UAS sequences drive expression of activated Hsap\RPS6KB1. Four mitogen-induced phosphorylation sites are mutated to aspartate and glutamate residues.
When Hsap\RPS6KB1D4.Scer\UAS is driven by Scer\GAL4Act5C.PP in wild-type flies a strong resistance to rapamycin is conferred.
Hsap\RPS6KB1D4.UAS/Scer\GAL4Act5C.PP is a suppressor of lethal phenotype of mTorEP2353/mTork17004
Hsap\RPS6KB1D4.UAS/Scer\GAL4Act5C.PP is a suppressor of lethal phenotype of mTorEP2353
Hsap\RPS6KB1D4.Scer\UAS markedly suppresses the reduction in ommatidial size seen in Tsc1Scer\UAS.T:Hsap\MYC; gigΔAkt-P.Scer\UAS.T:Zzzz\FLAG; Scer\GAL4GMR.PF flies.
The addition of Hsap\RPS6KB1D4.Scer\UAS (driven by Scer\GAL4Act5C.PP) to TorEP2353/TorEP2353 or TorEP2353/Tork17004 animals, rescues the Tor phenotype to viability. 74% of TorEP2353/Tork17004, Hsap\RPS6KB1D4.Scer\UAS animals survive to adulthood compared to 0% without Hsap\RPS6KB1D4.Scer\UAS.