Homozygous embryos derived from females carrying homozygous germ-line clones show defects in epithelial wound repair, failing to form a continuous actomyosin purse-string at the leading edge of wounds. There are significant delays in both the coalescence and contraction phases. Wound closure does occur, by local contraction of actin patches and protrusions.

The elongation of the dorsal most epidermal cells is impaired in maternal and zygotic mutant ed^F72 dorsal closure stage embryos. These cells fail to display actomyosin cable or filopodia formation.

Homozygous embryos (lacking zygotic ed function) show no obvious tracheal defects.

Mutant embryos lacking both maternal and zygotic ed function (mutant embryos derived from homozygous female germline clones) have highly convoluted tracheal tubes compared to wild type. In addition, the tracheal networks show abnormal branch fusion; there are breaks along the dorsal and lateral trunks and in the dorsal anastomoses in 56% of embryos and ectopic branch fusions are seen in 24% of embryos. The fusion cell triple ring structure appears thicker and less organised than normal in mutant stage 16 embryos.

ed^F72 mutant follicle cell clones display no detectable defects in growth or viability. Eggs produced by females bearing these follicle clones show groups of eggshell imprints with a smooth border. The smooth borders occur between the mutant follicle cells and adjacent heterozygous or homozygous wild-type cells, but the borders of mutant cells within clones appear normal. The smooth clone border phenotype is only observed at the apical side of the epithelium, while the basal aspect of the clone displays no obvious phenotype. The apical clone circumference is markedly reduced relative to the basal circumference, consistent with the presence of a contractile actin cable. Adherens junctions are destabilized at the border of the mutant clones.

The smooth clone border phenotype is completely penetrant in early stage egg chambers with ed^F72 clones. During stage 10, the border appears wild type, consistent with a disappearance in ed expression in wild-type cells at this stage. By stage 11 the phenotype reappears and persists for the rest of oogenesis.

The morphogenesis of appendage primordia is defective in egg chambers with ed^F72 follicle cell clones. At stage 11, the smooth border at the posterior of the roof cell domain, seen in wild-type cells at this stage, is abolished in ed^F72 clones. At stage 12, nascent appendage tubes from ed^F72 mutant primordia are shorter than wild-type tubes and exhibit a wider opening. In all phases of tube morphogenesis, the floor cells of both wild-type and mutant primordia elongate to a similar degree and project their apices toward the future tube floor midline. Prior to the tube extension phase, floor closure is incomplete in mutant primordia. During tube extension, the tube floor remained open in 16/17 cases observed. ed^F72 mutant appendages are severely reduced in length compared to those of wild-type egg-chambers, or fail to extend from the main body of the eggshell completely.

ed^F72 embryos that lack both maternal and zygotic contributions of ed exhibit defective dorsal closure. These embryos exhibit apparent irregularities in the progression of the leading edge during dorsal closure. The actomyosin cable that forms during dorsal stages in wild-type embryos fails to assemble in ed^F72 embryos and the dorsal epidermis appears to buckle towards the amnioserosa in ed^F72 embryos, suggesting that a lack of tension prevents the formation of a taut interface with the amnioserosa. The dorsal movement of the lateral epidermis is delayed compared with wild-type embryos, and discontinuities and puckering at the dorsal midline and misalignment of opposing segments are ultimately observed.