Fig. 3.
Increased phosphorylation of AKT1 is an indirect result of reduced inhibitory feedback by S6K. (A) Overexpressing a constitutively active form of S6k (S6kCA) suppresses the hyperphosphorylation of AKT1 in Smad2 mutant muscle. (B) Overexpression of S6kRNAi and S6kCA in wild-type muscle causes hyper-phosphorylation and hypo-phosphorylation of AKT1, respectively, indicating that the negative feedback loop from S6K to the InR-AKT1 axis functions efficiently in larval body wall muscle. (C) Overexpression of raptorRNAi to inhibit TORC1 activity results in an elevated pAKT1 level, whereas rictorRNAi inhibits TORC2 activity leading to decreased phosphorylation of AKT1. (D) The larval body wall tissue of Activin pathway mutants exhibits lower protein synthesis capacity, as assayed by the SUnSET method. (E) Rescue of decreased protein synthesis capacity by muscle-specific expression of Smad2 transgene. Values are mean±s.e.m. *P<0.05 from one-way ANOVA followed by Dunnett's test in which each genotype was compared with wt (A) or UAS-dicer2/+;Mef2-Gal4/+ control (B,C). Additionally, an unpaired t-test was performed in A as indicated by lines; ##P<0.01.