Fig. 5. 5EE-lacZ is regulated by ey, eya and so. (A-J) All panels show wing (A-F) or eye-antennal (G-J) discs from 5EE-lacZ transgenic lines stained to reveal ß-galactosidase reporter activity. (A) A wing imaginal disc from a 5EE-lacZ third instar larva shows weak enhancer activity (present in multiple transgenic lines). (B,C) Wing imaginal discs from 5EE-lacZ third instar larvae in which the expression of UAS-ey alone (B) or a combination of UAS-dpp, UAS-eya and UAS-so (C) is driven by 30A-Gal4. (B) ey alone, but not (C) a combination of UAS-dpp, UAS-eya and UAS-so, is capable of inducing 5EE-lacZ in the ring around the wing disc. (D-F) Wing imaginal discs from 5EE-lacZ third instar larvae in which the expression of UAS-ey is driven by dpp-Gal4 in wild-type (D), so¹ (E), eya² (F) or mutant backgrounds. Ectopic ey expression is able to induce ß-galactosidase reporter expression via 5EE at the AP boundary in all three cases. The activity is stronger in so¹ mutant wing discs than eya² mutant wing discs. (G,H) Eye-antennal imaginal discs from so¹ (G) or eya² (H) mutant 5EE-lacZ third instar larvae stained for ß-galactosidase activity. No reporter activity is detected in these mutant eye discs. (I,J) Eye-antennal imaginal discs from w; so¹; dpp-Gal4, 5EE-lacZ/UAS-ey and w; eya²; dpp-Gal4, 5EE-lacZ/UAS-ey third instar larvae. Strong induction of 5EE-lacZ is seen in the ventral antenna in both so¹ and eya² mutants (arrowheads in I and J, respectively). In addition, ß-galactosidase activity is restored at the posterior margin of so¹ mutant eye discs (arrow in I).