Role of SKN-1 in mediating CEH-60 transcriptional activity in oxidative stress response in C. elegans

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Oxidative stress is a state of imbalance between the activities of reactive oxygen species (ROS) and the activities of the antioxidants (AOX) that detoxify the reactive intermediates or repair the resulting damage. Impaired ROS management contributes to aging and disease through oxidative degradation of lipids in cell membranes disrupting the DNA, proteins, and cellular functions. In C. elegans animals undergoing oxidative stress, SKN-1 accumulates in the intestinal nuclei to induce downstream stress response genes to restore the redox balance. CEH-60/PBX is an intestinal transcription factor that opposes this pathway by repressing genes that promote longevity and stress responses. To uncover the activity of CEH-60 in oxidative stress response and the role of SKN-1 in mediating this activity, I measured the survival of ceh-60 mutants as well as animals with both CEH-60 and intestinal SKN-1 knocked out under oxidative stress conditions. I found that ceh-60 mutant animals with intestinal SKN-1 additionally knocked out displayed extended lifespan compared to ceh-60 single mutants, suggesting that loss of ceh-60 may not require SKN-1 to upregulate stress response genes. Thus, in wildtype animals, CEH-60 may have different mechanistic ways to repress stress response and longevity other than via SKN-1. Another possible explanation to my findings is that SKN-1 carries out most of its stress response activity in the non-intestinal tissues.

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