The transcriptional repressors VAL1 and VAL2 recruit PRC2 for genome-wide Polycomb silencing in Arabidopsis
文献类型: 外文期刊
作者: Yuan, Liangbing 1 ; Song, Xin 1 ; Zhang, Lu 1 ; Yu, Yaoguang 1 ; Liang, Zhenwei 1 ; Lei, Yawen 1 ; Ruan, Jiuxiao 1 ; Tan, 1 ;
作者机构: 1.Sun Yat Sen Univ, Sch Life Sci, State Key Lab Biocontrol, Guangdong Prov Key Lab Plant Resource, Guangzhou 510275, Peoples R China
2.Hainan Normal Univ, Coll Life Sci, Key Lab Trop Anim & Plant Ecol Hainan Prov, Minist Educ,Key Lab Ecol Trop Isl, Haikou 571158, Hainan, Peoples R China
3.South China Agr Univ, Coll Agr, Guangdong Key Lab Plant Mol Breeding, Guangzhou 510624, Peoples R China
4.Guangdong Acad Agr Sci, Agrobiol Gene Res Ctr, Guangdong Prov Key Lab Crop Germplasm Resources P, Guangzhou 510640, Peoples R China
期刊名称:NUCLEIC ACIDS RESEARCH ( 影响因子:16.971; 五年影响因子:15.542 )
ISSN: 0305-1048
年卷期: 2021 年 49 卷 1 期
页码:
收录情况: SCI
摘要: The Polycomb repressive complex 2 (PRC2) catalyzes histone H3 Lys27 trimethylation (H3K27me3) to repress gene transcription in multicellular eukaryotes. Despite its importance in gene silencing and cellular differentiation, how PRC2 is recruited to target loci is still not fully understood. Here, we report genome-wide evidence for the recruitment of PRC2 by the transcriptional repressors VIVIPAROUS1/ABI3-LIKE1 (VAL1) and VAL2 in Arabidopsis thaliana. We show that the val1 val2 double mutant possesses somatic embryonic phenotypes and a transcriptome strikingly similar to those of the swn clf double mutant, which lacks the PRC2 catalytic subunits SWINGER (SWN) and CURLY LEAF (CLF). We further show that VAL1 and VAL2 physically interact with SWN and CLF in vivo. Genome-wide binding profiling demonstrated that they colocalize with SWN and CLF at PRC2 target loci. Loss of VAL1/2 significantly reduces SWN and CLF enrichment at PRC2 target loci and leads to a genome-wide redistribution of H3K27me3 that strongly affects transcription. Finally, we provide evidence that the VAL1/VAL2-RY regulatory system is largely independent of previously identified modules for Polycomb silencing in plants. Together, our work demonstrates an extensive genome-wide interaction between VAL1/2 and PRC2 and provides mechanistic insights into the establishment of Polycomb silencing in plants.
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