ena-STUDY-MAX PLANCK INSTITUTE FOR PLANT BREEDING RESEARCH-10-03-2017-11:44:47:460-181
Telobox cis-elements recruit CLF-PRC2 for H3K27me3 deposition via TELOMERE REPEAT BINDING FACTORs (TRBs) in Arabidopsis
Polycomb Repressive Complex 2 (PRC2) deposits the repressive epigenetic H3K27me3 mark at target genes. In plants, different mechanisms for PRC2 recruitment have only been described for individual genes. Here we provide evidence of genome-wide PRC2 recruitment by TELOMERE REPEAT BINDING FACTORs (TRBs) in connection with the telobox cis-element. A trb1/2/3 mutant displayed a severe pleiotropic phenotype with thousands of misregulated genes and a transcriptome strikingly similar to that of strong PRC2 mutants. Furthermore, TRB1-3 physically interact with CLF, the catalytic unit of PRC2. ChIP-seq data show substantial redistribution of H3K27me3 in trb1/2/3, affecting 21.78 % of all Polycomb group (PcG) target genes. Loss of H3K27me3 is correlated to gene induction, TRB1 binding, and the presence of telobox elements. Mutation of a TRB1-bound telobox caused ectopic expression and H3K27me3 depletion of a SEP3 promoter-reporter construct. We propose that teloboxes recruit PRC2 for H3K27me3 deposition through an interaction between TRBs and CLF.
Polycomb Repressive Complex 2 (PRC2) deposits the repressive epigenetic H3K27me3 mark at target genes. In plants, different mechanisms for PRC2 recruitment have only been described for individual genes. Here we provide evidence of genome-wide PRC2 recruitment by TELOMERE REPEAT BINDING FACTORs (TRBs) in connection with the telobox cis-element. A trb1/2/3 mutant displayed a severe pleiotropic phenotype with thousands of misregulated genes and a transcriptome strikingly similar to that of strong PRC2 mutants. Furthermore, TRB1-3 physically interact with CLF, the catalytic unit of PRC2. ChIP-seq data show substantial redistribution of H3K27me3 in trb1/2/3, affecting 21.78 % of all Polycomb group (PcG) target genes. Loss of H3K27me3 is correlated to gene induction, TRB1 binding, and the presence of telobox elements. Mutation of a TRB1-bound telobox caused ectopic expression and H3K27me3 depletion of a SEP3 promoter-reporter construct. We propose that teloboxes recruit PRC2 for H3K27me3 deposition through an interaction between TRBs and CLF.