Germ cell ablation delays C. elegans aging, in part, because unconsumed fat triggers activation of the detoxification factor SKN-1/Nrf, which is regulated by lipid signals and maintains lipid homeostasis.

Increased production of ether lipids is required to extend lifespan in response to metformin, phenformin, and multiple, distinct, longevity-promoting manipulations, illuminating the possibility that raising ether lipid levels represents a new therapeutic strategy to support healthy aging.

Post-translational processing of the SKN-1A/Nrf1 transcription factor regulates proteasome expression.

Genetic analysis reveals NADPH oxidase generated reactive oxygen species as signals to re-establish cellular homeostasis during aging via activating a transcriptional response.

C. elegans nematodes can assess faithfully the threat that H₂O₂ poses by coupling the induction of their H₂O₂ defenses to the perception of high temperature—an inherent enhancer of the reactivity of H₂O₂.

SKN-1A/Nrf1 promotes healthy aging by activating protein degradation in response to accumulation of misfolded proteins.

Quantitative genetic analyses reveal remarkably broad genetic variation underlies the requirement for two critical regulatory inputs into a core embryonic gene regulatory network within one animal species.

C. elegans nematodes use a sensory-neuronal circuit to determine whether to defend themselves from hydrogen peroxide attack or to freeload off orthologous protective defenses from bacteria in their surrounding environment.

In C. elegans, neuronic TRPA-1 senses bacterial accumulation by detecting indole production to up-regulate lysozyme genes via FOXO/DAF-16 in the intestine, thereby delaying microbial dysbiosis.