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Silencing by plant Polycomb‐group genes requires dispersed trimethylation of histone H3 at lysine 27
Author(s) -
Schubert Daniel,
Primavesi Lucia,
Bishopp Anthony,
Roberts Gethin,
Doonan John,
Jenuwein Thomas,
Goodrich Justin
Publication year - 2006
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/sj.emboj.7601311
Subject(s) - biology , polycomb group proteins , histone h3 , chromatin immunoprecipitation , prc2 , gene silencing , histone , epigenetics , chromatin , genetics , methylation , microbiology and biotechnology , gene , repressor , promoter , gene expression
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.