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Cell. 2016 May 19;165(5):1197-1208. doi: 10.1016/j.cell.2016.04.011. Epub 2016 Apr 28.

Mitochondrial Stress Induces Chromatin Reorganization to Promote Longevity and UPR(mt).

Author information

1
Department of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, CA 94720, USA; The Glenn Center for Aging Research, University of California, Berkeley, Berkeley, CA 94720, USA.
2
Department of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, CA 94720, USA.
3
Department of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, CA 94720, USA; The Glenn Center for Aging Research, University of California, Berkeley, Berkeley, CA 94720, USA. Electronic address: dillin@berkeley.edu.

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.

PMID:
27133166
PMCID:
PMC4889216
DOI:
10.1016/j.cell.2016.04.011
[Indexed for MEDLINE]
Free PMC Article

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