Mitochondrial Stress Induces Chromatin Reorganization to Promote Longevity and UPRmt

作者：Tian Ye; Garcia Gilberto; Bian Qian; Steffen Kristan K; Joe Larry; Wolff Suzanne; Meyer Barbara J; Dillin Andrew

来源：Cell, 2016, 165(5): 1197-1208.

DOI：10.1016/j.cell.2016.04.011

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.

• 出版日期2016-5-19