TOR通过对H3K27me3的整体维护来抑制转录应激反应

表观遗传修饰H3K4me3和H3K27me3的组合暗示了双稳态特征，该特征在开启和关闭状态之间交替，从而允许在外部刺激下快速转录变化。

雷帕霉素（TOR）的靶标是将多种外部刺激与基因表达联系起来的中央感觉枢纽。但是，由TOR刺激特定转录重编程的基础机制仍然难以捉摸。我们在拟南芥中进行的生物信息分析表明，TOR阻遏的基因与双稳态或沉默染色质域相关。受TOR信号通路调控的两个结构域均与CURLY LEAF（CLF）在特定情况下与类异源染色质蛋白1（LHP1）沉积的高水平H3K27me3相关。染色质重塑剂SWI2 / SNF2 ATPase BRAHMA（BRM）仅在双稳态染色质域上激活TOR抑制的基因，以快速诱导生物应激反应。本文，我们生物信息预测和体内实验都证明了TOR通过对H3K27me3的整体维护来抑制转录应激反应。

Abstract

Combinations of epigenetic modifications H3K4me3 and H3K27me3 implicate bistable feature which alternates between on and off state allowing rapid transcriptional changes upon external stimuli. Target of Rapamycin (TOR) functions as a central sensory hub to link a wide range of external stimuli to gene expression. However, the mechanisms underlying stimulus-specific transcriptional reprogramming by TOR remains elusive. Our in silico analysis in Arabidopsis demonstrates that TOR-repressed genes are associated with either bistable or silent chromatin domains. Both domains regulated by TOR signaling pathway are associated with high level of H3K27me3 deposited by CURLY LEAF (CLF) in specific context with LIKE HETEROCHROMATIN PROTEIN1 (LHP1). Chromatin remodeler SWI2/SNF2 ATPase BRAHMA (BRM) activates TOR-repressed genes only at bistable chromatin domains to rapidly induce biotic stress responses. Here we demonstrated both in silico and in vivo that TOR represses transcriptional stress responses through global maintenance of H3K27me3.

来源：

https://www.biorxiv.org/content/10.1101/2021.03.28.437410v1.full.pdf

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