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. Author manuscript; available in PMC: 2013 May 2.
Published in final edited form as: Cell Metab. 2012 May 2;15(5):713–724. doi: 10.1016/j.cmet.2012.04.007

Figure 6. Rapamycin-induced lifespan extension may involve TORC1 and TORC2.

Figure 6

(A) Longevity from rapamycin requires skn-1 but not daf-16. (B, C) TORC2 inhibition (rict-1 RNAi) increases lifespan dependent upon skn-1 (B) but not daf-16 (C). (D) rict-1 RNAi extends lifespan in VP288, in which RNAi is active specifically in the intestine (see text). Representative (rapamycin) or composite (rict-1) experiments are shown, with statistics and additional analyses presented in Tables S6 and S7. (E) TORC2 or TOR kinase (let-363) inhibition by feeding RNAi increases SKN-1 nuclear occupancy. (F, G) SKN-1 nuclear accumulation in rict-1 mutants (F) and after rapamycin treatment (G) depends upon the food source. ***P< 0.0001, NS= not significant, chi2 method. L=Low, M=Medium, H=High. Error bars represent ± SEM