Fig. 5. Two independent Wnt pathways regulate salivary gland positioning. (A-I) Lateral views of stage 15-16 Drosophila embryos stained with FKH and CRB. (J) Graphical representation of phenotypic penetrance in embryos scored for salivary gland migration defects at stages 14-16. (A) Wild-type control. (B) Wnt4-null embryos have a ventral curving defect that affects a large portion of the salivary gland. (C,J) Embryos mutant for both Wnt4^EMS23 and Wnt5^D7 show an enhanced penetrance (68%) of the salivary gland guidance phenotype compared with the single mutants. (D) fz¹ mutant embryos show a phenotype very similar to that of Wnt4^EMS23. (E,F) Using the GAL4/UAS system, dominant-negative transgenes of either fz or fz2 were ectopically expressed in the salivary gland using a salivary-gland-specific driver. The loss of fz signaling in the gland resulted in guidance defects similar to those seen in Wnt4 mutants. (G,J) Furthermore, embryos mutant for both drl^R343 and fz¹ show a higher penetrance of salivary gland guidance defects than drl^R343 or fz¹ alone. (H,I) Expression of dominant-negative transgenes for Tcf or dsh in the salivary glands, using a salivary-gland-specific GAL4 driver, results in ventral curving of a large portion of the salivary gland.