Fig. 6. Early defects in cardiogenesis caused by Dorsocross mutation. (A-D) Expression of Tin and Eve in dorsal mesoderm. In wild-type mid-stage 11 embryos (A) each segment contains a cluster of three or four Eve⁺ cells (arrowhead), and during mid-stage 12 (C), two or three Eve⁺ cells (progenitors of Eve-PCs and muscles #1 and 10) are present. The number of Eve⁺ cells is increased in DocA mutant embryos at stage 11 (B) and 12 (D). At stage 12, fewer tin-expressing cells are present in DocA mutants, and almost none of them within the area normally occupied by the cardiogenic mesoderm (D, bracket). Almost all dorsal cells that maintain tin expression are Eve⁺. vm, visceral mesoderm. (E,F) Expression of pnr in the cardiogenic mesoderm visualized by anti-Pnr/anti-ß-Galactosidase staining of wild-type (E) and DocA mutant (F) stage 11 embryos carrying tinD-lacZ. Arrow indicates overlapping expression of Pnr and tinD-lacZ along the dorsal margin of the mesoderm in wild-type embryos and missing Pnr expression in DocA mutants. Pnr is still present in the dorsal ectoderm (ect) of DocA mutants (partially present in projection). The embryo shown in F has been rescued for amnioserosa expression of Doc2 via c381-GAL4, but results are identical without c381-driven Doc2.