Cited by 370Genetics, Aging, and Longevity in Model OrganismsEpigenetics and DNA MethylationGenomics and Chromatin Dynamics

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Mitochondrial stress induces chromatin reorganization to promote longevity and UPR(mt)

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Tian, Ye, Garcia, Gilberto, Bian, Qian, Steffen, Kristan K., Joe, Larry, Wolff, Suzanne, Meyer, Barbara J., Dillin, Andrew·2016·Cell

DOI 10.1016/j.cell.2016.04.011PMC PMC4889216

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Abstract

Organisms respond to mitochondrial stress through the upregulation of an array of protective genes, often perpetuating an early response to metabolic dysfunction across a lifetime. We find that mitochondrial stress causes widespread changes in chromatin structure through histone H3K9 di-methylation marks traditionally associated with gene silencing. Mitochondrial stress response activation requires the di-methylation of histone H3K9 through the activity of the histone methyltransferase met-2 and the nuclear co-factor lin-65. While globally the chromatin becomes silenced by these marks, remaining portions of the chromatin open up, at which point the binding of canonical stress responsive factors such as DVE-1 occurs. Thus, a metabolic stress response is established and propagated into adulthood of animals through specific epigenetic modifications that allow for selective gene expression and lifespan extension.

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Authors: Tian, Y., Garcia, G., Bian, Q., Steffen, K. K., Joe, L., Wolff, S., Meyer, B. J., & Dillin, A.
Affiliations: Howard Hughes Medical Institute (US)
Corresponding author: Dillin, Andrew
ORCID: Tian, Ye
Garcia, Gilberto
Bian, Qian
Joe, Larry
Meyer, Barbara J.
Dillin, Andrew
Venue: Cell
Publisher: Elsevier BV
Published: 2016-05
Volume: 165
Issue: 5
Pages: 1197-1208
ISSN: 0092-8674 (ISSN-L)
DOI: 10.1016/j.cell.2016.04.011
PMC: PMC4889216
OpenAlex: W2343051572
Cited by: 370
References: 43
Citations by year: 2026: 40 · 2025: 27 · 2024: 36 · 2023: 25 · 2022: 47 · 2021: 40 · 2020: 39 · 2019: 33 · 2018: 37 · 2017: 34 · 2016: 12
FWCI: 20.81
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 383 d)
Locations: Cell (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
eScholarship (California Digital Library) (submittedVersion)
Funders: National Institutes of Health (5r01gm030702-36)
National Institute on Aging (R37AG024365)
National Institute of General Medical Sciences (R01-GM030702)
National Center for Research Resources (S10RR029668, S10RR027303)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Keywords: mitochondrial stress, chromatin reorganization, MET-2, longevity, lifespan extension, epigenetic regulation, gene silencing, Caenorhabditis elegans, metabolic stress response
MeSH terms: Animals, Gene Expression Regulation, Histones, Longevity, Mitochondria, Histone-Lysine N-Methyltransferase, Caenorhabditis elegans, Caenorhabditis elegans Proteins, Chromatin Assembly and Disassembly, Epigenesis, Genetic, Unfolded Protein Response

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Mitochondrial stress induces chromatin reorganization to promote longevity and UPR(mt)

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