Homozygous eye clones result in defects in the shape of the rhabdomeres. No light-induced retinal degeneration is seen.
Mutant embryos exhibit a loss of epithelial integrity and cell shape.
First defects in zonula adherens formation are seen at the onset of germband extension on the dorsal side of the embryo in the developing amnioserosa. The distribution of adherens junction material at the apicolateral boundary is more irregular.
At stage 11 of embryogenesis ectodermal cells lose their normal columnar shape and round up. 1-2hr later cells form clusters, rather than a monolayer. Dead cells are often seen on the outside of the embryo. Vesicles form of cells retaining epithelial characteristics, and later secrete grains or vesicles of cuticle. Many cells fail to become integrated into an epithelial sheet. Degeneration is most extreme in the epidermis, the pharynx and the amnioserosa, and least extreme in the proventriculus and Malpighian tubules which develop almost normally.
sdtEH681, sdt7D, sdt2, sdt3, sdtK8 and Df(1)HA11 all have a similar phenotype. The sdt mutant phenotype is not enhanced by deleting the sdt gene from the maternal germline. The phenotype of amorphic sdt mutants is essentially the same as the phenotype of amorphic crb mutants. Embryos doubly mutant for sdt and crb mutants show the same phenotype as embryos singly mutant for either gene. Double mutants for Egfr and sdt or crb show an enhancement of the sdt or crb mutant phenotype. Phenotype is unaffected by a duplication for crb+, Dp(3;3)M95A+13.