Parental genomes in the endosperm are marked by differential DNA methylation and are therefore epigenetically distinct. This epigenetic asymmetry is established in the gametes and maintained after fertilization by unknown mechanisms. In this manuscript, we have addressed the key question whether parentally inherited differential DNA methylation affects de novo targeting of chromatin modifiers in the early endosperm. Our data reveal that polycomb‐mediated H3 lysine 27 trimethylation (H3K27me3) is preferentially localized to regions that are targeted by the DNA glycosylase DEMETER (DME), mechanistically linking DNA hypomethylation to imprinted gene expression. Our data furthermore suggest an absence of de novo DNA methylation in the early endosperm, providing an explanation how DME‐mediated hypomethylation of the maternal genome is maintained after fertilization. Lastly, we show that paternal‐specific H3K27me3‐marked regions are located at pericentromeric regions, suggesting that H3K27me3 and DNA methylation are not necessarily exclusive marks at pericentromeric regions in the endosperm.
Genomewide mapping of the epigenetic state in early plant endosperm links Polycomb to the maintenance of parental imprinting and explains how DNA hypomethylation of the maternal genome is maintained after fertilization.
The polycomb‐mediated histone mark H3K27me3 has a parent‐of‐origin‐specific distribution in the endosperm and determines the imprinting status of paternally expressed imprinted genes.
The early endosperm is largely devoid of CHH methylation, providing an explanation of how hypomethylation of the maternal genome is maintained after fertilization.
Paternal‐specific H3K27me3 is localized at pericentromeric regions and has no major impact on the regulation of maternally expressed imprinted genes.
The EMBO Journal (2016) 35: 1298–1311
- Received November 20, 2015.
- Revision received March 14, 2016.
- Accepted March 17, 2016.
- © 2016 The Authors
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