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

Figure 1.

Figure 1.

Reduction of Gprk2 modifies the phenotypes caused by a dominant-negative Smo. (A,B) A wild-type wing (A) or a wing expressing UAS-Smo−PKA12 with the C765 Gal4 driver (C765-Smo−PKA12) (B). (Arrow in B) Overexpression of Smo−PKA12 causes a partial fusion between vein 3 and vein 4. (C–F) Heterozygote for a Gprk2 deficiency (C), a P-element insertion allele of Gprk2 (Gprk206936) (D), an excision allele (Gprk2Δ15) (E), or Gprk2 RNAi (F) enhanced the fused wing phenotype caused by C765-Smo−PKA12. (G–J) C765-Smo−PKA12 reduces ptc expression (H), which is enhanced by the Gprk2Δ15 heterozygote (I) or Gprk2 RNAi (J).