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

Tullet, Jennifer M.A. and Green, James W. and Au, Catherine and Benedetto, Alexandre and Thompson, Maximillian A. and Clarke, Emily and Gilliat, Ann F. and Young, Adelaide and Schmisser, Kathrin and Gems, David (2017) The SKN-1/Nrf2 transcription factor can protect against oxidative stress and increase lifespan in C. elegans by distinct mechanisms. Aging Cell, 16 (5). pp. 1191-1194. ISSN 1474-9718. E-ISSN 1474-9726. (doi:https://doi.org/10.1111/acel.12627) (Full text available)

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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.

Item Type: Article
Subjects: Q Science > QH Natural history > QH581.2 Cell Biology
Divisions: Faculties > Sciences > School of Biosciences
Depositing User: Jennifer Tullet
Date Deposited: 17 May 2017 10:36 UTC
Last Modified: 13 Sep 2017 10:14 UTC
Resource URI: https://kar.kent.ac.uk/id/eprint/61758 (The current URI for this page, for reference purposes)
Tullet, Jennifer M.A.: https://orcid.org/0000-0002-2037-526X
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