A mutated form of arm, lacking the end of the N-terminal region (amino acids 101-139 are deleted), is expressed under the control of its own promoter. The protein is tagged with a Tag:MYC epitope at residue 784 in the Gly/Pro-rich region close to the C-terminus. arm 3' trailer sequences are also present. The protein produced shows slightly reduced levels of binding to shg protein compared to wild-type controls in a coimmunoprecipitation assay and binding to α-Cat protein is abolished.
Embryos expressing armS14.T:Hsap\MYC in an arm1 mutant background do not show a wg loss of function phenotype in the cuticle. The embryos have defects in the ventral epidermis and the head that resemble a weak to moderate shg mutant phenotype. In particular, there are foci of cell death in and around the optic placodes. The optic placode does form but loses its epithelial structure and fails to invaginate in late embryos.
The size of the primary branches of the tracheal system is largely unaffected in embryos carrying armS14.T:Hsap\MYC in an arm4 background, even though segments of the dorsal trunk are disconnected.
Photoreceptors are not rescued from death in ApcQ8 homozygotes carrying one copy of armS14.T:Hsap\MYC in an arm4/+ background.
Embryos do not exhibit segment polarity defects.
armS14.Tag:MYC partially rescues arm4
armS14.Tag:MYC partially rescues arm3
The phenotype seen in RP2 neurons in embryos that are zygotically arm4 but have wild-type maternal arm is rescued by armS14.T:Hsap\MYC.
Partial rescue of adherens junction defect.
Used in a coimmunoprecipitation assay to study shg binding and analysed by SDS-PAGE to study protein phosphorylation and stability.
Mutation abolished the ability of arm to bind α-Cat in vivo.