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Communications Biology:植物组蛋白乙酰化作用于创伤诱导的转录激活和细胞重编程

已有 715 次阅读 2019-11-7 17:02 |个人分类:每日摘要|系统分类:论文交流

Histone acetylation orchestrates wound-induced transcriptional activation and cellular reprogramming in Arabidopsis


First author: Bart Rymen; Affiliations: RIKEN Center for Sustainable Resource Science (日本理化研究所可持续资源科学中心): Kanagawa, Japan

Corresponding author: Keiko Sugimoto 


Plant somatic cells reprogram and regenerate new tissues or organs when they are severely damaged. These physiological processes are associated with dynamic transcriptional responses but how chromatin-based regulation contributes to wound-induced gene expression changes and subsequent cellular reprogramming remains unknown. In this study we investigate the temporal dynamics of the histone modifications H3K9/14ac, H3K27ac, H3K4me3, H3K27me3, and H3K36me3, and analyze their correlation with gene expression at early time points after wounding. We show that a majority of the few thousand genes rapidly induced by wounding are marked with H3K9/14ac and H3K27ac before and/or shortly after wounding, and these include key wound-inducible reprogramming genes such as WIND1ERF113/RAP2.6L and LBD16. Our data further demonstrate that inhibition of GNAT-MYST-mediated histone acetylation strongly blocks wound-induced transcriptional activation as well as callus formation at wound sites. This study thus uncovered a key epigenetic mechanism that underlies wound-induced cellular reprogramming in plants.




当遭受严重的损害时,植物的体细胞会经历重编程,然后再生出新的组织和器官。这些生理进程与动态的转录响应相关,但基于染色质的调控如何作用于创伤诱导的基因表达变化以及后续的细胞重编程还不是很清楚。本文中,作者研究了植物在遭受创伤后早期组蛋白修饰H3K9/14ac、H3K27ac、H3K4me3、H3K27me3和H3K36me3的时间动态变化,并分析它们与基因表达的相关性。作者的研究显示在数千个能够快速响应创伤诱导的基因中,大部分在创伤之前或者在创伤之后很短的时间内具有明显的H3K9/14ac和H3K27ac标记,这些基因包括关键的创伤诱导性重编程基因,比如WIND1ERF113/RAP2.6LLBD16。本文的数据进一步揭示了GNAT-MYST介导的组蛋白乙酰化抑制强烈阻断了创伤诱导的转录激活,同时也阻断了创伤位点上愈伤组织的形成。因此,本文的研究揭示了一个植物中作用于创伤诱导的细胞重编程的关键表观机制。



通讯:Keiko Sugimoto (http://www.riken.jp/en/research/labs/csrs/cell_funct/)


研究方向在不断变化的环境中,植物如何整合发育和环境信号最大限度地促进器官生长



doi: https://doi.org/10.1038/s42003-019-0646-5


Journal: Communications Biology

Published date: November 04, 2019


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http://blog.sciencenet.cn/blog-3158122-1205258.html

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