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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.

Author information

1
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.
2
Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, China.

Abstract

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.

KEYWORDS:

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

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