Maternal H3K27me3 controls DNA methylation-independent imprinting

Azusa Inoue, Lan Jiang, Falong Lu, Tsukasa Suzuki and Yi Zhang ()
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Azusa Inoue: Howard Hughes Medical Institute, Boston Children’s Hospital
Lan Jiang: Howard Hughes Medical Institute, Boston Children’s Hospital
Falong Lu: Howard Hughes Medical Institute, Boston Children’s Hospital
Tsukasa Suzuki: Howard Hughes Medical Institute, Boston Children’s Hospital
Yi Zhang: Howard Hughes Medical Institute, Boston Children’s Hospital

Nature, 2017, vol. 547, issue 7664, 419-424

Abstract: Abstract Mammalian sperm and oocytes have different epigenetic landscapes and are organized in different fashions. After fertilization, the initially distinct parental epigenomes become largely equalized with the exception of certain loci, including imprinting control regions. How parental chromatin becomes equalized and how imprinting control regions escape from this reprogramming is largely unknown. Here we profile parental allele-specific DNase I hypersensitive sites in mouse zygotes and morula embryos, and investigate the epigenetic mechanisms underlying these allelic sites. Integrated analyses of DNA methylome and tri-methylation at lysine 27 of histone H3 (H3K27me3) chromatin immunoprecipitation followed by sequencing identify 76 genes with paternal allele-specific DNase I hypersensitive sites that are devoid of DNA methylation but harbour maternal allele-specific H3K27me3. Interestingly, these genes are paternally expressed in preimplantation embryos, and ectopic removal of H3K27me3 induces maternal allele expression. H3K27me3-dependent imprinting is largely lost in the embryonic cell lineage, but at least five genes maintain their imprinted expression in the extra-embryonic cell lineage. The five genes include all paternally expressed autosomal imprinted genes previously demonstrated to be independent of oocyte DNA methylation. Thus, our study identifies maternal H3K27me3 as a DNA methylation-independent imprinting mechanism.

Date: 2017
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DOI: 10.1038/nature23262

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