Fig. 9. Current model of cardioblast development and the roles of Dorsocross, tinman and pannier. Dorsocross is involved in multiple steps of early cardiogenesis. First (stage 10), positional information transmitted by Dpp and Wg signals is integrated within dorsal cells of the mesodermal A domain, in which the Doc genes are activated. In parallel, tin is activated by Dpp in the entire dorsal mesoderm. Second (stage 11), the cardiogenic mesoderm becomes delineated with the Doc- and tin-dependent activation of pnr, which itself is required for maintained expression of tin and Doc. During this stage, cells start to align at the dorsal mesodermal margin, while ectodermal pnr maintains dpp expression along the dorsal leading edge. The combined action of Doc, tin and pnr selects a pool of progenitors for all cells of the dorsal vessel, including those of the lymph gland, with the exception of the Eve-pericardial progenitors, which are Doc independent. Third (early stage 12), refined co-expression of Doc, tin and pnr leads to the activation of specific target genes in presumptive cardioblasts or their progenitor cells, thereby promoting cardioblast specification. Owing to additional localized inputs (particularly on svp, which additionally requires extrinsic Hh signals) (Ponzielli et al., 2002), cardioblast fate diversifications are also initiated during this process. Other regulators, including mid and hand, are turned on in all cardioblasts. During the second half of stage 12, tin and Doc are re-activated in complementary subsets of cardioblasts through the actions of mid and svp, respectively, as indicated (broken arrow indicates permissive role of svp on Doc; S. Zaffran, I.R. and M.F., unpublished). Tin and Doc, either alone or in combination with uniformly expressed cardioblast factors, then activate various regulatory and differentiation genes in the respective subtypes of cardioblasts. In the heart portion, which is defined by abd-A expression within cardioblasts, Doc-positive cardioblasts form ostial cells marked by wg expression, whereas the Tin-positive cells form `regular' myocardial cells marked by Sulfonylurea receptor (Sur) expression.