1RIKEN Center for Sustainable Resource Science, 1-7-22 Suehiro-cho, Tsurumi, Yokohama, Kanagawa 230-0045 Japan.
2Department of Biological Sciences, Faculty of Science, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8654 Japan.
Commun Biol. 2019 Nov 4;2:404. doi: 10.1038/s42003-019-0646-5. eCollection 2019.
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 , and . 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.
当植物体细胞受到严重损伤时,它们会重新编程并再生新的组织或器官。这些生理过程与动态转录反应有关,但染色质调控如何促进损伤诱导的基因表达变化以及随后的细胞重编程仍然未知。在这项研究中,我们研究了组蛋白修饰 H3K9/14ac、H3K27ac、H3K4me3、H3K27me3 和 H3K36me3 的时间动态,并分析了它们与损伤后早期基因表达的相关性。我们发现,几千个快速诱导损伤的基因中的大多数在损伤之前和/或损伤后不久就被 H3K9/14ac 和 H3K27ac 标记,其中包括关键的损伤诱导重编程基因,如 、 和 。我们的数据还表明,抑制 GNAT-MYST 介导的组蛋白乙酰化强烈阻止了损伤诱导的转录激活以及损伤部位的愈伤组织形成。因此,这项研究揭示了一个关键的表观遗传机制,它是植物损伤诱导细胞重编程的基础。