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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.

Regulation of Synaptic nlg-1/Neuroligin Abundance by the skn-1/Nrf Stress Response Pathway Protects against Oxidative Stress