X–chromosome inactivation during differentiation of female teratocarcinoma stem cells in vitro

Nature ◽  
1978 ◽  
Vol 271 (5643) ◽  
pp. 329-333 ◽  
Author(s):  
Gail R. Martin ◽  
Charles J. Epstein ◽  
Bruce Travis ◽  
Georgianne Tucker ◽  
Shaul Yatziv ◽  
...  
Keyword(s):  
Stem Cells ◽  
X Chromosome ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation

scholarly journals A novel approach to differentiate rat embryonic stem cells in vitro reveals a role for RNF12 in activation of X chromosome inactivation

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Aristea Magaraki ◽  
Agnese Loda ◽  
Cristina Gontan ◽  
Sarra Merzouk ◽  
Esther Sleddens-Linkels ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
X Chromosome ◽  
Embryonic Stem ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation ◽  
Novel Approach

Aberrant Patterns of X Chromosome Inactivation in a New Line of Human Embryonic Stem Cells Established in Physiological Oxygen Concentrations

2014 ◽  
Vol 10 (4) ◽  
pp. 472-479 ◽  
Author(s):  
Juliana Andrea de Oliveira Georges ◽  
Naja Vergani ◽  
Simone Aparecida Siqueira Fonseca ◽  
Ana Maria Fraga ◽  
Joana Carvalho Moreira de Mello ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
X Chromosome ◽  
Human Embryonic Stem Cells ◽  
Embryonic Stem ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation ◽  
Oxygen Concentrations

scholarly journals Histone H3 Lysine 36 Trimethylation Is Established over theXistPromoter by AntisenseTsixTranscription and Contributes to RepressingXistExpression

2015 ◽  
Vol 35 (22) ◽  
pp. 3909-3920 ◽  
Author(s):  
Tatsuya Ohhata ◽  
Mika Matsumoto ◽  
Martin Leeb ◽  
Shinwa Shibata ◽  
Satoshi Sakai ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
X Chromosome ◽  
Antisense Rna ◽  
Histone H3 ◽  
Embryonic Stem ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation ◽  
X Chromosomes ◽  
Histone H3.3

One of the two X chromosomes in female mammals is inactivated by the noncodingXistRNA. In mice, X chromosome inactivation (XCI) is regulated by the antisense RNATsix, which repressesXiston the active X chromosome. In the absence ofTsix, PRC2-mediated histone H3 lysine 27 trimethylation (H3K27me3) is established over theXistpromoter. Simultaneous disruption ofTsixand PRC2 leads to derepression ofXistand in turn silencing of the single X chromosome in male embryonic stem cells. Here, we identified histone H3 lysine 36 trimethylation (H3K36me3) as a modification that is recruited byTsixcotranscriptionally and extends over theXistpromoter. Reduction of H3K36me3 by expression of a mutated histone H3.3 with a substitution of methionine for lysine at position 36 causes a significant derepression ofXist. Moreover, depletion of the H3K36 methylaseSetd2leads to upregulation ofXist, suggesting H3K36me3 as a modification that contributes to the mechanism ofTsixfunction in regulating XCI. Furthermore, we found that reduction of H3K36me3 does not facilitate an increase in H3K27me3 over theXistpromoter, indicating that additional mechanisms exist by whichTsixblocks PRC2 recruitment to theXistpromoter.

scholarly journals X-chromosome inactivation in monkey embryos and pluripotent stem cells

2012 ◽  
Vol 371 (2) ◽  
pp. 146-155 ◽  
Author(s):  
Masahito Tachibana ◽  
Hong Ma ◽  
Michelle L. Sparman ◽  
Hyo-Sang Lee ◽  
Cathy M. Ramsey ◽  
...  
Keyword(s):  
Stem Cells ◽  
X Chromosome ◽  
Pluripotent Stem Cells ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation

scholarly journals SPEN is required for Xist upregulation during initiation of X chromosome inactivation

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Teresa Robert-Finestra ◽  
Beatrice F. Tan ◽  
Hegias Mira-Bontenbal ◽  
Erika Timmers ◽  
Cristina Gontan ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
X Chromosome ◽  
Female Mouse ◽  
Antisense Transcript ◽  
Embryonic Stem ◽  
Mouse Embryonic Stem Cells ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation ◽  
Chromatin Remodelers

AbstractAt initiation of X chromosome inactivation (XCI), Xist is monoallelically upregulated from the future inactive X (Xi) chromosome, overcoming repression by its antisense transcript Tsix. Xist recruits various chromatin remodelers, amongst them SPEN, which are involved in silencing of X-linked genes in cis and establishment of the Xi. Here, we show that SPEN plays an important role in initiation of XCI. Spen null female mouse embryonic stem cells (ESCs) are defective in Xist upregulation upon differentiation. We find that Xist-mediated SPEN recruitment to the Xi chromosome happens very early in XCI, and that SPEN-mediated silencing of the Tsix promoter is required for Xist upregulation. Accordingly, failed Xist upregulation in Spen−/− ESCs can be rescued by concomitant removal of Tsix. These findings indicate that SPEN is not only required for the establishment of the Xi, but is also crucial in initiation of the XCI process.

scholarly journals X-Chromosome Inactivation during Preimplantation Development and in Pluripotent Stem Cells

2020 ◽  
Vol 160 (6) ◽  
pp. 283-294 ◽  
Author(s):  
Paola Rebuzzini ◽  
Maurizio Zuccotti ◽  
Silvia Garagna
Keyword(s):  
Stem Cells ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Pluripotent Stem Cells ◽  
Mammalian Cells ◽  
Gene Dosage ◽  
X Chromosome Inactivation ◽  
Preimplantation Development ◽  
Chromosome Inactivation ◽  
Transcriptional Gene Silencing

X dosage compensation between XX female and XY male mammalian cells is achieved by a process known as X-chromosome inactivation (XCI). XCI initiates early during preimplantation development in female cells, and it is subsequently stably maintained in somatic cells. However, XCI is a reversible process that occurs in vivo in the inner cell mass of the blastocyst, in primordial germ cells or in spermatids during reprogramming. Erasure of transcriptional gene silencing can occur though a mechanism named X-chromosome reactivation (XCR). XCI and XCR have been substantially deciphered in the mouse, whereas they still remain debated in the human. In this review, we summarized the recent advances in the knowledge of X-linked gene dosage compensation during mouse and human preimplantation development and in pluripotent stem cells.

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