Animals expressing dshΔDIX.Scer\UAS under the control of Scer\GAL4arm.PS display a loss of denticles. The arrangement of cells and cell morphology are greatly disrupted.
Expression of dshΔDIX.Scer\UAS under the control of Scer\GAL4hs.PB produces a weak phenotype in the wing.
dshΔDIX.UAS/Scer\GAL4da.G32 is an enhancer of embryonic/first instar larval cuticle phenotype of wgl-17
dshΔDIX.UAS/Scer\GAL469B is a suppressor of amnioserosa phenotype of hep1
dshΔDIX.UAS/Scer\GAL469B is a suppressor of embryonic dorsal epidermis phenotype of hep1
dshΔDIX.UAS/Scer\GAL469B is a suppressor of embryonic leading edge cell & actin filament phenotype of hep1
dshΔDIX.UAS/Scer\GAL469B is a suppressor of embryonic/first instar larval cuticle | dorsal phenotype of hep1
dshΔDIX.UAS/Scer\GAL4da.G32 is a non-suppressor of denticle | ectopic phenotype of wgl-17
dshΔDIX.Scer\UAS; Scer\GAL4da.G32 does not suppress the transformation of naked ventral cuticle into denticles in cuticles from wgl-17 homozygous embryos. The resulting cuticles are even shorter and more puckered than those from wgl-17 homozygous embryos, have an enlarged dorsal hole.
The dorsal hole phenotype, loss of leading edge actin cable, and loss of adhesion between the amnioserosa and dorsal epidermis of hep1 mutant embryos are all partially suppressed by Scer\GAL469B with dshΔDIX.Scer\UAS.