Fig. 6. Loss of Dorsocross causes abnormal development and premature breakdown of the amnioserosa. Homozygous Df(3L)DocA mutant embryos (A,C,E,G) and heterozygous control embryos (B,D,F,H) were stained for amnioserosa markers as indicated. (A,B) Expression of hnt, as determined with anti-Hnt antibodies, initiates in the absence of Dorsocross (A), but fails to the reach wild-type levels especially in anterior areas of the amnioserosa by stage 9 (arrowheads; compare with B). Note comparable levels of Hnt in midgut primordia (amg, pmg) in A and B. (C-H) Anti-C15 antibody staining of stage 9 (C,D), late stage 12 (E,F) and stage 14 (G,H) embryos. C15 expression is not reduced in early DocA mutants (C) and large flattened nuclei are present in the amnioserosa similar to the wild-type situation (D). However, in DocA mutants there are some abnormally small nuclei in the amnioserosa (arrow) and germ band elongation is slightly aberrant. (E) C15 staining of a stage 12 DocA mutant embryo reveals a decrease in the size of most amnioserosa nuclei (arrow) and a broadening of the ectodermal C15 expression domain (arrowhead) when compared with F. Around stage 14, no large amnioserosa cells expressing C15 can be found in DocA mutants (G), there is a dorsal hole lacking C15 (arrowhead) and the germ band is not retracted. In the control embryo (H), C15 expression in the amnioserosa is still strong during this stage and in the dorsal ectoderm it shows a well-defined segmented pattern. DocA mutants were initially identified via absence of balancer-derived anti-ß-galactosidase staining. Various morphological features (reduction of dorsal head structures, incomplete germ band extension associated with an inwardly kinked posterior germ band, absence of germ band retraction, yolk displacement) were found to be consistently present in mutants, which allows reliable discrimination of mutant and control embryos without anti-ß-galactosidase staining after stage 8.

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