Fig. 6. A dfer gain-of-function mutant affects dorsal closure, the morphology of leading edge and amnioserosal cells. (A,B) Late stage 16 wild-type embryo (A), stained for the cell adhesion molecule Fasciclin 3, is dorsally closed, whereas an equivalently staged dfer^gof embryo (B) is still open. (C) At stage 14, wild-type leading edge cells develop an actomyosin cable (up arrowhead; white, Alexa568-Phalloidin), and numerous filopodia (down arrowhead). F-actin is enriched at amnioserosal cell borders (double arrowhead; same embryo as is shown in Fig. 4D). (D) In dfer^gof mutants, the actomyosin cable is thinner (up arrowhead), and the filopodia less abundant (down arrowheads). Amnioserosal cells show weaker F-actin staining at cell-cell junctions (double arrowhead). Contraction of individual amnioserosal cells still occurs (up arrow). (E) In wild-type embryos, GFP-Actin highlights the actomyosin cable (up arrowhead), filopodia (down arrowhead) and cortical enrichment in amnioserosal cells (double arrowhead; UAS-GFP-Actin/+; daGAL4/+; stage 14). (F) In dfer^gof embryos, the actomyosin cable and filopodia are reduced, and amnioserosal cells show less cortical actin and a more motile morphology (arrowhead; UAS-GFP-Actin/+;daGAL4,dfer^gof/dfer^gof; stage 14).