In homozygous embryos the pushing force generated by ectodermal cell intercalation is impaired or lacking. Germband extension is desynchronized from mesoderm and endoderm invaginations. Germband extension arrests, and defects in ventral midlien closure occur. The phenotype is variable, some embryos arrest at very early stages. Other embryos develop further and show a "double line" denticle belt phenotype. Some embryos hatch to first instar larvae.

Homozygous lethal. Mutant embryos show abnormal germband extension movements. There is a desynchronization between germband extension and mesodermal and endodermal invaginations, and a premature termination of movements. The ventral midline closure is often incomplete. At apparent stage 7, the ectodermal cells of homozygous embryos have a round apex, presenting only few intercellular connecting structures. Cell adhesion is impaired. The apical projections of the cells are reduced and the apico-basal localisation of junctional structures is altered.