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. 2010 Sep 15;24(18):2054–2067. doi: 10.1101/gad.1948710

Figure 2.

Figure 2.

Genetic characterization of Gprk2. (A–C) A Gprk2-lacZ enhancer trap is expressed along the A/P border (A), and is induced ectopically by misexpression of either Hh (B) or an activated form of Ci (C) using MS1096 Gal4 driver. (D–F″) A-compartment Gprk2Δ15 mutant cells near the A/P boundary (marked by the lack of GFP) (arrows in D–D″,F–F″) exhibited reduced expression of ptc (D′) and en (F′). Insets in D′ and D″ show enlarged images of the region indicated by the arrows. (E–E″) P-compartment Gprk2Δ15 mutant cells abutting the A/P boundary did not affect ptc expression. (G–J) Wing discs expressing SmoΔSAID (G,H) or SmoSD123 (I,J) with (H,J) or without (G,I) multiple copies of a Gprk2 RNAi transgene using MS1096 were immunostained to show en expression. SmoΔSAID but not SmoSD123 induced ectopic expression of en when Gprk2 was knocked down. (K–N) Gprk2Δ15 mutant discs expressing a wild-type Gprk2 (L), a kinase-dead Gprk2 (Gprk2KM) (M), or a mammalian GRK5 (mGRK5) (N) with MS1096 were immunostained to show en expression. Expression of the wild-type Gprk2 or mGRK5 but not Gprk2KM rescued anterior en expression in Gprk2Δ15 mutant discs. The red lines demarcate the A/P border based on Ci expression (not shown).