| First Author | Wang J | Year | 2001 |
| Journal | Nat Genet | Volume | 28 |
| Issue | 4 | Pages | 371-5 |
| PubMed ID | 11479595 | Mgi Jnum | J:70724 |
| Mgi Id | MGI:2138044 | Doi | 10.1038/ng574 |
| Citation | Wang J, et al. (2001) Imprinted X inactivation maintained by a mouse Polycomb group gene. Nat Genet 28(4):371-5 |
| abstractText | 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 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. |
