| Autor: |
Zhou Y; Max Planck Institute for Plant Breeding Research, Department of Plant Developmental Biology, Köln, Germany., Wang Y; National Key Laboratory of Plant Molecular Genetics, CAS Center for Excellence in Molecular Plant Sciences, Institute of Plant Physiology and Ecology, Shanghai Institute for Biological Sciences, Shanghai, China.; University of Chinese Academy of Sciences, Shanghai, China., Krause K; Max Planck Institute for Plant Breeding Research, Department of Plant Developmental Biology, Köln, Germany., Yang T; Max Planck Institute for Plant Breeding Research, Department of Plant Developmental Biology, Köln, Germany., Dongus JA; Max Planck Institute for Plant Breeding Research, Department of Plant Microbe Interactions, Köln, Germany., Zhang Y; National Key Laboratory of Plant Molecular Genetics, CAS Center for Excellence in Molecular Plant Sciences, Institute of Plant Physiology and Ecology, Shanghai Institute for Biological Sciences, Shanghai, China.; University of Chinese Academy of Sciences, Shanghai, China., Turck F; Max Planck Institute for Plant Breeding Research, Department of Plant Developmental Biology, Köln, Germany. turck@mpipz.mpg.de. |
| Abstrakt: |
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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