Mitochondrial stress induces chromatin reorganization to promote longevity and UPRmt

• Autores: Ye Tian, Gilberto Garcia, Qian Bian
• Localización: Cell, ISSN 0092-8674, Vol. 165, Nº. 5, 2016, págs. 1197-1208
• Idioma: inglés
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• Resumen

  • 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.