Fig. 4. Effects of Dorsocross mutation on pericardial cell and dorsal somatic muscle formation. (A) Lateral view of stage 14 control embryo that carries the amnioserosa rescue constructs c381-GAL4/UAS-Doc2, but is otherwise wild type. Staining for Zfh-1, Odd and Eve allows discrimination of lymph gland (LG) and Odd-pericardial cells (Odd-PC) (yellow, Odd⁺ + Zfh-1⁺) from Eve-pericardial cells (Eve-PC, purple, Eve⁺ + Zfh-1⁺) and from pericardial cells that express only Zfh-1 (Tin-PC and other tissues, red). Odd is also expressed in ectodermal stripes (green), and Eve in DA1 (#1) muscles (blue). (B) DocA mutant embryo with amnioserosa rescue constructs stained as in A. Odd⁺ pericardial and lymph gland cells as well as the great majority of Tin-PCs are absent, while Eve-PCs and DA1 muscles are present. (C,D) Expression of the dorsal muscle marker proteins Eve (red) and Runt (green) in stage 14 embryos carrying amnioserosa rescue constructs. In control embryos (C), Eve is present in the nuclei of DA1 muscles and pericardial cells (Eve-PC, red) and Runt in DO2 (#10) muscles. In amnioserosa-rescued homozygous DocA mutants (D) muscles DA1 and DO2 are largely unaffected. Ectodermal runt (ect) is dorsally expanded owing to the function of Doc in the dorsolateral ectoderm. (E,F) Anti-ß-Galactosidase staining of stage 16 embryos carrying the 1010 B2-lacZ-reporter gene to visualize nuclei of dorsal muscles. (E) Wild-type embryo (dorsal view) with multi-nucleated dorsal muscles. (F) Homozygous DocA mutant embryo showing the presence of dorsal muscles, albeit distorted owing to the morphogenetic defects of these embryos.