We have initiated an extensive analysis of wing vein development as a model system for studying a binary cell fate choice (Sturtevant and Bier, 1995). Based on these studies, we proposed a sequential model of vein formation. The first step, which takes place during embryogenesis and early larval development, is subdivision of the anterior-posterior (A/P) axis of the wing segment into a series of alternating sectors. The boundaries between these discrete sectors define discontinuities which induce the formation of vein primordia. Vein development is initiated independently on both the dorsal and ventral surfaces of the wing disc through the action of opposing vein promoting genes (e.g. mutants lack one or more veins) and vein suppression genes (e.g. mutants have ectopic veins).
In the case of the second longitudinal vein (L2), we have established a link between signals emanating from the A/P compartment boundary and induction of the vein developmental program (Sturtevant et al., 1997; Fig. 5). Thus, the Dpp protein, which is produced in a narrow stripe of cells along the A/P compartment boundary, diffuses in both anterior and posterior directions to activate expression of the transcription factor spalt (sal) in a broad central domain. The anterior boundary of the sal expression domain then induces expression of rhomboid (rho) in the L2 primordium (Sturtevant et al., 1997). This localized expression of rho promotes EGF-R signaling (see Rho-EGF-R page) and causes cells to differentiate as vein cells rather than intervein cells (Sturtevant et al., 1993; Noll et al., 1994).
Once vein development is initiated, at least three different types of cell-cell communication contribute to the differentiation of continuous and straight veins: 1) lateral inhibitory signal(s) elaborated by presumptive vein cells restrict vein formation to the center of broad vein competent domains, 2) dorsal-to-ventral signal(s) maintain vein fates in cells on the ventral surface of the wing, and 3) vein continuity signal(s) promote vein formation in straight lines along the axis of vein extension. These various signals presumably collaborate to insure that the dorsal and ventral components of veins are strictly aligned and uninterrupted. It is likely that Dpp, which is expressed in veins, functions as a vein continuity signal and that Sog expression in intervein cells constrains Dpp autoactivation to narrow straight channels (Yu et al., 1996).
We are currently conducting genetic screens to identify new wing vein mutants. Goals of future studies of vein formation are to identify genes functioning upstream of the Dpp and EGF-R signaling pathways through suppressor/enhancer mutant screens, to assess the contribution of different Dpp-Receptor subunits to promoting vein continuity versus lateral inhibition, to isolate new genes involved in initiating vein formation at sector boundaries, and to identify components of the dorsal-to-ventral signaling pathway.
