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. 2022 Feb 18;12:18. doi: 10.1186/s13578-022-00747-0

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Mechanism of UPR^mt in C. elegans. When mitochondrial proteostasis is disturbed, signaling molecules of UPR^mt mediate mitochondria-to-nucleus retrograde communication. Transcription factors, including ATFS-1, DVE-1, and DAF-16, are activated by upstream signals and bind to the promoters of target genes, thus inducing the transcription of UPR^mt-related genes. A1 Under nonstress conditions, ATFS-1 enters the mitochondria through the MTS and is subsequently degraded. A2 Under mitochondrial stress conditions, ATFS-1 is transported to the nucleus in an NLS-dependent manner. B ULP-4-mediated deSUMOylation of ATFS-1 and DVE-1 enhances ATFS-1- and DVE-1-dependent transcription programs. C JMJD-1.2-, JMJD-3.1- and CBP-1-dependent epigenetic modifications facilitate the formation of a nucleosome conformation that is conducive to transcription. D Additionally, MET-2- and LIN-65-mediated chromatin silencing of non-UPR^mt gene regions is crucial for triggering UPR^mt. Consequently, the activation of UPR^mt promotes the recovery of mitochondria from damage, enhances mitochondrial function, and prolongs the lifespan of C. elegans