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Imprinted X inactivation maintained by a mouse Polycomb group gene

Nature Genetics volume 28, pages 371–375 (2001)Cite this article

Abstract

In mammals, dosage compensation of X-linked genes is achieved by the transcriptional silencing of one X chromosome in the female (reviewed in ref. 1). This process, called X inactivation, is usually random in the embryo proper. In marsupials and the extra-embryonic region of the mouse, however, X inactivation is imprinted: the paternal X chromosome is preferentially inactivated whereas the maternal X is always active. Having more than one active X chromosome is deleterious to extra-embryonic development in the mouse2. Here we show that the gene eed (embryonic ectoderm development)3,4, a member of the mouse Polycomb group (Pc-G) of genes, is required for primary and secondary trophoblast giant cell development in female embryos. Results from mice carrying a paternally inherited X-linked green fluorescent protein (GFP) transgene implicate eed in the stable maintenance of imprinted X inactivation in extra-embryonic tissues. Based on the recent finding that the Eed protein interacts with histone deacetylases, we suggest that this maintenance activity involves hypoacetylation of the inactivated paternal X chromosome in the extra-embryonic tissues.

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Figure 1: Trophoblast giant cell defects in eed−/− male and female embryos.
Figure 2: Reactivation of paternal XGFP in eed−/− female embryos.
Figure 3: Loss of imprinted X inactivation in eed−/− females.
Figure 4: Loss of imprinted paternal X inactivation in eed−/hypomorph females.

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Acknowledgements

This work was supported by an NIH grant to T.M.

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Author notes

  1. Jianbo Wang

    Present address: UCSD School of Medicine, 9500 Gilman Drive, La Jolla, California, 92093, USA

  2. Jianbo Wang and Jesse Mager: These authors contributed equally to this work.

Authors and Affiliations

  1. Department of Genetics, CB 7264, The University of North Carolina, 102 Mason Farm Road, Chapel Hill, 27599-7264, North Carolina, USA

    Jianbo Wang, Jesse Mager, Yijing Chen, Elizabeth Schneider & Terry Magnuson

  2. Department of Biochemistry and Molecular Biology, Genes and Development Research Group, University of Calgary, Calgary, Alberta, Canada

    James C. Cross

  3. Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada

    Andras Nagy

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Correspondence to Terry Magnuson.

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Wang, J., Mager, J., Chen, Y. et al. Imprinted X inactivation maintained by a mouse Polycomb group gene. Nat Genet 28, 371–375 (2001). https://doi.org/10.1038/ng574

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