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Imprinted inactivation

Jonathan B Weitzman

Genome Biology 2001, 2:spotlight-20010730-01  doi:10.1186/gb-spotlight-20010730-01

The electronic version of this article is the complete one and can be found online at:

Published:30 July 2001

© 2001 BioMed Central Ltd

Research news

The eed (embryonic ectoderm development) gene is a member of the mouse Polycomb group (Pc-G) and is required for early gastrulation. In the Advance Online issue of Nature Genetics, Jianbo Wang and colleagues from the University of North Carolina define a role for eed in X chromosome inactivation. They analysed trophoblast giant cells in eed-null embryonic deciduas and found developmental defects in eed-null females but not in male embryos. To investigate the role of paternal X inactivation, Wang et al. crossed the eed-mutant mice with mice carrying a paternally inherited X-linked green fluorescent protein (GFP) transgene. The presence of fluorescent extra-embryonic cells in eed-null females suggests that eed is essential for maintaining paternal X-inactivation. The authors propose a model in which interaction between the Eed protein and histone deacetylases maintains gene silencing on the imprinted X chromosome in mouse extra-embryonic tissues.


  1. The Polycomb-group gene eed is required for normal morphogenetic movements during gastrulation in the mouse embryo.

    PubMed Abstract | Publisher Full Text OpenURL

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    Nature Genetics

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    University of North Carolina

  4. Non-invasive sexing of preimplantation stage mammalian embryos

    PubMed Abstract | Publisher Full Text OpenURL

  5. Transcriptional repression mediated by the human polycomb-group protein EED involves histone deacetylation.

    PubMed Abstract | Publisher Full Text OpenURL