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Telobox motifs recruit CLF/SWN-PRC2 for H3K27me3 deposition via TRB factors in Arabidopsis.

Yue ZhouYuejun WangKristin KrauseTingting YangJoram A DongusYijing ZhangFranziska Turck
Published in: Nature genetics (2018)
Polycomb repressive complexes (PRCs) control organismic development in higher eukaryotes through epigenetic gene repression1-4. 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.
Keyphrases
  • genome wide
  • dna methylation
  • dna binding
  • transcription factor
  • copy number
  • genome wide identification
  • poor prognosis
  • rna seq
  • crispr cas
  • long non coding rna