SUMO peptidase ULP-4 regulates mitochondrial UPR-mediated innate immunity and lifespan extension.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 30642431.
- Also identified by DOI 10.7554/eLife.41792 and PMC identifier 6355198.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Animals respond to mitochondrial stress with the induction of mitochondrial unfolded protein response (UPR<sup>mt</sup>). A cascade of events occur upon UPR<sup>mt</sup> 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 <i>C. elegans</i> UPR<sup>mt</sup> to control SUMOylation status of DVE-1 and ATFS-1. SUMOylation affects these two axes in the transcriptional program of UPR<sup>mt</sup> 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.
Medical subject headings
- Caenorhabditis elegans
- Caenorhabditis elegans Proteins
- Cysteine Endopeptidases
- Immunity, Innate
- Longevity
- Mitochondria
- Unfolded Protein Response