Fig. 1. Progenitors of the mesodermal Eve lineage adopt a muscle cell fate when their asymmetric divisions are blocked. (A-D) Antibody staining of Eve (red) and Mef2 (green) in stage 13 embryos. Five hemisegments of segment A2-A7 are shown in each panel. (A) Six Mef2-expressing myocardial cells, two EPCs, and one DA1 muscle are present in each hemisegment in wild-type stage 13 embryos. (B) In CycA mutants, the number of Mef2 myocardial cells is reduced to four per hemisegment; no EPCs are specified, but the DA1 muscles are present. (C) In Rca1 mutants, four myocardial cells are present in each hemisegment; most EPCs are absent. (D) Pan-mesodermal expression of dap reduces the number of myocardial cells to four and the EPCs to one per hemisegment. The DA1 muscles are present. (E) In the mesodermal Eve lineage model of Park et al. (Park et al., 1998), two progenitors are formed per hemisegment, each giving rise to an EPC and a muscle founder. (F) In the model of Carmena et al. (Carmena et al., 1998), two progenitors are also formed in each hemisegment, but one (P2) gives rise to both EPCs and one muscle founder, whereas the other (P15) generates only the DA1 founder. This EPC progenitor is a daughter cell of an asymmetric cell division that also generates the DO2 muscle founder.