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

The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.

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

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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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Crossref · 10.1016/j.cell.2016.04.011

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Metadata

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
Venue
Cell
Publisher
Elsevier BV
Published
2016-05
Volume
165
Issue
5
Pages
1197-1208
ISSN
0092-8674 (ISSN-L)
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
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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