FIGURE 5.

Autophagy and the UPR^mt, but not mitophagy, are required for the enhanced longevity of sgk‐1 mutants upon PHB depletion. (a–f) Lifespan of wild‐type worms (left) and sgk‐1 mutants (right) with or without the PHB complex (phb‐1(RNAi)) upon inhibition of autophagy (a and b), inhibition of the UPR^mt (c and d) and inhibition of mitophagy (e and f). Replicates and statistics are shown in Table S1. (g) Quantification of the autophagy reporter Ex[Pnxh‐2::mCherry::LGG‐1] in wild‐type animals, phb‐1(RNAi) treated worms, sgk‐1(ok538) mutants and sgk‐1;phb‐1 depleted mutants at day 5 of adulthood upon inhibition of the UPR^mt (atfs‐1(RNAi)) and mitophagy (pink‐1(RNAi)). ***p < 0.001, **p < 0.01, *p < 0.1, ns not significant; Mann–Whitney test. Combination of at least three independent replicates. (h) SGK‐1 protein levels during ageing, at day 1, 5 and 10 of adulthood, upon PHB depletion and inhibition of either the UPR^mt (atfs‐1(RNAi)) or mitophagy (pink‐1(RNAi)). Mean ± SD; ***p < 0.001, **p < 0.01, *p < 0.1, ns not significant; ANOVA test. Combination of at least three independent replicates is shown