Imprinted X inactivation maintained by a mouse Polycomb group gene.

TitleImprinted X inactivation maintained by a mouse Polycomb group gene.
Publication TypeJournal Article
Year of Publication2001
AuthorsWang J, Mager J, Chen Y, Schneider E, Cross JC, Nagy A, Magnuson T
JournalNature genetics
Date Published2001 Aug
KeywordsAcetylation, Animals, Cell Count, Crosses, Genetic, Dosage Compensation, Genetic, Female, Genomic Imprinting, Green Fluorescent Proteins, Histone Deacetylases, Homozygote, Luminescent Proteins, Male, Mice, Mice, Transgenic, Multigene Family, Placenta, Placental Lactogen, Repressor Proteins, Sex Factors, Transgenes, Trophoblasts
AbstractIn 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 mouse. Here we show that the gene eed (embryonic ectoderm development), 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.
Alternate JournalNat. Genet.
PubMed ID11479595