Females, homozygous for scra⁴, lay morphologically normal eggs that fail to hatch. These mutant embryos exhibit cellularisation defects. In embryos from scra⁵/scra⁴ mothers, early furrow canals lack the characteristic `tear-drop' shape. As these embryos progress through cellularisation, the contractile rings fail to form. During gastrulation, the transition from a hexagonal network into contractile rings fails, with a broken, hexagonal mesh in place of the normal lattice of rings. The cellularisation front is disorganised and nuclei are mis-positioned, with the newly formed cells open at their bases. Embryos of the genotype scra⁷/scra⁴ survive to pupation but die before eclosion. Imaginal discs in scra⁷/scra⁴ 3rd instar larvae are much smaller than in wild-type and are hard to identify. The rudimentary discs contain many large bi-nucleate cells.

Cellularising embryos from scra⁴/scra⁵ mothers lack the microfilament rings seen at the base of furrow canals in wild-type embryos at this stage. The furrow canals themselves are collapsed and lack the early bulb-like or the late flask-like morphology of the wild type. Viewed from the embryo surface, the basal openings of the furrow canals are not round, as in wild-type, but are irregular in shape and sharply angular. The sides remain straight and show no waviness that would indicate a lack of tension.

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.

homozygous viable but lethal over the deficiency.