Lipid-mediated regulation of SKN-1/Nrf in response to germ cell absence
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Narasimhan, Sri Devi
Robida-Stubbs, Stacey
Moronetti Mazzeo, Lorenza E
Dreyfuss, Jonathan M
Raghavan, Prashant
Operaña, Theresa N
Esmaillie, Reza
Blackwell, T Keith
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https://doi.org/10.7554/eLife.07836Metadata
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Steinbaugh, Michael J, Sri Devi Narasimhan, Stacey Robida-Stubbs, Lorenza E Moronetti Mazzeo, Jonathan M Dreyfuss, John M Hourihan, Prashant Raghavan, Theresa N Operaña, Reza Esmaillie, and T Keith Blackwell. 2015. “Lipid-mediated regulation of SKN-1/Nrf in response to germ cell absence.” eLife 4 (1): e07836. doi:10.7554/eLife.07836. http://dx.doi.org/10.7554/eLife.07836.Abstract
In Caenorhabditis elegans, ablation of germline stem cells (GSCs) extends lifespan, but also increases fat accumulation and alters lipid metabolism, raising the intriguing question of how these effects might be related. Here, we show that a lack of GSCs results in a broad transcriptional reprogramming in which the conserved detoxification regulator SKN-1/Nrf increases stress resistance, proteasome activity, and longevity. SKN-1 also activates diverse lipid metabolism genes and reduces fat storage, thereby alleviating the increased fat accumulation caused by GSC absence. Surprisingly, SKN-1 is activated by signals from this fat, which appears to derive from unconsumed yolk that was produced for reproduction. We conclude that SKN-1 plays a direct role in maintaining lipid homeostasis in which it is activated by lipids. This SKN-1 function may explain the importance of mammalian Nrf proteins in fatty liver disease and suggest that particular endogenous or dietary lipids might promote health through SKN-1/Nrf. DOI: http://dx.doi.org/10.7554/eLife.07836.001Other Sources
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4541496/pdf/Terms of Use
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