Border cell migration fails in egg chambers that contain follicle cell epithelia entirely mutant for shd². Larger clones result in more severe migration delays.

Border cell migration appears normal when the germline is mutant for shd².

Mutant embryos show defects in dorsal closure, head involution and midgut constrictions. The mutant embryos stall in tracheal branching morphogenesis at stage 14. Despite the stall in morphogenesis, the embryos move within their eggshell and accumulate chitin in the epidermis during stages 16 and 17. A 2 hour exposure of 5-7 hour embryos to 20-hydroxy-ecdysone is sufficient to rescue the morphogenetic defects and produce viable first instar larvae, but treatment of older embryos has little rescuing effect.

Early embryonic development of shd² mutants is normal until approximately stage 14. At stages 15-16, abnormal morphogenetic movements are apparent that involve failure of head involution, defects in dorsal closure, and aberrant gut looping. shd¹/shd²; shd^Scer\UAS.cPa; Scer\GAL4^twi.2PE animals survive to be viable adults. Howver, females of this genotype are sterile, with egg chambers that arrest and degenerate at about stage 8-9 of oogenesis.