Journal
CELL
Volume 165, Issue 5, Pages 1197-1208Publisher
CELL PRESS
DOI: 10.1016/j.cell.2016.04.011
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Funding
- NIH [S10RR029668, S10RR027303, R37 AG024365]
- Gordon and Betty Moore Foundation
- Glenn Foundation for Medical Research Postdoctoral Fellowship
- Jane Coffin Childs Memorial Fund for Medical Research
- Glenn Foundation for Medical Research
- Howard Hughes Medical Institute
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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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