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Telobox motifs recruit CLF/SWN–PRC2 for H3K27me3 deposition via TRB factors in Arabidopsis
First author: Yue Zhou; Affiliations: Max Planck Institute for Plant Breeding Research (德国马克斯普朗克遗传发育生物学研究所): Köln, Germany
Corresponding author: Franziska Turck
Polycomb repressive complexes (PRCs; 多梳抑制复合物) control organismic development in higher eukaryotes through epigenetic gene repression. PRC proteins do not contain DNA-binding domains, thus prompting questions regarding how PRCs find their target loci. Here we present genome-wide evidence of PRC2 recruitment by telomere-repeat-binding factors (TRBs) through telobox-related motifs in Arabidopsis. A triple trb1-2, trb2-1, and trb3-2 (trb1/2/3) mutant with a developmental phenotype and a transcriptome strikingly similar to those of strong PRC2 mutants showed redistribution of trimethyl histone H3 Lys27 (H3K27me3) marks and lower H3K27me3 levels, which were correlated with derepression (去阻遏) of TRB1-target genes. TRB1–3 physically interacted with the PRC2 proteins CLF and SWN. A SEP3 reporter gene with a telobox mutation showed ectopic expression, which was correlated with H3K27me3 depletion, whereas tethering (拴住) TRB1 to the mutated cis element partially restored repression. We propose that telobox-related motifs recruit PRC2 through the interaction between TRBs and CLF/SWN, a mechanism essential for H3K27me3 deposition at a subset of target genes.
在高等真核生物中,多梳抑制复合物PRCs通过表观基因抑制控制着器官的发育。PRC蛋白并不含有DNA结合结构域,因此PRCs是如何结合到其靶基因位点的还是一个有待解决的问题。本文报道了拟南芥中端粒重复结合因子TRB通过telobox基序招募PRC2。trb1-2、trb2-1和trb3-2三突变体的表型和转录组与PRC2突变体较为相似,两者均显示H3K27me3的再分配以及低水平的H3K27me3,这与TRB1靶基因的去阻遏相关。TRB1–3能够与PRC2蛋白CLF和SWN相互作用。一个带有telobox突变的SEP3报告基因显示出异位表达,这与H3K27me3的耗尽相关,会将TRB1紧紧拴在突变了的顺式作用元件上,部分恢复抑制作用。作者假设telobox基序通过TRBs与CLF/SWN之间的相互作用招募PRC2,该机制能够促进H3K27me3在一些靶基因上的沉积。
通讯:Franziska Turck (http://www.mpipz.mpg.de/turck)