SKN-1 regulates stress resistance downstream of amino catabolism pathways
Phillip A. Frankino, Talha F. Siddiqi, Theodore Bolas, Raz Bar‐Ziv, Holly K. Gildea, Hanlin Zhang, Ryo Higuchi‐Sanabria, Andrew Dillin
Abstract
activates a unique subset of SKN-1 regulated genes. Interestingly, this transcriptional program is independent of canonical P38-MAPK signaling components but requires ELT-3, NHR-49 and MDT-15. This activation of SKN-1 is dependent on upstream histidine catabolism genes HALY-1 and Y51H4A.7/UROC-1 and may occur through accumulation of a catabolite, 4-imidazolone-5-propanoate. Activating SKN-1 results in increased oxidative stress resistance but decreased survival to heat stress. Together, our data suggest that SKN-1 acts downstream of key catabolic pathways to influence physiology and stress resistance.
Topics & Concepts
CatabolismGene knockdownTranscription factorBiologyCell biologyOxidative stressGeneSignal transductionUpstream and downstream (DNA)Metabolic pathwayBiochemistryMetabolismComputer scienceComputer networkUpstream (networking)Genetics, Aging, and Longevity in Model OrganismsGenomics, phytochemicals, and oxidative stressAdipose Tissue and Metabolism