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. 2000 Nov 1;14(21):2712–2724. doi: 10.1101/gad.835000

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Copyright © 2000, Cold Spring Harbor Laboratory Press

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dTOR interacts with dS6K. (A) Immunoblot of extracts from Drosophila S₂ cells transfected with HA-tagged dS6K, visualized with anti-HA antibodies. dS6K migrates as a doublet, and the slower migrating band (top), which represents phosphorylated dS6K, is abolished by treatment with rapamycin (lane 2; Stewart et al. 1996). Phosphorylation of dS6K is maintained in the presence of rapamycin when dTOR^S1956T (dTOR^RR, lane 6) but not kinase-inactive dTOR^S1956T (dTOR^RRKD, lane 5) is cotransfected with dS6K. (B) Constitutive expression of activated human p70^S6K1 rescues dTOR flies to viability. Genotypes: (Left) dTOR^P2 UAS-p70^S6K1-D4/dTOR^P1; Act5c-Gal4/+; (right) dTOR^P2 UAS-p70^S6K1-D4/CyO; Act5c-Gal4/+. Note that the rescued dTOR fly (left) is smaller than the control. (C) Constitutive expression of dS6K provides rapamycin resistance. UAS-dS6K/+; Act5c-Gal4/+ flies cultured with 1 μM rapamycin eclose ∼3 d earlier than wild-type controls.