| First Author | Harris C | Year | 2019 |
| Journal | Elife | Volume | 8 |
| PubMed ID | 30938678 | Mgi Jnum | J:275851 |
| Mgi Id | MGI:6306588 | Doi | 10.7554/eLife.44258 |
| Citation | Harris C, et al. (2019) Conversion of random X-inactivation to imprinted X-inactivation by maternal PRC2. Elife 8:e44258 |
| abstractText | Imprinted X-inactivation silences genes exclusively on the paternally-inherited X-chromosome and is a paradigm of transgenerational epigenetic inheritance in mammals. Here, we test the role of maternal vs. zygotic Polycomb repressive complex 2 (PRC2) protein EED in orchestrating imprinted X-inactivation in mouse embryos. In maternal-null (Eed(m-/-)) but not zygotic-null (Eed(-/-)) early embryos, the maternal X-chromosome ectopically induced Xist and underwent inactivation. Eed(m-/-) females subsequently stochastically silenced Xist from one of the two X-chromosomes and displayed random X-inactivation. This effect was exacerbated in embryos lacking both maternal and zygotic EED (Eed(mz-/-)), suggesting that zygotic EED can also contribute to the onset of imprinted X-inactivation. Xist expression dynamics in Eed(m-/-) embryos resemble that of early human embryos, which lack oocyte-derived maternal PRC2 and only undergo random X-inactivation. Thus, expression of PRC2 in the oocyte and transmission of the gene products to the embryo may dictate the occurrence of imprinted X-inactivation in mammals. |
