A ubiquitin promoter drives expression of shg that lacks amino acid residues 734-1316 and which is tagged at the C-terminal end with EGFP.

The ventral epidermis and tracheal defects of shg^R69 are almost completely rescued by shg^{DEΔ734-1316.Ubi.T:Avic\GFP-EGFP}. The head defects are not rescued by shg^{DEΔ734-1316.Ubi.T:Avic\GFP-EGFP} and the primary defects appear to occur in the anterior terminal region before stage 11.

When shg^{DEΔ734-1316.Ubi.T:Avic\GFP-EGFP} is present, shg^R69 mutant cell clones are able to grow in size in the epithelia. These epithelia developed normally into adult tissues.

When shg^{DEΔ734-1316.Ubi.T:Avic\GFP-EGFP} is present in the background, egg chambers containing shg^R69 mutant germ-line clones show normal development.

Cellularization occurs normally in embryos mutant for both maternal and zygotic shg^R69 that carry shg^{DEΔ734-1316.Ubi.T:Avic\GFP-EGFP}. Similarly, in the presence of shg^{DEΔ734-1316.Ubi.T:Avic\GFP-EGFP}, posterior invagination occurs normally, and the ectoderm initiates extension and maintains epithelial integrity in embryos mutant for both maternal and zygotic shg^R69. However, ectopic furrows transiently appear and the extension is slightly affected, presumably because of failure in mesoderm invagination.

Stage 12 and older embryos mutant for both maternal and zygotic shg^R69 that carry shg^{DEΔ734-1316.Ubi.T:Avic\GFP-EGFP} show disorganized epidermal ectoderm, particularly in the head and ventral regions. These embryos also show defects in ventral furrow formation: the two lines of the ventral midline cells either fail to meet or only meet partially.

Apical constrictions when cell shapes change are initiated relatively normally but subsequently decelerate in maternal and zygotic shg^R69 mutants carrying shg^{DEΔ734-1316.Ubi.T:Avic\GFP-EGFP}. Catastrophic disruption of the junctional network follows the defective apical constriction in the mutant embryos.