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This article is part of a special issue on epigenomics.

Open Access Open Badges Research

Contribution of the epigenetic mark H3K27me3 to functional divergence after whole genome duplication in Arabidopsis

Lidija Berke1*, Gabino F Sanchez-Perez123 and Berend Snel1

Author Affiliations

1 Theoretical Biology and Bioinformatics, Department of Biology, Faculty of Science, Utrecht University, Padualaan 8, 3584 CH Utrecht, Netherlands

2 Netherlands Consortium for Systems Biology, Science Park 904, 1098 XH Amsterdam, The Netherlands

3 Applied Bioinformatics, PRI, Wageningen UR, Droevendaalsesteeg 1, 6708 PB Wageningen, Netherlands

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Genome Biology 2012, 13:R94  doi:10.1186/gb-2012-13-10-r94

Published: 3 October 2012



Following gene duplication, retained paralogs undergo functional divergence, which is reflected in changes in DNA sequence and expression patterns. The extent of divergence is influenced by several factors, including protein function. We examine whether an epigenetic modification, trimethylation of histone H3 at lysine 27 (H3K27me3), could be a factor in the evolution of expression patterns after gene duplication. Whereas in animals this repressive mark for transcription is deposited on long regions of DNA, in plants its localization is gene-specific. Because of this and a well-annotated recent whole-genome duplication, Arabidopsis thaliana is uniquely suited for studying the potential association of H3K27me3 with the evolutionary fate of genes.


Paralogous pairs with H3K27me3 show the highest coding sequence divergence, which can be explained by their low expression levels. Interestingly, they also show the highest similarity in expression patterns and upstream regulatory regions, while paralogous pairs where only one gene is an H3K27me3 target show the highest divergence in expression patterns and upstream regulatory sequence. These trends in divergence of expression and upstream regions are especially pronounced for transcription factors.


After duplication, a histone modification can be associated with a particular fate of paralogs: H3K27me3 is linked to lower expression divergence yet higher coding sequence divergence. Our results show that H3K27me3 constrains expression divergence after duplication. Moreover, its association with higher conservation of upstream regions provides a potential mechanism for the conserved H3K27me3 targeting of the paralogs.