The role of maternal-specific H3K9me3 modification in establishing imprinted X-chromosome inactivation and embryogenesis in mice

Atsushi Fukuda, Junko Tomikawa, Takumi Miura, Kenichiro Hata, Kazuhiko Nakabayashi, Kevin Eggan, Hidenori Akutsu () and Akihiro Umezawa
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Atsushi Fukuda: National Research Institute for Child Health and Development
Junko Tomikawa: National Research Institute for Child Health and Development
Takumi Miura: National Research Institute for Child Health and Development
Kenichiro Hata: National Research Institute for Child Health and Development
Kazuhiko Nakabayashi: National Research Institute for Child Health and Development
Kevin Eggan: The Howard Hughes Medical Institute, Harvard University
Hidenori Akutsu: National Research Institute for Child Health and Development
Akihiro Umezawa: National Research Institute for Child Health and Development

Nature Communications, 2014, vol. 5, issue 1, 1-14

Abstract: Abstract Maintaining a single active X-chromosome by repressing Xist is crucial for embryonic development in mice. Although the Xist activator RNF12/RLIM is present as a maternal factor, maternal Xist (Xm-Xist) is repressed during preimplantation phases to establish imprinted X-chromosome inactivation (XCI). Here we show, using a highly reproducible chromatin immunoprecipitation method that facilitates chromatin analysis of preimplantation embryos, that H3K9me3 is enriched at the Xist promoter region, preventing Xm-Xist activation by RNF12. The high levels of H3K9me3 at the Xist promoter region are lost in embryonic stem (ES) cells, and ES-cloned embryos show RNF12-dependent Xist expression. Moreover, lack of Xm-XCI in the trophectoderm, rather than loss of paternally expressed imprinted genes, is the primary cause of embryonic lethality in 70–80% of parthenogenotes immediately after implantation. This study reveals that H3K9me3 is involved in the imprinting that silences Xm-Xist. Our findings highlight the role of maternal-specific H3K9me3 modification in embryo development.

Date: 2014
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DOI: 10.1038/ncomms6464

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