Transcriptome analysis in individual mouse blastocyst with Xist deletion
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ABSTRACT:
PROVIDER: PRJNA552802 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9645600.fastq.gz | Fastqsanger.gz | |||
| SRR9645610.fastq.gz | Fastqsanger.gz | |||
| SRR9645601.fastq.gz | Fastqsanger.gz | |||
| SRR9645611.fastq.gz | Fastqsanger.gz | |||
| SRR9645602.fastq.gz | Fastqsanger.gz |
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Project description:We reprot transcriptome states in mouse blastocyst cultured with various conditons as well as Xist deletion. By comparing the gene expression states of blastocyst grown in different culture conditions with Xist deletion, we identified the differentially expressed genes, which are dependent culture conditions and Xist RNA.
2019-11-06 | GSE133845 | GEO
Project description:RNA-seq of Xist deletion mouse models
| PRJEB33688 | ENA
Project description:Purpose: The goals of this study are to establish a dynamic roadmap of imprinted X chromosome inactivation and the role of Xist by elucidation of the transcriptome of Xist KO embryos during mouse preimplantation development. Methods: mRNA profiles of the preimplantation embryos WT and KO for Xist were elucidated by RNA-seq at various stages. Trophoblasts isolated from blastocyst outgrowths were also included. The sequence reads for samples where gender could be determined and that passed quality filters were analyzed at the level of autosomes, X chromosome as well as single genes. Results: Female embryos fail to silence the X chromosome at late preimplantation development. General autosomal gene expression is not affected in embryos lacking Xist. Conclusions: Xist is crucial for iXCI. In preimplantation embryos, the main in vivo function of Xist is to regulate iXCI in females.
2016-10-11 | GSE75951 | GEO
Project description:Determine the tissue specific impact of Xist loss on dosage compensation in various somatic tissues of the mouse
2020-01-30 | E-MTAB-8161 | biostudies-arrayexpress
Project description:The long noncoding RNA, Xist, is critical for initiation and establishment of X- chromosome inactivation during embryogenesis in mammals but it is unclear whether its continued expression is required for maintaining X inactivation in vivo. By using an inactive X chromosome-linked MeCP2-GFP reporter, which allowed us to enumerate reactivation events in the mouse brain even when they occur in very few cells, we found that deletion of Xist in the brain after establishment of X chromosome inactivation leads to reactivation in 2-5% of neurons and in a smaller fraction of astrocytes. In contrast to global loss of both H3 lysine 27 tri-methylation (H3K27m3) and histone H2A lysine 119 monoubiquitylation (H2AK119ub1) we observed upon Xist deletion, alterations in CpG methylation were subtle, and this was mirrored by only minor alterations in X- chromosome-wide gene expression levels. Our results demonstrate that Xist is required for maintaining tight transcriptional repression on the inactive X-chromosome and that partial loss of X-dosage compensation in the absence of Xist in the brain is well tolerated.
2018-08-28 | GSE119066 | GEO
Project description:We show that a deletion encompassing the entire Xist 5’ m6A region results in a modest reduction in Xist-mediated silencing.
