Fig. 2. Progenitors of the Svp lineage adopt a myocardial cell fate when their asymmetric divisions are blocked. (A-D) Antibody staining of Tinman (red) and Eve (green), (E,F) Odd (red) and Eve (green), (G) Lbe (red) and Eve (green), and (H) Lbe (red) and ß-Gal (green). Five stage 13 A2-A7 hemisegments are shown in each panel. (A) In wild-type embryos, four out of six myocardial cells are labeled with Tinman. (B) In CycA mutants, the number of Tinman myocardial cells is reduced to two per hemisegment; no EPCs, only DA1 muscles, are specified. (C) In Rca1 mutants, two Tinman myocardial cells are present per hemisegment; EPCs are usually absent but sometimes appear as a single cell. (D) Mesodermal overexpression of dap: two Tinman myocardial cells, one EPC and normal DA1 muscles forms in each hemisegment. (E) In wild type, four pericardial cells express odd (OPC) in each hemisegment. (F) In CycA mutants, the number of Odd pericardial cells is reduced to one per hemisegment. (G) In wild type, two lbe-expressing myocardial cells (TLMC) and two lbe-expressing pericardial cells (LPC) are present in each hemisegment. (H) In CycA mutants, only one TLMC and one LPC are present in each hemisegment. emeA-lacZ shows two Eve lineage derived muscle founders form in each hemisegment (see also Fig. 6C).

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