Figure 2: NMD is required for the long lifespan of insulin/IGF-1 receptor daf-2 mutants.

(a) The long lifespan of daf-2(e1370) (daf-2(−)) mutants was significantly suppressed by smg-2(qd101) (smg-2(−)) mutations. (b) smg-2 RNAi from L4 stage significantly decreased the longevity of daf-2(−) animals. (c) smg-2 mutations significantly reduced the long lifespan conferred by daf-2 mutations without FUdR treatment. (d–f) Longevity induced by isp-1(qm150) (isp-1(−)) (d), eat-2(ad1116) (eat-2(−)) (e) or glp-1(e2141) (glp-1(−)) mutations (f) was suppressed by smg-2 mutations. (g,h) smg-2 mutations had no effect on the long lifespan of vhl-1(ok161) (vhl-1(−)) (g) or osm-5(p813) (osm-5(−)) (h) mutants. Please see Supplementary Fig. 2c–f for data regarding the effects of smg-2 RNAi on the longevity of isp-1, eat-2, glp-1 and vhl-1 mutants. Specific lifespan-decreasing effects of smg-2 RNAi on daf-2 mutants may be due to variability in RNAi efficiency, as we did not perform all the RNAi-based lifespan assays using various longevity mutants in the same experimental set. smg-2 mutations also partially suppressed delayed age-dependent declines in the body movement of daf-2 mutants (Supplementary Fig. 5). See Supplementary Data 1 for statistical analysis and additional repeats.