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

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 adult

SUBMITTER: Tian Y 

PROVIDER: S-EPMC4889216 | biostudies-literature | 2016 May

REPOSITORIES: biostudies-literature