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Journal ArticleDOI

Regulation of X-chromosome inactivation by the X-inactivation centre

Sandrine Augui, +2 more
- 01 Jun 2011 - 
- Vol. 12, Iss: 6, pp 429-442
TLDR
The recent discovery of the plasticity of the inactive state during early development, or during cloning, and induced pluripotency have contributed to the X chromosome becoming a gold standard in reprogramming studies.
Abstract
X-chromosome inactivation (XCI) ensures dosage compensation in mammals and is a paradigm for allele-specific gene expression on a chromosome-wide scale. Important insights have been made into the developmental dynamics of this process. Recent studies have identified several cis- and trans-acting factors that regulate the initiation of XCI via the X-inactivation centre. Such studies have shed light on the relationship between XCI and pluripotency. They have also revealed the existence of dosage-dependent activators that trigger XCI when more than one X chromosome is present, as well as possible mechanisms underlying the monoallelic regulation of this process. The recent discovery of the plasticity of the inactive state during early development, or during cloning, and induced pluripotency have also contributed to the X chromosome becoming a gold standard in reprogramming studies.

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Citations
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Journal ArticleDOI

DNA methylation: roles in mammalian development

TL;DR: Key concepts in the function of DNA methylation in mammals are discussed, stemming from more than two decades of research, including many recent studies that have elucidated when and whereDNA methylation has a regulatory role in the genome.
Journal ArticleDOI

lincRNAs: genomics, evolution, and mechanisms.

TL;DR: This Review outlines the emerging understanding of lincRNAs in vertebrate animals, with emphases on how they are being identified and current conclusions and questions regarding their genomics, evolution and mechanisms of action.
Journal ArticleDOI

Dynamic Imaging of Genomic Loci in Living Human Cells by an Optimized CRISPR/Cas System

TL;DR: Using an EGFP-tagged endonuclease-deficient Cas9 protein and a structurally optimized small guide (sg) RNA, robust imaging of repetitive elements in telomeres and coding genes in living cells is demonstrated by repurposing the bacterial CRISPR/Cas system.
References
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Journal ArticleDOI

Establishment in culture of pluripotential cells from mouse embryos

TL;DR: The establishment in tissue culture of pluripotent cell lines which have been isolated directly from in vitro cultures of mouse blastocysts are reported, able to differentiate either in vitro or after innoculation into a mouse as a tumour in vivo.
Journal ArticleDOI

Gene Action in the X -chromosome of the Mouse ( Mus musculus L.)

TL;DR: Ohno and Hauschka1 showed that in female mice one chromosome of mammary carcinoma cells and of normal diploid cells of the ovary, mammary gland and liver was heteropyKnotic and suggested that the so-called sex chromatin was composed of one heteropyknotic X-chromosome.
Journal ArticleDOI

Directly Reprogrammed Fibroblasts Show Global Epigenetic Remodeling and Widespread Tissue Contribution

TL;DR: Genome-wide analysis of two key histone modifications indicated that iPS cells are highly similar to ES cells, and data show that transcription factor-induced reprogramming leads to the global reversion of the somatic epigenome into an ES-like state.
Journal ArticleDOI

Polycomb Proteins Targeted by a Short Repeat RNA to the Mouse X Chromosome

TL;DR: In this article, a 1.6-kilobase ncRNA (RepA) was found within Xist and identified the Polycomb complex, PRC2, as its direct target.
PatentDOI

Connecting microrna genes to the core transcriptional regulatory circuitry of embryonic stem cells

TL;DR: The transcriptional regulatory circuitry of ES cells that incorporates protein-coding and miRNA genes based on high-resolution ChIP-seq data, systematic identification of miRNA promoters, and quantitative sequencing of short transcripts in multiple cell types reveals how key ES cell transcription factors promote the ES cell miRNA expression program and integrate miRNAs into the regulatory circuitry controlling ES cell identity.
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