Signals from the pouch and notum restrict JAK/STAT signaling to the hinge to insure proper wing development. Erika Bach, Aidee Ayala-Camargo, Aloma Rodrigues, Marc Amoyel, Maria Sol Flaherty. Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, NY.

   JAK/STAT pathway activity localizes to the hinge domain of the wing disc, but its function there has not been reported. Here we show that STAT activity is necessary and sufficient for hinge development through autonomous induction of hinge-specific factors. We find that mutual negative interactions between Iroquois-complex factors and Stat92E repress JAK/STAT pathway activity from the notum. The pouch factor Nubbin represses Unpaired, the JAK/STAT ligand, and STAT activity out of the pouch. These data suggest that JAK/STAT signaling in the pouch is deleterious to wing development. Indeed, mis-expression of Unpaired within the presumptive pouch causes small, stunted adult wings. Within the hinge, JAK/STAT pathway activity becomes restricted to the gap domain in cells that lack Nubbin and Teashirt. We report the autonomous lack of growth of gap domain cells lacking STAT function. Finally, JAK/STAT signaling does not perturb the Wingless inner or outer ring, indicating that JAK/STAT and Wingless pathways control hinge growth independently. We conclude that JAK/STAT signaling is critical for hinge fate specification and growth of the gap domain.