Mitochondrial stress induces chromatin reorganization to promote longevity and UPRmt
收藏干细胞与再生医学数据中心2022-02-20 更新2024-03-06 收录
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Organisms respond to mitochondrial stress throughthe upregulation of an array of protective genes,often perpetuating an early response to metabolicdysfunction across a lifetime. We find that mitochondrialstress causes widespread changes in chromatinstructure through histone H3K9 di-methylationmarks traditionally associated with gene silencing.Mitochondrial stress response activation requiresthe di-methylation of histone H3K9 through the activityof the histone methyltransferase met-2 and thenuclear co-factor lin-65. While globally the chromatinbecomes silenced by these marks, remaining portionsof the chromatin open up, at which point thebinding of canonical stress responsive factors suchas DVE-1 occurs. Thus, a metabolic stress responseis established and propagated into adulthood ofanimals through specific epigenetic modificationsthat allow for selective gene expression and lifespanextension.
提供机构：
University of California, Berkeley
创建时间：
2022-02-20
