UAS regulatory sequences drive expression of a constitutively active form of arm that lacks the N-terminal part of the protein (amino acids 155-843 are present). The protein is tagged at the N-terminal end with a myristoylation signal (MGNKCCSKRQGTMAGNI) followed by two copies of the Tag:HA epitope. Sequence encoding an inactive nuclear localization signal has been added at the C-terminal end of the protein.
Co-expression of CbydsRNA.Scer\UAS.WIZ in a armF1α, armΔ.Scer\UAS.T:Ivir\HA1, Scer\GAL4arm.PS background leads to increased naked cuticle compared to armF1α, armΔ.Scer\UAS.T:Ivir\HA1, Scer\GAL4arm.PS embryos.
armF1α, armΔ.Scer\UAS.T:Ivir\HA1, CbydsRNA.Scer\UAS.WIZ (driven by Scer\GAL4arm.PS) germ-line clones exhibit a naked cuticle phenotype. When CbydsRNA.Scer\UAS.WIZ is driven by Scer\GAL4arm.PS in a armΔ.Scer\UAS.T:Ivir\HA1 germ-line clone background, the ectopic denticle phenotype is enhanced.
Expression of armΔ.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4da.G32 has no effect on the cuticle phenotype of pygoS28 or pygoS123 mutant embryos which lack both maternal and zygotic pygo function.
Coexpression of both armΔ.Scer\UAS.T:Ivir\HA1 and tshScer\UAS.cGa in clones under the control of Scer\GAL4Act5C.PI suppresses eye development in both the dorsal and ventral domains and both in marginal and internal regions of the eye disc. Some of these clones are associated with tissue overgrowth in the adult eye. Coexpression of both armΔ.Scer\UAS.T:Ivir\HA1 and tshScer\UAS.cGa under the control of Scer\GAL4dpp.blk1 results in complete suppression of the eye. Coexpression of both armΔ.Scer\UAS.T:Ivir\HA1 and tshScer\UAS.cGa under the control of Scer\GAL4bi-omb-Gal4 results in eyes which are reduced in both the dorsal and ventral margins in discs and in adults. Coexpression of both wgScer\UAS.cAa and tshScer\UAS.cGa in clones under the control of Scer\GAL4Act5C.PI results in eye suppression in the dorsal eye disc. Coexpression of both wgScer\UAS.cAa and tshScer\UAS.cGa under the control of Scer\GAL4dpp.blk1 results in suppression of eye fate at the dorsal and ventral margins of the eye.
Co-expression of armΔ.Scer\UAS.T:Ivir\HA1 and tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL4ey.PH in the eye disc often results in ectopic morphogenetic furrow formation from the anterior margin of the disc and a reduction in posterior differentiation.
The phenotype caused by expression of armΔ.Scer\UAS.T:Ivir\HA1 in clones in the eye disc under the control of Scer\GAL4Act5C.PP is not rescued if the clones are also co-expressing tkvQ253D.Scer\UAS.cNb. Clones expressing Ras85DV12.Scer\UAS in the eye disc under the control of Scer\GAL4Act5C.PP show ectopic photoreceptor formation anterior or posterior to the morphogenetic furrow. This ectopic photoreceptor formation is not prevented by coexpression of armΔ.Scer\UAS.T:Ivir\HA1.
Co-expression of armΔ.Scer\UAS.T:Ivir\HA1 and Hsap\ESR1Scer\UAS.cKa under the control of Scer\GAL4GMR.PY results in a marked increase in apoptosis in third larval instar eye discs compared to controls. Treatment with estradiol significantly increases the rate of apoptosis in these double mutant flies. Co-expression of armΔ.Scer\UAS.T:Ivir\HA1 and Hsap\ESR1Scer\UAS.cKa under the control of Scer\GAL4GMR.PY synergistically enhances the rough eye phenotype seen when either is expressed alone. Treatment of the double mutant flies with estrogen further aggravates the severity of the eye phenotype.