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. Author manuscript; available in PMC: 2014 Dec 26.
Published in final edited form as: Cell Rep. 2013 Dec 12;5(6):1600–1610. doi: 10.1016/j.celrep.2013.11.018

Figure 1. Double mutations in daf-2 and rsks-1 lead to synergistically prolonged longevity that requires DAF-16.

Figure 1

(A) The daf-2 rsks-1 double mutant showed synergistically prolonged longevity (454% extension compared to N2) that is dependent on DAF-16. (B) Inhibition of TOR by rapamycin led to increased lifespan extension in daf-2 compared to N2. Rapamycin (100 μM) extended N2 and daf-2 lifespan by 26% and 45%, respectively (log-rank, p < 0.0001). Animals treated with the vehicle (DMSO) alone did not show significantly affected lifespan (log-rank, p > 0.05). Quantitative data and statistical analyses are included in Table S1. (C) daf-2 rsks-1 animals showed significantly increased DAF-16 transcriptional activity. mRNA levels of DAF-16 targets that are either activated (sod-3 and hsp-12.3) or inhibited (sams-1) by DAF-16 were quantified using qRT-PCR. Asterisks indicate statistical differences using two-tailed t tests: ***, p < 0.001.