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. Author manuscript; available in PMC: 2022 Apr 11.
Published in final edited form as: Free Radic Biol Med. 2022 Feb 1;181:52–61. doi: 10.1016/j.freeradbiomed.2022.01.030

Fig. 3.

Fig. 3.

Overexpression of daf-16 and lgg-1 extends lifespan, alleviates locomotor deficits, and improves stress response in hSOD1G93A worms. (A-C) Survival curves for hSOD1G93A::daf-16, hSOD1G93A::lgg-1, and lgg-1::daf-16 worms. (D, E) Motor neuron survival and morphology in transgenic worms. Overexpression of lgg-1 but not daf-16 protected against hSOD1G93A-induced neurotoxicity (D) and restored motor neuron morphology (E) in hSOD1G93A worms. (F) Western blot analysis of protein extracts from hSOD1G93A transgenic strains. Lgg-1 overexpression reduced the level of hSOD1 protein in hSOD1G93A worms, whereas daf-16 overexpression had no effect. (G) Locomotor behavior in hSOD1 transgenic worms overexpressing daf-16 or lgg-1. Locomotion was restored in hSOD1G93A::lgg-1 worms, and to a lesser extent in hSOD1G93A::daf-16 worms. (H, I) Oxidative stress response in hSOD1G93A transgenic worms, hSOD1G93A worms over expressing lgg-1 and exposed to paraquat showed increased longevity compared to hSOD1G93A worms. Overexpression of daf-16 had no obvious effect on hSOD1 protein degradation, but partly restored the oxidative stress response that was diminished by hSOD1G93A mutation. ****P<0.0001, **P <0.001 (N ~ 100 worms per condition from 3 independent experiments).