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The SKN-1/Nrf2 transcription factor can protect against oxidative stress and increase lifespan in C. elegans by distinct mechanisms

Research output: Contribution to journalJournal articlepeer-review

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  • Jennifer M.a. Tullet
  • James W. Green
  • Catherine Au
  • Alexandre Benedetto
  • Maximillian A. Thompson
  • Emily Clark
  • Ann F. Gilliat
  • Adelaide Young
  • Kathrin Schmeisser
  • David Gems
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<mark>Journal publication date</mark>10/2017
<mark>Journal</mark>Aging Cell
Issue number5
Volume16
Number of pages4
Pages (from-to)1191-1194
Publication StatusPublished
Early online date14/06/17
<mark>Original language</mark>English

Abstract

In C. elegans, the skn-1 gene encodes a transcription factor that resembles mammalian Nrf2 and activates a detoxification response. skn-1 promotes resistance to oxidative stress (Oxr) and also increases lifespan, and it has been suggested that the former causes the latter, consistent with the theory that oxidative damage causes aging. Here, we report that effects of SKN-1 on Oxr and longevity can be dissociated. We also establish that skn-1 expression can be activated by the DAF-16/FoxO transcription factor, another central regulator of growth, metabolism, and aging. Notably, skn-1 is required for Oxr but not increased lifespan resulting from over-expression of DAF-16; concomitantly, DAF-16 over-expression rescues the short lifespan of skn-1 mutants but not their hypersensitivity to oxidative stress. These results suggest that SKN-1 promotes longevity by a mechanism other than protection against oxidative damage.