Figure 7. ‘Weak point’ in the wing imaginal disc is responsive to Upd1 ligand and model for notum to wing transdetermination.

(A, B) Wing discs with dilp8-GFP and vgQE-RFP reporters: control (A), and dpp-GAL4, UAS-upd1 (B). Note the specific expression of dilp8-GFP along the posterior edge of the notum and in the wing pouch (arrows). (C) Overexpression of UAS-upd1 by heat-shock induced flip-out clones (hs-FLP, Act<stop<GAL4) marked with UAS-RFP. Note the specific area in the notum that responds to Upd1 by expressing dilp8-GFP (arrows). (D) Model for how JAK/STAT and JNK/AP-1 signaling work together to trigger a fate change and the growth of an ectopic pouch. Damage to the normal wing pouch generates both Egr and Upd ligands. The weak point, an area near the anterior/posterior compartment boundary in the notum responds to Upd ligands and the resulting JAK/STAT signaling disrupts the normal notum identity (as observed with the disruption of the notum Wg stripe). JNK activity within a field of JAK/STAT activity leads to the expression of Wg, which triggers cells to adopt the new wing pouch fate. Then, as in the regenerating wing pouch, additional cells are recruited to generate a new pouch. CtBP functions, either directly or indirectly, to antagonize these pathways.

Figure 7—figure supplement 1. The notum and wing pouch respond to the overexpression of UAS-upd1 by dpp-GAL4.

(A–B) JAK/STAT activity as shown by the STAT-DGFP reporter in late L3 wing discs in the control (A) and dpp>upd1 (B). Note the specific activation of STAT-DGFP in the notum and wing pouch but not in-between. (C–D) Apoptosis (DCP-1) in control (C) and dpp>upd1 (D) wing discs, with the dilp8-GFP reporter and a wing pouch reporter (vestigial quadrant enhancer, vgQE-RFP). Note the increase in DCP-1 staining following the overexpression of UAS-upd1, which is mostly adjacent to the areas of dilp8-GFP expression (arrows). (E) The adult phenotype of dpp>upd1. Note the disruption of the thorax including the loss of many bristles and macrochaetes.