Females, homozygous for scra¹, lay morphologically normal eggs that fail to hatch. These mutant embryos exhibit cellularisation defects. Despite defects in furrow canal structure and septin targeting, the cellularisation front still ingresses in scra⁵/scra¹ mutant embryos. In comparison to wild-type, the initiation phase of ingression is eliminated. Instead, a cellularisation front begins to ingress as soon as mitosis is completed, at a roughly constant slow rate. A distinct transition to a faster rate can be observed, but both slow and fast rates of ingression are slower than their wild-type counterparts. As the cellularisation front ingresses, extensive abnormalities become apparent. Furrow canals are malformed, appearing narrow or absent. Embryos in slow phase exhibit both paired plasma membranes and lines of vesicles in different areas of the same specimen, while those embryos in fast phase exhibit only lines of vesicles, in place of paired plasma membranes between nuclei. In scra⁵/scra¹-derived embryos the pole cells are properly formed and enclosed by intact spherical plasma membranes, as in wild-type.

Eggs derived from homozygous females form a syncytial blastoderm and begin to cellularise normally, but cellularisation is often not completed. Gastrulation takes place but is usually very abnormal. The embryos form pieces of cuticle. Homozygous viable, hemizygous lethal.