Fig. 7. Model for the control of Drosophila wing growth by feed-forward autoregulation of vg mediated by the QE and fueled by Wg. During the first larval instar (L1), tsh and vg are coexpressed in the nascent wing disc, the latter driven at least in part by the vg priming enhancer (PE). Wg signaling in early L2 represses tsh in the distal portion of the disc, segregating the disc into heritably distinct hinge/notum and pre-blade primordia. Both primordia are then subdivided into dorsal (D) and ventral (V) compartments in mid-L2. After the D-V segregation, vg expression becomes dependent on DSL-Notch signaling (orange) across the D-V boundary, which activates both wg and vg expression in D-V border cells, the latter driven by vg boundary enhancer (BE) elements. By early L3, Wg (blue) and the Vg-dependent feed-forward signal (yellow) sent by border cells activate vg quadrant enhancer (QE) elements in neighboring cells, upregulating vg expression (red). During the mid- and late L3, the domain of vg-expressing cells expands dramatically by reiterative cycles of short-range feed-forward signaling, fueled by long-range Wg and Dpp signaling from D-V border and A-P border cells (for simplicity, Dpp and the A-P compartment boundary are not shown). Feed-forward autoregulation is required both to recruit new cells to express vg, as well as to maintain vg expression in cells already recruited; Wg and Dpp are also required for the survival and proliferation of cells already recruited. Lastly, Vg-expressing cells produce a signal (green) that stimulates proliferation in the surrounding, `rn-only' cells, sustaining the cell population from which wing cells are recruited. Short-range (DSL-N, Feed-forward and Growth) and long-range (Wg) signals are indicated, respectively, by arrowheads and arrows.