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Xist-seeded nucleation sites form local concentration gradients of silencing proteins to inactivate the X-chromosome [II]

ABSTRACT: Xist-seeded nucleation sites form local concentration gradients of silencing proteins to inactivate the X-chromosome [II]

PROVIDER: PRJNA751096 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15309300_1.fastq.gz	Fastqsanger.gz
	SRR15309300_2.fastq.gz	Fastqsanger.gz
	SRR15309301_1.fastq.gz	Fastqsanger.gz
	SRR15309301_2.fastq.gz	Fastqsanger.gz
	SRR15309302_1.fastq.gz	Fastqsanger.gz

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Xist-seeded nucleation sites form local concentration gradients of silencing proteins to inactivate the X-chromosome

Project description:Xist-seeded nucleation sites form local concentration gradients of silencing proteins to inactivate the X-chromosome

| PRJNA751089 | ENA

Xist-seeded nucleation sites form local concentration gradients of silencing proteins to inactivate the X-chromosome [I]

Project description:Xist-seeded nucleation sites form local concentration gradients of silencing proteins to inactivate the X-chromosome [I]

| PRJNA680314 | ENA

Xist-seeded nucleation sites form local concentration gradients of silencing proteins to inactivate the X-chromosome [II]

Project description:The long non-coding RNA Xist exploits numerous effector proteins to gradually induce gene silencing across the X chromosome. Here, we show that formation of the inactive X (Xi)-compartment is induced by ~50 locally confined granules, where two Xist RNA molecules nucleate supra-molecular complexes (SMCs) of interacting proteins. Xist-SMCs are dynamic structures that concentrate rapidly recycling proteins on the X by increasing their binding affinity, thereby facilitating their access to the entire chromosome. We find that gene silencing originates at Xist-SMCs and propagates across the entire X chromosome over time. The propagation of silencing is achieved by Polycomb-mediated coalescence of chromatin regions and aggregation of the critical silencing enzyme SPEN, via its intrinsically disordered domains. Our observations suggest a new model for X Chromosome Inactivation, whereby Xist RNA triggers macromolecular crowding of heterochromatinizing proteins at distinct sites to ultimately increase their occupancy throughout the X chromosome. This mechanism enables deterministic gene silencing across an entire chromosome without the need for Xist ribonucleoprotein complex-chromatin interactions at each target gene. Our findings uncover a spatial organization mechanism by which few RNA molecules can regulate a broad nuclear compartment through the recruitment and local concentration of dynamic effector proteins, and provide a quantitative framework for studying such compartments.

2021-10-27 | GSE181235 | GEO

Xist-seeded nucleation sites form local concentration gradients of silencing proteins to inactivate the X-chromosome [I]

Project description:The long non-coding RNA Xist exploits numerous effector proteins to gradually induce gene silencing across the X chromosome. Here, we show that formation of the inactive X (Xi)-compartment is induced by ~50 locally confined granules, where two Xist RNA molecules nucleate supra-molecular complexes (SMCs) of interacting proteins. Xist-SMCs are dynamic structures that concentrate rapidly recycling proteins on the X by increasing their binding affinity, thereby facilitating their access to the entire chromosome. We find that gene silencing originates at Xist-SMCs and propagates across the entire X chromosome over time. The propagation of silencing is achieved by Polycomb-mediated coalescence of chromatin regions and aggregation of the critical silencing enzyme SPEN, via its intrinsically disordered domains. Our observations suggest a new model for X Chromosome Inactivation, whereby Xist RNA triggers macromolecular crowding of heterochromatinizing proteins at distinct sites to ultimately increase their occupancy throughout the X chromosome . This mechanism enables deterministic gene silencing across an entire chromosome without the need for Xist ribonucleoprotein complex-chromatin interactions at each target gene. Our findings uncover a spatial organization mechanism by which few RNA molecules can regulate a broad nuclear compartment through the recruitment and local concentration of dynamic effector proteins, and provide a quantitative framework for studying such compartments.

2021-10-27 | GSE162011 | GEO

Xist-seeded nucleation sites form local concentration gradients of silencing proteins to inactivate the X-chromosome

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

2021-10-26 | GSE181236 | GEO

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

2012-12-21 | E-GEOD-39757 | biostudies-arrayexpress

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]

2024-02-01 | GSE249829 | GEO

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

2024-02-01 | GSE249828 | GEO