Fig. 1.

AMPK mediates ROS-induced longevity. (A–E) Paraquat (0.25 mM) treatment increased the lifespan of wild-type animals. This lifespan extension was suppressed by mutations in genes encoding AMPK pathway components, including aak-2(ok524) (A and B), aak-2(rr48) (C), aakb-2(rr88) (D), and par-4(tm2986) (E). (F) Percent changes in the lifespan of various C. elegans mutants upon 0.25 mM paraquat treatment are shown. ROS-induced longevity was not suppressed by mutations in sir-2.1(ok434), hsf-1(sy441), daf-12(rh61rh411), skn-1(zu67), or haf-1(ok705). (G and H) Western blot analysis showed that the levels of phosphorylated AAK-2 (p-AAK-2) were increased by paraquat (0.25 mM) treatment in wild-type animals (n = 4) (G) and by clk-1(qm30) or isp-1(qm150) mutations (n = 4) (H). α-Tubulin was used as a loading control. The number below each lane indicates the relative band intensity of p-AAK-2. See SI Appendix, Fig. S1 for detailed analysis. (I and J) Lifespan curves of transgenic animals expressing only coinjection marker (Control) and a truncated form of AMPK catalytic subunit (CA-aak-2::gfp) with or without paraquat treatment (I) and the percent changes in their lifespans (J). See individual lifespan curves in SI Appendix, Fig. S1F and SI Appendix, Table S1 for statistical analysis and additional repeats of lifespan data. Also see the legend of SI Appendix, Fig. S1 for a discussion regarding the comparison of our lifespan data with those presented in a previous paper (14). Error bars indicate SEM.