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• W2039464456 endingPage "e1004100" @default.
• W2039464456 startingPage "e1004100" @default.
• W2039464456 abstract "The Nrf family of transcription factors mediates adaptive responses to stress and longevity, but the identities of the crucial Nrf targets, and the tissues in which they function in multicellular organisms to promote survival, are not known. Here, we use whole transcriptome RNA sequencing to identify 810 genes whose expression is controlled by the SKN-1/Nrf2 negative regulator WDR-23 in the nervous system of Caenorhabditis elegans. Among the genes identified is the synaptic cell adhesion molecule nlg-1/neuroligin. We find that the synaptic abundance of NLG-1 protein increases following pharmacological treatments that generate oxidative stress or by the genetic activation of skn-1. Increasing nlg-1 dosage correlates with increased survival in response to oxidative stress, whereas genetic inactivation of nlg-1 reduces survival and impairs skn-1-mediated stress resistance. We identify a canonical SKN-1 binding site in the nlg-1 promoter that binds to SKN-1 in vitro and is necessary for SKN-1 and toxin-mediated increases in nlg-1 expression in vivo. Together, our results suggest that SKN-1 activation in the nervous system can confer protection to organisms in response to stress by directly regulating nlg-1/neuroligin expression." @default.
• W2039464456 created "2016-06-24" @default.
• W2039464456 creator A5032997650 @default.
• W2039464456 creator A5046190178 @default.
• W2039464456 creator A5087163606 @default.
• W2039464456 creator A5089677894 @default.
• W2039464456 date "2014-01-16" @default.
• W2039464456 modified "2023-10-14" @default.
• W2039464456 title "Regulation of Synaptic nlg-1/Neuroligin Abundance by the skn-1/Nrf Stress Response Pathway Protects against Oxidative Stress" @default.
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• W2039464456 doi "https://doi.org/10.1371/journal.pgen.1004100" @default.
• W2039464456 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3894169" @default.
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• W2039464456 hasPublicationYear "2014" @default.
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