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Updated: Dec 9, 2025

Measurements of Physiological Stress Responses in C. Elegans
Published on: May 21, 2020
PER1 interaction with GPX1 regulates metabolic homeostasis under oxidative stress
Qi Sun1, Yunxia Yang2, Zhongqiu Wang3
1Center for Molecular Metabolism, Nanjing University of Science & Technology, Nanjing, 210094, China; Key Laboratory of Cardiovascular and Cerebrovascular Diseases, Bengbu Medical College, Bengbu, 233030, China.
Abstract:
Metabolism serves mammalian feeding and active behavior, and is controlled by circadian clock. The molecular mechanism by which clock factors regulate metabolic homeostasis under oxidative stress is unclear. Here, we have characterized that the daily oxygen consumption rhythm was deregulated in Per1 deficient mice. Per1 deficiency impaired daily mitochondrial dynamics and deregulated cellular GPx-related ROS fluctuations in the peripheral organs. We identified that PER1 enhanced GPx activity through PER1/GPX1 interaction in cytoplasm, consequently improving the oxidative phosphorylation efficiency of mitochondria. Per1 expression was specifically elevated in the fasting peripheral organs for protecting mitochondrial from oxidation stress. These observations reveal that Per1-driven mitochondrial dynamics is a critical effector mechanism for the regulation of mitochondrial function in response to oxidation stress.
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