The transcriptional repressors VAL1 and VAL2 recruit PRC2 for genome-wide Polycomb silencing in Arabidopsis.

The transcriptional repressors VAL1 and VAL2 recruit PRC2 for genome-wide Polycomb silencing in Arabidopsis.
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DOI:
10.1093/nar/gkaa1129
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发表时间:
2021-01-11
影响因子:
14.9
通讯作者:
Li C
Li C
中科院分区:
生物学2区
文献类型:
--
作者:
Yuan L;Song X;Zhang L;Yu Y;Liang Z;Lei Y;Ruan J;Tan B;Liu J;Li C

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多梳抑制复合物2(PRC 2)催化组蛋白H3 Lys 27三甲基化(H3 K27 me 3)以抑制多细胞真核生物中的基因转录。尽管它在基因沉默和细胞分化中的重要性,但PRC 2如何被募集到靶位点仍然没有完全理解。在这里,我们报告了全基因组范围内的证据PRC 2招聘的转录抑制因子VIVIPAROUS 1/ABI 3-LIKE 1(VAL 1)和VAL 2在拟南芥。我们发现,val 1 val 2双突变体具有体细胞胚胎表型和转录组惊人的swn clf双突变体,缺乏PRC 2催化亚基SWINGER(SWN)和卷曲叶(CLF)的相似。我们进一步表明,VAL 1和VAL 2物理相互作用与SWN和CLF在体内。全基因组结合分析表明,它们与SWN和CLF在PRC 2靶位点共定位。VAL 1/2的缺失显著降低了PRC 2靶基因座处的SWN和CLF富集,并导致H3 K27 me 3在全基因组范围内的重新分布,这强烈影响转录。最后,我们提供的证据表明,VAL 1/VAL 2-RY调节系统是在很大程度上独立于以前确定的模块Polycomb沉默植物。总之,我们的工作证明了VAL 1/2和PRC 2之间广泛的全基因组相互作用,并为植物中Polycomb沉默的建立提供了机制见解。
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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