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Analysis of chromatin accessibility of WT & XIST deficient type 1 conventional DCs in female mice

ABSTRACT: Analysis of chromatin accessibility of WT & XIST deficient type 1 conventional DCs in female mice

PROVIDER: PRJNA1113325 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29079114_1.fastq.gz	Fastqsanger.gz
	SRR29079114_2.fastq.gz	Fastqsanger.gz
	SRR29079115_1.fastq.gz	Fastqsanger.gz
	SRR29079115_2.fastq.gz	Fastqsanger.gz
	SRR29079116_1.fastq.gz	Fastqsanger.gz

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Analysis of chromatin accessibility of WT & XIST deficient type 1 conventional DCs in female mice

Project description:To investigate the cooperative function of Xist (X-inactive specific transcript) in type 1 conventional DCs in relation to TLR & XCR1 signaling

2024-05-24 | GSE267828 | GEO

Analysis of transcriptomes of WT & XIST deficient type 1 conventional DCs in mice

Project description:To investigate the cooperative function of Xist (X-inactive specific transcript) in type 1 conventional DCs in relation to TLR & XCR1 signaling

2024-05-24 | GSE267829 | GEO

Analysis of transcriptomes of WT & XIST deficient type 1 conventional DCs in mice

Project description:Analysis of transcriptomes of WT & XIST deficient type 1 conventional DCs in mice

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Comparision of transcriptomes between murine WT type 1 conventional DCs to XCR1-deficient type 1 conventional DCs

Project description:We sought to compare the overall transcriptomic differences between TLR stimulated WT and XCR1-deficient type 1 conventional DCs. In addition, we also wanted to investigate functional role of XCR1 signaling in WT type 1 conventional DCs by treating recombinant murine XCL1, a ligand of XCR1 to these cells as well

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Comparision of transcriptomes between murine WT type 1 conventional DCs to XCR1-deficient type 1 conventional DCs

Project description:Comparision of transcriptomes between murine WT type 1 conventional DCs to XCR1-deficient type 1 conventional DCs

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Xist recruits the X chromosome to the nuclear lamina to enable chromosome-wide silencing

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

Transcriptomic analysis of XIST+ and XIST- hES cells

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

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Female mice lacking Xist RNA show partial dosage compensation and survive to term

Project description:X chromosome inactivation (XCI) compensates for differences in X-chromosome number between male and female mammals. XCI is orchestrated by Xist RNA, whose expression in early development leads to transcriptional silencing of one X-chromosome in the female. Knockout studies have established a requirement for Xist, with inviability of female embryos that inherit an Xist deletion from the father. Here, we report that female mice lacking Xist RNA can, surprisingly, develop and survive to term. Xist-null females are born at lower frequency and are smaller at birth, but organogenesis is mostly normal. Transcriptomic analysis indicates significant overexpression of hundreds of X-linked genes across multiple tissues. Therefore, Xist-null mice can develop to term in spite of a deficiency of dosage compensation. However, the degree of X-autosomal dosage imbalance was less than anticipated (1.14- to 1.36-fold). Thus, partial dosage compensation can be achieved without Xist, supporting the idea of inherent genome balance. Nevertheless, to date, none of the mutant mice has survived beyond weaning stage. Sudden death is associated with failure of postnatal organ maturation. Our data suggest Xist-independent mechanisms of dosage compensation and demonstrate that small deviations from X-autosomal balance can have profound effects on overall fitness. RNA-sequencing of tail-tip fibroblasts (TTFs), spleen, liver and heart tissue from Xist-null and control female mice. Sequencing performed with 50nt read length on Illumina HiSeq2000 or 2500. Data consists of 3 biological replicates for TTFs (6 datasets) and 2 biological replicates for tissues (12 datasets).

2016-08-19 | E-GEOD-84665 | biostudies-arrayexpress

Xist ribonucleoprotein particles promote female sex-biased autoimmunity [10X multi-ome]

Project description:Autoimmune diseases disproportionately affect females more than males. The XX sex chromosome complement is strongly associated with susceptibility to autoimmunity. Xist long noncoding RNA (lncRNA) is expressed only in females to randomly inactivate one of the two X chromosomes to achieve gene dosage compensation. Here, we show that the Xist ribonucleoprotein (RNP) complex, comprised of numerous autoantigenic components, is an important driver of sex-biased autoimmunity. Inducible transgenic expression of a non-silencing form of Xist in male mice introduced Xist RNP complexes and sufficed to produce autoantibodies. Male SJL/J mice expressing transgenic Xist developed more severe multiorgan pathology in pristane-induced model of lupus than wild-type males. Xist expression in males reprogrammed T and B cell population and chromatin states to more resemble wild type females. Human patients with autoimmune diseases displayed significant autoantibodies to multiple components of XIST RNP. Thus, a sex-specific lncRNA scaffolds ubiquitous RNP components to drive sex-biased immunity.

2024-02-01 | GSE249829 | GEO

Xist ribonucleoprotein particles promote female sex-biased autoimmunity [bulk RNA-seq]

2024-02-01 | GSE249828 | GEO