ArticleDevelopment (Cambridge, England)2012
Failure of extra-embryonic progenitor maintenance in the absence of dosage compensation.
Article in Development (Cambridge, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- XIST drives X-chromosome inactivation and safeguards female extraembryonic cells in humans.Nature communications · 2026Article
- Compensation of gene dosage on the mammalian X.Development (Cambridge, England) · 2024Review
- Roles of the Rlim-Rex1 axis during X chromosome inactivation in mice.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Modeling X-chromosome inactivation and reactivation during human development.Current opinion in genetics & development · 2023Review
- Polycomb repressive complexes 1 and 2 are each essential for maintenance of X inactivation in extra-embryonic lineages.Nature cell biology · 2023Article
- Placenta-specific lncRNA 1600012P17Rik is expressed in spongiotrophoblast and glycogen trophoblast cells of mouse placenta.Histochemistry and cell biology · 2022Article
- Transposable elements shape the evolution of mammalian development.Nature reviews. Genetics · 2021Review
- Xist/Tsix expression dynamics during mouse peri-implantation development revealed by whole-mount 3D RNA-FISH.Scientific reports · 2019Article
- The Role of Xist in X-Chromosome Dosage Compensation.Trends in cell biology · 2018Review
- Transcription factor ASCL2 is required for development of the glycogen trophoblast cell lineage.PLoS genetics · 2018Article
- Round Spermatid Injection Rescues Female Lethality of a Paternally Inherited Xist Deletion in Mouse.PLoS genetics · 2016Article
- SHAPE reveals transcript-wide interactions, complex structural domains, and protein interactions across the Xist lncRNA in living cells.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The "lnc" between 3D chromatin structure and X chromosome inactivation.Seminars in cell & developmental biology · 2016Review
- Epigenesis and plasticity of mouse trophoblast stem cells.Cellular and molecular life sciences : CMLS · 2016Review
- A rapid passage through a two-active-X-chromosome state accompanies the switch of imprinted X-inactivation patterns in mouse trophoblast stem cells.Epigenetics & chromatin · 2015Article
- X chromosome regulation: diverse patterns in development, tissues and disease.Nature reviews. Genetics · 2014Review
- Understanding the X chromosome inactivation cycle in mice: a comprehensive view provided by nuclear transfer.Epigenetics · 2014Article
- RNAi-mediated knockdown of Xist does not rescue the impaired development of female cloned mouse embryos.The Journal of reproduction and development · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Proper regulation of X-linked gene expression, termed dosage compensation, is required for the normal development of mammalian embryos. Through the process of X chromosome inactivation (XCI), somatic cells of mammalian females inactivate one of their two X chromosomes in order to balance X-linked gene dosage with their male counterparts. The process of XCI is dependent upon the long non-coding RNA Xist, which is expressed from and coats the inactivated X chromosome (Xi) in cis. During mouse embryogenesis, imprinted XCI inactivates the paternally inherited X chromosome (Xp) within the extra-embryonic lineages. Consequently, females harboring a paternally derived Xist mutation (X/X(Xist-)) die owing to failure of imprinted XCI and, presumably, poor trophoblast development. Here, we investigate the consequence of two active X chromosomes in the extra-embryonic ectoderm (ExE) of X/X(Xist-) female embryos. At embryonic day (E) 6.5, we find that the X/X(Xist-) ExE lacks the transcriptional regulator CDX2, a factor required to maintain the ExE in a progenitor state. In addition, spongiotrophoblast progenitors are not maintained. Surprisingly, we observe evidence of an Xi in a subpopulation of X/X(Xist-) ExE cells. We demonstrate further that trophectodermal stem cells derived from X/X(Xist-) embryos completely reverse normal imprinted XCI patterns. Taken together, our data suggest that, much like in the cells of the epiblast, the initial imprint that establishes imprinted XCI is probably erased in ExE cells. Conversely, unlike the epiblast, in which XCI is not required for progenitor cell maintenance, we demonstrate that dosage compensation is indispensable for the maintenance of trophoblast progenitors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.