期刊
NATURE GENETICS
卷 50, 期 5, 页码 638-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41588-018-0109-9
关键词
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资金
- Max Planck Society
- Chinese Scholarship Council
- National Natural Science Foundation of China [31570319]
Polycomb repressive complexes (PRCs) control organismic development in higher eukaryotes through epigenetic gene repression(1-4). PRC proteins do not contain DNA-binding domains, thus prompting questions regarding how PRCs find their target loci(5). 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 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 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.
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