Research Paper Volume 2, Issue 7 pp 393—414

Figure 9. Lack of Tor1p does not impair the life-extending effect of LCA and abolishes the dependence of the anti-aging efficacy of LCA on the number of available calories. (A and B) Effect of LCA on the mean (A) and maximum (B) life spans of chronologically aging tor1Δ strain. Data are presented as means ± SEM (n = 4-7; ***p < 0.001). (C and D) Effect of LCA on the fold increase in the mean (C) or maximum (D) life spans of chronologically aging tor1Δ and WT strains. Data are presented as means ± SEM (n = 4-7). Cells in A to D were cultured in medium initially containing 0.2%, 0.5%, 1% or 2% glucose in the presence of LCA (50 μM) or in its absence. Survival data are provided in Supplementary Figure 10. (E and F) Outline of pro- and anti-aging processes that are controlled by the TOR and/or cAMP/PKA signaling pathways and are modulated by LCA in tor1Δcells grown under non-CR (E) or CR (F) conditions.