Zhang Dong, Jing Yanjun, Jiang Zhimin, Lin Rongcheng
Key Laboratory of Photobiology, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China University of the Chinese Academy of Sciences, Beijing 100049, China.
Key Laboratory of Photobiology, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China.
Plant Cell. 2014 Jun;26(6):2472-2485. doi: 10.1105/tpc.113.121848. Epub 2014 Jun 10.
Plant cell elongation is controlled by endogenous hormones, including brassinosteroid (BR) and gibberellin (GA), and by environmental factors, such as light/darkness. The molecular mechanisms underlying the convergence of these signals that govern cell growth remain largely unknown. We previously showed that the chromatin-remodeling factor PICKLE/ENHANCED PHOTOMORPHOGENIC1 (PKL/EPP1) represses photomorphogenesis in Arabidopsis thaliana. Here, we demonstrated that PKL physically interacted with PHYTOCHROME-INTERACTING FACTOR3 (PIF3) and BRASSINAZOLE-RESISTANT1 (BZR1), key components of the light and BR signaling pathways, respectively. Also, this interaction promoted the association of PKL with cell elongation-related genes. We found that PKL, PIF3, and BZR1 coregulate skotomorphogenesis by repressing the trimethylation of histone H3 Lys-27 (H3K27me3) on target promoters. Moreover, DELLA proteins interacted with PKL and attenuated its binding ability. Strikingly, brassinolide and GA inhibited H3K27me3 modification of histones associated with cell elongation-related loci in a BZR1- and DELLA-mediated manner, respectively. Our findings reveal that the PKL chromatin-remodeling factor acts as a critical node that integrates light/darkness, BR, and GA signals to epigenetically regulate plant growth and development. This work also provides a molecular framework by which hormone signals regulate histone modification in concert with light/dark environmental cues.
植物细胞伸长受包括油菜素内酯（BR）和赤霉素（GA）在内的内源激素以及光照/黑暗等环境因素的控制。这些调控细胞生长的信号相互整合的分子机制在很大程度上仍不清楚。我们之前表明，染色质重塑因子PICKLE/增强光形态建成1（PKL/EPP1）在拟南芥中抑制光形态建成。在此，我们证明PKL分别与光信号通路和BR信号通路的关键组分——光敏色素相互作用因子3（PIF3）和抗油菜素唑1（BZR1）发生物理相互作用。此外，这种相互作用促进了PKL与细胞伸长相关基因的结合。我们发现PKL、PIF3和BZR1通过抑制靶启动子上组蛋白H3赖氨酸-27（H3K27me3）的三甲基化共同调控暗形态建成。此外，DELLA蛋白与PKL相互作用并减弱其结合能力。引人注目的是，油菜素内酯和GA分别以BZR1和DELLA介导的方式抑制与细胞伸长相关基因座的组蛋白H3K27me3修饰。我们的研究结果表明，PKL染色质重塑因子作为一个关键节点，整合光照/黑暗、BR和GA信号，以表观遗传方式调控植物生长发育。这项工作还提供了一个分子框架，通过该框架激素信号与光照/黑暗环境信号协同调节组蛋白修饰。
