UAS regulatory sequences drive expression of the extracellular and transmembrane domains of kek1 fused to the entire Egfr cytoplasmic domain. A G901R mutation (which disrupts ATP binding) has been introduced within the Egfr kinase domain, abolishing kinase activity. The chimeric protein is tagged at the C-terminal end with GFP.
Expression of Egfr::kek1KEgG.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4CY2 results in eggs with ventralised chorions. Expression of Egfr::kek1KEgG.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4GMR.PF results in a rough eye phenotype.
Egfr::kek1KEgG.UAS.GFP, Scer\GAL4GMR.PF has visible phenotype, suppressible by Egfr[+]/EgfrSOK2
Egfr::kek1KEgG.UAS.GFP, Scer\GAL4GMR.PF has eye phenotype, suppressible by Egfr[+]/EgfrSOK2
Egfr::kek1KEgG.UAS.GFP, Scer\GAL4GMR.PF has ommatidium phenotype, suppressible by Egfr[+]/EgfrSOK2
The rough eye phenotype caused by expression of Egfr::kek1KEgG.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4GMR.PF is strongly suppressed by EgfrSOK2/+.