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

ABSTRACT: Xist ribonucleoprotein particles promote female sex-biased autoimmunity [bulk ATAC-seq]

PROVIDER: PRJNA1050813 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27166610_1.fastq.gz	Fastqsanger.gz
	SRR27166610_2.fastq.gz	Fastqsanger.gz
	SRR27166611_1.fastq.gz	Fastqsanger.gz
	SRR27166611_2.fastq.gz	Fastqsanger.gz
	SRR27166612_1.fastq.gz	Fastqsanger.gz

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Xist ribonucleoprotein particles promote female sex-biased autoimmunity.

Project description:Xist ribonucleoprotein particles promote female sex-biased autoimmunity.

| PRJNA1050811 | ENA

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

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 | GSE249827 | GEO

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

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

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

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

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

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

| PRJNA1050815 | ENA

Xist ribonucleoprotein particles promote female sex-biased autoimmunity.

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-02-01 | GSE249830 | GEO

Xist ribonucleoproteins promote female sex-biased autoimmunity.

Project description:Autoimmune diseases disproportionately affect females more than males. The XX sex chromosome complement is strongly associated with susceptibility to autoimmunity. Xist long non-coding 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 comprising 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 multi-organ pathology in a pristane-induced lupus model than wild-type males. Xist expression in males reprogrammed T and B cell populations 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.

| S-EPMC10949934 | biostudies-literature

The role of XIST in X-inactivation maintenance in B cells (CRISPRi screen)

Project description:The long noncoding RNA (lncRNA) XIST establishes X chromosome inactivation (XCI) in female cells in early development and thereafter is thought to be largely dispensable. Here we show XIST is continually required in adult human B cells to silence a subset of X-linked immune genes such as TLR7. XIST-dependent genes lack promoter DNA methylation and require continual XIST-dependent histone deacetylation. XIST RNA-directed proteomics and CRISPRi screen reveal distinctive somatic cell-specific XIST complexes, and identify TRIM28 that mediates Pol II pausing at promoters of X-linked genes in B cells. XIST dysregylation, reflected by escape of XIST-dependent genes, occurs in CD11c+ atypical memory B cells across single-cell transcriptome data in patients with female-biased autoimmunity and COVID-19 infection. XIST inactivation with TLR7 agonism suffices to promote isotype-switched atypical B cells. These results suggest cell-type-specific diversification of lncRNA-protein complexes increase lncRNA functionalities, and expand roles for XIST in sex-differences in biology and medicine.

2021-01-12 | GSE164593 | GEO

The role of XIST in X-inactivation maintenance in B cells (RNA-seq)

2021-01-12 | GSE164595 | GEO