Li Wenjuan, Zhang Xiaoling, Zhang Qingche, Li Qingzhu, Li Yanzhuo, Lv Yanfang, Liu Yue, Cao Ying, Wang Huamei, Chen Xiangsong, Yang Hongchun
State Key Laboratory of Hybrid Rice, College of Life Sciences, Wuhan University, Wuhan 430072, China.
Hubei Hongshan Laboratory, Wuhan 430072, China.
Plant Physiol. 2024 Oct 1;196(2):1080-1094. doi: 10.1093/plphys/kiae369.
Chromatin dynamics play essential roles in transcriptional regulation. The chromodomain helicase DNA-binding domain 3 chromatin remodeler PICKLE (PKL) and HISTONE DEACETYLASE6 (HDA6) are required for transcriptional gene silencing, but their coordinated function in gene repression requires further study. Through a genetic suppressor screen, we found that a point mutation at PKL could partially restore the developmental defects of a weak Polycomb repressive complex 1 (PRC1) mutant (ring1a-2 ring1b-3), in which RING1A expression is suppressed by a T-DNA insertion at the promoter. Compared to ring1a-2 ring1b-3, the expression of RING1A is increased, nucleosome occupancy is reduced, and the histone 3 lysine 9 acetylation (H3K9ac) level is increased at the RING1A locus in the pkl ring1a-2 ring1b-3 triple mutant. HDA6 interacts with PKL and represses RING1A expression similarly to PKL genetically and molecularly in the ring1a-2 ring1b-3 background. Furthermore, we show that PKL and HDA6 suppress the expression of a set of genes and transposable elements (TEs) by increasing nucleosome density and reducing H3K9ac. Genome-wide analysis indicated they possibly coordinately maintain DNA methylation as well. Our findings suggest that PKL and HDA6 function together to reduce H3K9ac and increase nucleosome occupancy, thereby facilitating gene/TE regulation in Arabidopsis (Arabidopsis thaliana).
染色质动力学在转录调控中发挥着至关重要的作用。染色质结构域解旋酶DNA结合结构域3染色质重塑因子PICKLE（PKL）和组蛋白去乙酰化酶6（HDA6）是转录基因沉默所必需的，但它们在基因抑制中的协同功能尚需进一步研究。通过遗传抑制子筛选，我们发现PKL上的一个点突变可以部分恢复弱多梳抑制复合体1（PRC1）突变体（ring1a-2 ring1b-3）的发育缺陷，在该突变体中，RING1A的表达因启动子处的T-DNA插入而受到抑制。与ring1a-2 ring1b-3相比，在pkl ring1a-2 ring1b-3三重突变体的RING1A基因座处，RING1A的表达增加，核小体占有率降低，组蛋白3赖氨酸9乙酰化（H3K9ac）水平升高。在ring1a-2 ring1b-3背景下，HDA6与PKL相互作用，并在遗传和分子水平上与PKL类似地抑制RING1A的表达。此外，我们表明PKL和HDA6通过增加核小体密度和降低H3K9ac来抑制一组基因和转座元件（TE）的表达。全基因组分析表明它们可能也协同维持DNA甲基化。我们的研究结果表明，PKL和HDA6共同发挥作用，降低H3K9ac并增加核小体占有率，从而促进拟南芥（Arabidopsis thaliana）中的基因/TE调控。
