Fig. 5.

Interactions between Gprk2 and the intracellular domain of Smo. (A) Phenotype caused by the expression of the Smo phosphomimic form SmoSD123 in the wing blade at 25°C. (B and C) Phenotype caused by ectopic expression of a Smo intracellular deletion (638-Gal4/UAS-SmoΔC2; B) and severe loss-of-Hh signaling phenotype resulting from the coexpression of Gprk2 RNAi in this genetic background (638-Gal4/UAS-SmoΔC2+UAS-Gprk2i; C). (D–F) Expression of Smo (D), En (E), and Ptc (F) in wing discs of 638-Gal4/+; UAS-Smo^SD123 /+ genotype. Note the expansion of Smo, En, and Ptc domains of expression to the entire anterior compartment. (G–I) Expression of Smo (G), En (H), and Ptc (I) in wing discs of 638-Gal4/+; UAS-Smo^SD123 /UAS-Gprk2i genotype. The anterior expression of En (H) and Ptc (I) is now suppressed upon a reduction in Gprk2 levels. Despite of the presence of the Smo^SD123 protein in the cell membrane of anterior cells (G), the pathway does not activate the expression of the high-level targets En and Ptc.