Fig. 8. A model for the development of the wing hinge. The figure represents the evolution of gene expression during development in cells of the dorsal wing hinge. In second instar larvae vg (red) and tsh (grey) are expressed in complementary patterns (1). The vg-expressing cells correspond to the presumptive wing pouch. A signal coming from the vg-expressing cells activates nub and rn expression in slightly broader domains (2). In early third instar larvae, cells expressing rn and nub but not vg (green) are competent to activate the wg IR enhancer (yellow) when induced by a signal coming from the vg-expressing cells (3). wg expression stimulates local cell proliferation that expands the different domains and moves the IR domain several cells away from vg-expressing cells (4). At this time, Wg signalling activates hth expression in the IR (orange). The combination of both Wg-dependent Hth and Vg-dependent Rn activates a Vg-independent mechanism that maintains wg expression in the IR. As soon as local cell proliferation moves rn-expressing cells away from the Vg domain, they lose rn expression, and consequently also lose wg and hth expression. Thus, wg expression in the IR is maintained at the border of the Rn domain, which proximally restricts the IR domain. In this process three new domains have been generated by local cell interactions that do not involve any cell lineage restriction. Note that the cells that belong to the new domain of rn-expressing cells between the IR and the Vg domain (green cells in 4) loses the ability to activate wg by a mechanism that, we propose, involves a Vg-dependent repressor. Therefore, the IR domain is proximally and distally restricted.