生物
召回
转录因子
神经科学
染色质
炎症
表观遗传学
组蛋白
刺激(心理学)
细胞生物学
免疫学
认知心理学
基因
遗传学
心理学
作者
Samantha B. Larsen,Christopher Cowley,Sairaj M. Sajjath,Douglas Barrows,Yihao Yang,Thomas Carroll,Elaine Fuchs
出处
期刊:Cell Stem Cell
[Elsevier]
日期:2021-10-01
卷期号:28 (10): 1758-1774.e8
被引量:105
标识
DOI:10.1016/j.stem.2021.07.001
摘要
Known for nearly a century but through mechanisms that remain elusive, cells retain a memory of inflammation that equips them to react quickly and broadly to diverse secondary stimuli. Using murine epidermal stem cells as a model, we elucidate how cells establish, maintain, and recall inflammatory memory. Specifically, we landscape and functionally interrogate temporal, dynamic changes to chromatin accessibility, histone modifications, and transcription factor binding that occur during inflammation, post-resolution, and in memory recall following injury. We unearth an essential, unifying role for the general stress-responsive transcription factor FOS, which partners with JUN and cooperates with stimulus-specific STAT3 to establish memory; JUN then remains with other homeostatic factors on memory domains, facilitating rapid FOS re-recruitment and gene re-activation upon diverse secondary challenges. Extending our findings, we offer a comprehensive, potentially universal mechanism behind inflammatory memory and less discriminate recall phenomena with profound implications for tissue fitness in health and disease.
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