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Elife. 2019 Jan 15;8. pii: e41792. doi: 10.7554/eLife.41792.

SUMO peptidase ULP-4 regulates mitochondrial UPR-mediated innate immunity and lifespan extension.

Gao K1, Li Y1,2, Hu S2, Liu Y1.

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State Key Laboratory of Membrane Biology, Institute of Molecular Medicine, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, and Peking-Tsinghua Center for Life Sciences, Peking University, Beijing, China.
Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, China.


Animals respond to mitochondrial stress with the induction of mitochondrial unfolded protein response (UPRmt). A cascade of events occur upon UPRmt activation, ultimately triggering a transcriptional response governed by two transcription factors: DVE-1 and ATFS-1. Here we identify SUMO-specific peptidase ULP-4 as a positive regulator of C. elegans UPRmt to control SUMOylation status of DVE-1 and ATFS-1. SUMOylation affects these two axes in the transcriptional program of UPRmt with distinct mechanisms: change of DVE-1 subcellular localization vs. change of ATFS-1 stability and activity. Our findings reveal a post-translational modification that promotes immune response and lifespan extension during mitochondrial stress.


C. elegans; cell biology; mitochondria; stress response; sumoylation

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