Figure 2.

pfd-6 is required for the longevity of daf-2 mutants. (A,B) pfd-6(gk493446) [pfd-6(−)] point mutation causing a T16I change with pfd-6 RNAi partly suppressed the longevity of daf-2(e1370) [daf-2(−)] mutants with (A) or without (B) FUdR. (A) pfd-6 RNAi during adulthood slightly decreased the short life span of pfd-6; daf-2 double mutants but did not affect that of pfd-6 mutants (two out of four trials). (C) pfd-6 RNAi partially suppressed the longevity conferred by osm-5(p813) [osm-5(−)] mutations. (D–G) pfd-6 RNAi did not decrease the longevity of eat-2(ad1116) [eat-2(−)] (D), isp-1(qm150) [isp-1(−)] (E), rsks-1(tm1714) [rsks-1(−)] (F), and vhl-1(ok161) [vhl-1(−)] (G) animals. (H) pfd-6 mutation did not decrease the life span of hsb-1(cg116) [hsb-1(−)] mutants. Considering our data suggesting that pfd-6 mediates the longevity effects of HSF-1, it is surprising to find that genetic inhibition of pfd-6 did not decrease the longevity of rsks-1 or hsb-1 mutants, which require HSF-1 for a longer life span (Chiang et al. 2012; Seo et al. 2013). We speculate that up-regulation of HSF-1 by rsks-1 and hsb-1 mutations may affect pfd-6 differently than that by daf-2 and osm-5 mutations, which will be interesting to examine in future studies. See Supplemental Table S3 for statistical analysis and additional repeats.