2020-02-01 | GSE142270 | GEO
Project description:Purpose: Compare the transcriptome of homogeneous XIST+ and XIST- hES cell populations. Methods: We isolated homogeneous XIST+ and XIST- cell populations. The XIST+ cells correspond to cells with a XIST cloud and one ATRX pinpoint. The XIST- cells correspond to cells with no XIST cloud and one ATRX pinpoint. Results: We took advantage of the clonal pattern of X-chromosome inactivation in H9 cells and analyzed the data in an allelic manner. By comparing the RNA-Seq data with known H9 SNPs, we identified genomic positions which were relaxed from XCI in XIST- cells compared to XIST+ cells. Conclusions: Genic as well as unannotated transcripts are massively relaxed from XCI in H9 cells when XIST expression is lost, however, this reactivation is only partial and a large region around the centromere is protected from relaxation of silencing. Total RNA (rRNA depleted) profiles of XIST+ and XIST- human embryonic stem cells
2012-12-21 | E-GEOD-39757 | biostudies-arrayexpress
Project description:Xist orchestrates X chromosome inactivation, a process that entails chromosome-wide silencing and remodeling of the 3-dimensional structure of the X chromosome. Yet, it remains unclear whether these changes in nuclear structure are mediated by Xist and whether they are required for silencing. Here we show that Xist directly interacts with the Lamin B Receptor (LBR), an integral component of the nuclear lamina, and that this interaction is required for Xist-mediated silencing. We show that this interaction recruits the inactive X to the nuclear lamina and by doing so enables Xist to spread to actively transcribed genes across the X. Our results demonstrate that lamina recruitment changes the accessibility of DNA thereby enabling Xist, and its silencing proteins, to spread across the X to silence transcription. We examined the genomic localization of the Xist lncRNA using RNA Antisense Purification (RAP) in male mouse ES cells where the endogenous Xist promoter is replaced by a tet-inducible one (pSM33) containing 1) wild-type Xist (WT), 2) A-repeat deletion Xist (dA), 3) LBR binding site deletion Xist (dLBS), 4) dLBS-Xist rescued with LMNB1 (LMNB1Res), 5) LBR CRISPRi knock down (LBRKD), or 6) SHARP CRISPRi knock down (SHARPKD).
2016-07-24 | E-GEOD-80510 | biostudies-arrayexpress
Project description:Cloning mammals by somatic cell nuclear transfer (SCNT) is highly inefficient. Most SCNT-generated embryos die after implantation because of unidentified, complex epigenetic errors in the process of postimplantation embryonic development. Here, we identified the most upstream level of dysfunction leading to impaired development of clones by using RNA interference (RNAi) against Xist, a gene responsible for X chromosome inactivation (XCI). A prior injection of Xist-specific short interfering (si)RNA into reconstructed oocytes efficiently corrected the SCNT-specific aberrant Xist expression at the morula stage, but failed to do so thereafter at the blastocyst stage. However, we found that shortly after implantation this aberrant XCI status in cloned embryos had been corrected autonomously in both embryonic and extraembryonic tissues, probably through a newly established XCI control for postimplantation embryos. Embryo transfer experiments revealed that the siRNA-treated embryos showed 10 times higher survival than controls as early as embryonic day 5.5 and this high survival persisted until term, resulting in a remarkable improvement in cloning efficiency (12% vs. 1% in controls). Importantly, unlike control clones, these Xist-siRNA clones at birth showed only a limited dysregulation of their gene expression, indicating that correction of Xist expression in preimplantation embryos had a long-term effect on their postnatal normality. Thus, contrary to the general assumption, our results suggest that the fate of cloned embryos is determined almost exclusively before implantation by their XCI status. Furthermore, our strategy provides a promising breakthrough for mammalian SCNT cloning because RNAi treatment of oocytes is readily applicable to most mammal species. Gene expression were measured in mouse in vitro fertilized and somatic cell cloned embryos. Four biological replicates were performed in each group of Xist- or Control-siRNA.
2011-11-17 | E-GEOD-33208 | biostudies-arrayexpress
Project description:The inner cell mass in blastocyst is the origin of all the somatic and germ cells in mammals, and of pluripotent stem cells in vitro. As the conserved principles between pig and human, here we performed comprehensive single-cell RNA-seq for porcine early embryos from oocyte to early blastocyst. We show the specification of inner cell mass and trophectoderm in morula, and the molecular signature of the precursors. We demonstrate the existence of naïve pluripotency signature in morula and inner cell mass of early blastocyst, and the specific pluripotent genes and the activity of signalling pathways highlight the characteristics of the naïve pluripotency. We observe absence of dosage compensation with respect to X-chromosome in morula, and incomplete dosage compensation in early blastocyst. However, the dynamics of dosage compensation may be independent on the expression of XIST induced X-chromosome inactivation. Our study describes molecular landmarks of embryogenesis in pig that will provide a better strategy for derivation of porcine pluripotent stem cells and improve the research in regenerative medicine.
2019-10-29 | GSE139512 | GEO