Silencing by plant Polycomb-group genes requires dispersed trimethylation of histone H3 at lysine 27

• Published in: The EMBO journal Vol. 25; no. 19; pp. 4638 - 4649
• Main Authors: Schubert, Daniel, Primavesi, Lucia, Bishopp, Anthony, Roberts, Gethin, Doonan, John, Jenuwein, Thomas, Goodrich, Justin
• Format: Journal Article
• Language: English
• Published: Chichester, UK John Wiley & Sons, Ltd 04.10.2006; Blackwell Publishing Ltd
• Subjects: AGAMOUS Protein, Arabidopsis - metabolism; Alleles; Amino Acid Sequence; Arabidopsis - metabolism; Arabidopsis Proteins - chemistry; Arabidopsis Proteins - metabolism; Carrier Proteins - metabolism; Cell division; Cell Nucleus - metabolism; Cold Temperature; DNA-Binding Proteins; flowering; Flowers & plants; Gene Silencing; Genes; Genes, Plant - genetics; histone methylation; Histones - metabolism; Homeodomain Proteins - chemistry; Homeodomain Proteins - metabolism; Leaves; Lysine - metabolism; MADS Domain Proteins - metabolism; Methylation; Mitosis; Models, Genetic; Molecular biology; Molecular Sequence Data; Nuclear Proteins - metabolism; Plant Leaves - cytology; Plant Roots - cytology; Plants; Point Mutation - genetics; Polycomb; Polycomb-Group Proteins; Protein Structure, Tertiary; Proteins; Repressor Proteins - genetics; Transgenes
• ISSN: 0261-4189; 1460-2075
• DOI: 10.1038/sj.emboj.7601311

The plant Polycomb‐group (Pc‐G) protein CURLY LEAF (CLF) is required to repress targets such as AGAMOUS (AG) and SHOOTMERISTEMLESS (STM). Using chromatin immunoprecipitation, we identify AG and STM as direct targets for CLF and show that they carry a characteristic epigenetic signature of dispersed histone H3 lysine 27 trimethylation (H3K27me3) and localised H3K27me2 methylation. H3K27 methylation is present throughout leaf development and consistent with this, CLF is required persistently to silence AG. However, CLF is not itself an epigenetic mark as it is lost during mitosis. We suggest a model in which Pc‐G proteins are recruited to localised regions of targets and then mediate dispersed H3K27me3. Analysis of transgenes carrying AG regulatory sequences confirms that H3K27me3 can spread to novel sequences in a CLF‐dependent manner and further shows that H3K27me3 methylation is not sufficient for silencing of targets. We suggest that the spread of H3K27me3 contributes to the mitotic heritability of Pc‐G silencing, and that the loss of silencing caused by transposon insertions at plant Pc‐G targets reflects impaired spreading.