrailed; Hh, Hedgehog; Ptc, Patched; RNAi, RNA interference; wt, wild-type.