gish is required for high levels of Hh pathway activity and genetically interacts with gprk2.

(A–J) Adult wings of the indicated genotypes. MS>Smo^DN caused a fusion between veins 3 and 4 (A). MS>Smo^DN wing carrying gish^P clones exhibited an enhanced phenotype (C). Heterozygosity for gish^Df (D) or gish^Δ4 (E) but not gish^P (B) enhanced the fused wing phenotype caused by MS>Smo^DN. Overexpression of wild-type Gish (F) but not Gish^KD (G) or Gish^ΔC (H) rescued the fused wing phenotype caused by MS>Smo^DN in gish heterozygous background. Heterozygosity for gprk2^Δ15 also enhanced the MS>Smo^DN phenotype (I). gprk2^Δ15 and gish^Δ4 double heterozygosity enhanced the MS>Smo^DN phenotype more dramatically than either gprk2^Δ15 or gish^Δ4 single heterozygosity (J compared with E and H). (K–N‴) Late third instar wild type wing discs (K, K', M, M') or wing discs carrying gish^Δ4 mutant clones induced at 24–48 h after egg laying (AEL) (L–L‴, N–N'') were immunostained to show the expression of Ci (red), Gish (green), En (blue in K', L", L‴), or Smo (blue in M', N", N‴). gish^Δ4 mutant cells abutting the A/P boundary (demarcated by dashed lines) exhibited reduced En and Smo staining (arrows in L", N").