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Conversion of random X-inactivation to imprinted X-inactivation by maternal PRC2

Harris, Clair and Cloutier, Marissa and Trotter, Megan and Hinten, Michael and Gayen, Srimonta and Du, Zhenhai and Xie, Wei and Kalantry, Sundeep (2019) Conversion of random X-inactivation to imprinted X-inactivation by maternal PRC2. In: ELIFE, 8 .

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Official URL: https://doi.org/10.7554/eLife.44258


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.

Item Type: Journal Article
Publication: ELIFE
Additional Information: copyright for this article belongs to the Authors
Department/Centre: Division of Biological Sciences > Molecular Reproduction, Development & Genetics
Date Deposited: 11 Jul 2019 07:28
Last Modified: 11 Jul 2019 07:28
URI: http://eprints.iisc.ac.in/id/eprint/62974

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