ArticlePLoS genetics2006
The Polycomb group protein EED is dispensable for the initiation of random X-chromosome inactivation.
Article in PLoS genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed.
- Deletion of Xist repeat B disrupts cell cycle and asymmetric cell division through Usp9x hyperactivation in mice.Nucleic acids research · 2025Article
- Denaturing purifications demonstrate that PRC2 and other widely reported chromatin proteins do not appear to bind directly to RNA in vivo.Molecular cell · 2024Article
- Review
- Regulatory non-coding RNAs: everything is possible, but what is important?Nature methods · 2022Article
- Activation of Xist by an evolutionarily conserved function of KDM5C demethylase.Nature communications · 2022Article
- Gene regulation in time and space during X-chromosome inactivation.Nature reviews. Molecular cell biology · 2022Review
- The control of polycomb repressive complexes by long noncoding RNAs.Wiley interdisciplinary reviews. RNA · 2021Review
- Article
- Xist Repeats A and B Account for Two Distinct Phases of X Inactivation Establishment.Developmental cell · 2020Article
- Progress toward understanding chromosome silencing by Xist RNA.Genes & development · 2020Review
- Approaches for Understanding the Mechanisms of Long Noncoding RNA Regulation of Gene Expression.Cold Spring Harbor perspectives in biology · 2019Review
- The role of Xist-mediated Polycomb recruitment in the initiation of X-chromosome inactivation.EMBO reports · 2019Article
- Article
- Alteration of Epigenetic Regulation by Long Noncoding RNAs in Cancer.International journal of molecular sciences · 2018Review
- The Ever-Evolving Concept of the Gene: The Use of RNA/Protein Experimental Techniques to Understand Genome Functions.Frontiers in molecular biosciences · 2018Review
- Experimental Analysis of Imprinted Mouse X-Chromosome Inactivation.Methods in molecular biology (Clifton, N.J.) · 2018Article
- Progress in understanding the molecular mechanism ofPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Polycomb complexes in X chromosome inactivation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Long non-coding RNAs as an epigenetic regulator in human cancers.Cancer science · 2017Review
- How do lncRNAs regulate transcription?Science advances · 2017Review
1 more citing papers are in PubMed but not listed here.
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2 authors.
Funding
Abstract
The Polycomb group (PcG) proteins are thought to silence gene expression by modifying chromatin. The Polycomb repressive complex 2 (PRC2) plays an essential role in mammalian X-chromosome inactivation (XCI), a model system to investigate heritable gene silencing. In the mouse, two different forms of XCI occur. In the preimplantation embryo, all cells undergo imprinted inactivation of the paternal X-chromosome (Xp). During the peri-implantation period, cells destined to give rise to the embryo proper erase the imprint and randomly inactivate either the maternal X-chromosome or the Xp; extraembryonic cells, on the other hand, maintain imprinted XCI of the Xp. PRC2 proteins are enriched on the inactive-X during early stages of both imprinted and random XCI. It is therefore thought that PRC2 contributes to the initiation of XCI. Mouse embryos lacking the essential PRC2 component EED harbor defects in the maintenance of imprinted XCI in differentiating trophoblast cells. Assessment of PRC2 requirement in the initiation of XCI, however, has been hindered by the presence of maternally derived proteins in the early embryo. Here we show that Eed-/- embryos initiate and maintain random XCI despite lacking any functional EED protein prior to the initiation of random XCI. Thus, despite being enriched on the inactive X-chromosome, PcGs appear to be dispensable for the initiation and maintenance of random XCI. These results highlight the lineage- and differentiation state-specific requirements for PcGs in XCI and argue against PcG function in the formation of the facultative heterochromatin of the inactive X-chromosome.
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