生物
DNA损伤
细胞生物学
DNA修复
早衰
核糖体生物发生
染色质重塑
染色质
抄写(语言学)
秀丽隐杆线虫
组蛋白
DNA
遗传学
基因
核糖核酸
核糖体
哲学
语言学
作者
Siyao Wang,David Meyer,Björn Schumacher
标识
DOI:10.1038/s41594-020-00513-1
摘要
DNA damage causes cancer, impairs development and accelerates aging. Transcription-blocking lesions and transcription-coupled repair defects lead to developmental failure and premature aging in humans. Following DNA repair, homeostatic processes need to be reestablished to ensure development and maintain tissue functionality. Here, we report that, in Caenorhabditis elegans, removal of the WRAD complex of the MLL/COMPASS H3K4 methyltransferase exacerbates developmental growth retardation and accelerates aging, while depletion of the H3K4 demethylases SPR-5 and AMX-1 promotes developmental growth and extends lifespan amid ultraviolet-induced damage. We demonstrate that DNA-damage-induced H3K4me2 is associated with the activation of genes regulating RNA transport, splicing, ribosome biogenesis and protein homeostasis and regulates the recovery of protein biosynthesis that ensures survival following genotoxic stress. Our study uncovers a role for H3K4me2 in coordinating the recovery of protein biosynthesis and homeostasis required for developmental growth and longevity after DNA damage.
科研通智能强力驱动
Strongly Powered by AbleSci AI