Journal
NATURE STRUCTURAL & MOLECULAR BIOLOGY
Volume 24, Issue 3, Pages 226-+Publisher
NATURE PORTFOLIO
DOI: 10.1038/nsmb.3365
Keywords
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Funding
- Region Ile-de-France (DIM STEMPOLE)
- Paris Alliance of Cancer Research Institutes (PACRI-ANR)
- ERC Advanced Investigator award (ERC-AdG) [250367]
- EU [242129, 259743]
- La Ligue
- Fondation de France
- Labex DEEP, IDEX Idex PSL [ANR-11-LBX-0044, ANR-10-IDEX-0001-02 PSL]
- ABS4NGS [ANR-11-BINF-0001]
- France Genomique National infrastructure [ANR-10-INBS-09]
- CELLECTCHIP [ANR-14-CE10-0013]
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The long noncoding RNA Xist is expressed from only the paternal X chromosome in mouse preimplantation female embryos and mediates transcriptional silencing of that chromosome. In females, absence of Xist leads to postimplantation lethality. Here, through single-cell RNA sequencing of early preimplantation mouse embryos, we found that the initiation of imprinted X-chromosome inactivation absolutely requires Xist. Lack of paternal Xist leads to genome-wide transcriptional misregulation in the early blastocyst and to failure to activate the extraembryonic pathway that is essential for postimplantation development. We also demonstrate that the expression dynamics of X-linked genes depends on the strain and parent of origin as well as on the location along the X chromosome, particularly at the first 'entry' sites of Xist. This study demonstrates that dosage-compensation failure has an effect as early as the blastocyst stage and reveals genetic and epigenetic contributions to orchestrating transcriptional silencing of the X chromosome during early embryogenesis.
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