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. 2014 Oct 24;289(49):34205–34213. doi: 10.1074/jbc.M114.587170

FIGURE 6.

FIGURE 6.

E2F (EFL-1) regulation of C. elegans longevity requires FOXO (DAF-16). A and B, reducing expression of EFL-1 by feeding wild-type worms bacteria expressing either of two different RNAi efl-1 clones, compared with a control clone, extended lifespan (A, left), (**, p < 0.001 for efl-1#1 or efl-1#2 RNAi versus control RNAi), but not efl-2 RNAi (A, right) (not significant for efl-2#1 or efl-2#2 RNAi versus control RNAi). Daf-16 (mu86), a putative null mutation of FOXO, doesn't extend lifespan, when knockdown efl-1 (B) (not significant for efl-1#1 or efl-1#2 RNAi versus control RNAi). C–D, increased longevity of efl-1 knockdown worms correlates with increased levels of stress response genes sod3, mtl-1, and sip1. Relative mRNA levels of the indicated genes were determined by quantitative real-time qPCR in wild type (C) (t test, **, p < 0.01; n = 3) and daf-16 (mu86) worms (D) (t test, *, p < 0.05; n = 3), fed bacteria as in A and B. E, GFP-DAF-16 transgenic worms were used for subcellular localization analysis of DAF-16. EFL-1 did not affect the subcellular localization of DAF-16 in worms (not significant for efl-2#1 or efl-2#2 RNAi versus control RNAi).