Nature Genetics28, 371 - 375 (2001)
Published online: 23 July 2001; | doi:10.1038/ng574
Imprinted X inactivation maintained by a mouse Polycomb group gene
Jianbo Wang1, 2, 5, Jesse Mager1, 5, Yijing Chen1, Elizabeth Schneider1, James C. Cross3, Andras Nagy4
& Terry Magnuson1
1
Department of Genetics, CB 7264, The University of North Carolina, 102 Mason Farm Road, Chapel Hill, North Carolina 27599-7264, USA.
2
Present address: UCSD School of Medicine, 9500 Gilman Drive, La Jolla, California 92093, USA.
3
Department of Biochemistry and Molecular Biology, Genes and Development Research Group, University of Calgary, Calgary, Alberta, Canada.
4
Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.
5
These authors contributed equally to this work.
Correspondence should be addressed to Terry Magnuson trm4@med.unc.edu
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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