sad^unspecified mutants are embryonic lethal. When an artificial pulse of 20E is applied to sad^unspecified embryos, 40% survive to the first larval instar but all fail to develop further and die before molting to the second instar.

Mutant embryos have alterations in embryonic morphology. No epidermal folds are found below the ventral nerve cord. Instead of stretching dorsally, the ectoderm appears to fold like an accordion in the anterior-posterior axis. As a consequence the gut is frequently pushed outside the embryo. By the end of embryogenesis the ventral folding of the epidermis pushes the ventral nerve cord further deep into the embryo. Beside the dorsal closure phenotypes, defects are also seen during head involution and in gut morphology. Mutant embryos also appear to more cells in the ventral neuron cluster. Mutant embryos also typically have fused commissure phenotypes where anterior and posterior commissures are not separated. Longitudinal connectives are found closer to the midline than wild-type. Glial cell organisation is severely affected in mutants. Mutants have a significant increase in the number of midline glial cells. An average of about 6 are seen per neuromere.

In mutant embryos, commissures are fused but connectives are not affected. Embryos show a compacted phenotype with the dorsal edges remaining open for much longer than wild type. Dorsal closure does happen in the end. The PNS often shows defasciculating axons and an increase in the number of sensory neurons.

sad^unspecified mutant embryos show no differentiation of cuticle or head skeleton. The posterior of the embryo is condensed.