生物
染色质
组蛋白甲基转移酶
表观遗传学
组蛋白
组蛋白甲基化
细胞生物学
遗传学
染色质重塑
DNA甲基化
组蛋白密码
基因表达调控
基因表达
基因
核小体
作者
Ye Tian,Gilberto Garcia,Qian Bian,Kristan K. Steffen,Larry Joe,Suzanne Wolff,Barbara J Meyer,Andrew Dillin
出处
期刊:Cell
[Elsevier]
日期:2016-05-01
卷期号:165 (5): 1197-1208
被引量:298
标识
DOI:10.1016/j.cell.2016.04.011
摘要
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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