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Jpx RNA controls Xist induction through spatial reorganization of the mouse X-inactivation center

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE283643 | GEO | 2025/06/11

REPOSITORIES: GEO

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Jpx RNA controls Xist induction through spatial reorganization of the mouse X-inactivation center [CHART-seq]

Project description:Known to regulate chromosome looping on a genome-wide scale, the noncoding Jpx RNA was originally shown to control X-chromosome counting and induce Xist expression during X-chromosome inactivation (XCI). Not fully understood is how Jpx upregulates Xist in coordination with Tsix downregulation in cis. Here, by integrating epigenomic data and polymer modeling in a mouse embryonic stem cell model, we demonstrate that Jpx controls architectural and transcriptional dynamics within anti- and pro-XCI zones of the X-inactivation center. Distinct topological changes occur on the future active (Xa) and inactive (Xi) chromosomes. Jpx binds the enhancer of Tsix on the future Xi and alters loop formation to favor Xist induction, coordinately releasing CTCF from Tsix and Xist in cis on the future Xi. Thus, by controlling a dynamic rewiring of functional loops, Jpx flips a transcriptional switch to control mutually exclusive Tsix and Xist expression in cis.

2025-06-11 | GSE283642 | GEO

Jpx RNA controls Xist induction through spatial reorganization of the mouse X-inactivation center [RNA-Seq]

2025-06-11 | GSE283641 | GEO

Jpx RNA controls Xist induction through spatial reorganization of the mouse X-inactivation center [Capture Hi-C]

2025-06-11 | GSE225226 | GEO

Jpx RNA controls Xist induction through spatial reorganization of the mouse X-inactivation center

Project description:Jpx RNA controls Xist induction through spatial reorganization of the mouse X-inactivation center

| PRJNA1194957 | ENA

Jpx RNA controls Xist induction through spatial reorganization of the mouse X-inactivation center [RNA-Seq]

Project description:Jpx RNA controls Xist induction through spatial reorganization of the mouse X-inactivation center [RNA-Seq]

| PRJNA1194960 | ENA

Jpx RNA controls Xist induction through spatial reorganization of the mouse X-inactivation center [CHART-seq]

Project description:Jpx RNA controls Xist induction through spatial reorganization of the mouse X-inactivation center [CHART-seq]

| PRJNA1194964 | ENA

Jpx RNA controls Xist induction through spatial reorganization of the mouse X-inactivation center [Capture Hi-C]

Project description:Jpx RNA controls Xist induction through spatial reorganization of the mouse X-inactivation center [Capture Hi-C]

| PRJNA934376 | ENA

Jpx RNA activates Xist by evicting CTCF.

Project description:In mammals, dosage compensation between XX and XY individuals occurs through X chromosome inactivation (XCI). The noncoding Xist RNA is expressed and initiates XCI only when more than one X chromosome is present. Current models invoke a dependency on the X-to-autosome ratio (X:A), but molecular factors remain poorly defined. Here, we demonstrate that molecular titration between an X-encoded RNA and an autosomally encoded protein dictates Xist induction. In pre-XCI cells, CTCF protein represses Xist transcription. At the onset of XCI, Jpx RNA is upregulated, binds CTCF, and extricates CTCF from one Xist allele. We demonstrate that CTCF is an RNA-binding protein and is titrated away from the Xist promoter by Jpx RNA. Thus, Jpx activates Xist by evicting CTCF. The functional antagonism via molecular titration reveals a role for long noncoding RNA in epigenetic regulation.

| S-EPMC3777401 | biostudies-literature

Chd8 regulates X chromosome inactivation in mouse through fine-tuning control of Xist expression.

Project description:Female mammals achieve dosage compensation by inactivating one of their two X chromosomes during development, a process entirely dependent on Xist, an X-linked long non-coding RNA (lncRNA). At the onset of X chromosome inactivation (XCI), Xist is up-regulated and spreads along the future inactive X chromosome. Contextually, it recruits repressive histone and DNA modifiers that transcriptionally silence the X chromosome. Xist regulation is tightly coupled to differentiation and its expression is under the control of both pluripotency and epigenetic factors. Recent evidence has suggested that chromatin remodelers accumulate at the X Inactivation Center (XIC) and here we demonstrate a new role for Chd8 in Xist regulation in differentiating ES cells, linked to its control and prevention of spurious transcription factor interactions occurring within Xist regulatory regions. Our findings have a broader relevance, in the context of complex, developmentally-regulated gene expression.

| S-EPMC8050208 | biostudies-literature

Species-specific regulation of XIST by the JPX/FTX orthologs.

Project description:X chromosome inactivation (XCI) is an essential process, yet it initiates with remarkable diversity in various mammalian species. XIST, the main trigger of XCI, is controlled in the mouse by an interplay of lncRNA genes (LRGs), some of which evolved concomitantly to XIST and have orthologues across all placental mammals. Here, we addressed the functional conservation of human orthologues of two such LRGs, FTX and JPX. By combining analysis of single-cell RNA-seq data from early human embryogenesis with various functional assays in matched human and mouse pluripotent stem- or differentiated post-XCI cells, we demonstrate major functional differences for these orthologues between species, independently of primary sequence conservation. While the function of FTX is not conserved in humans, JPX stands as a major regulator of XIST expression in both species. However, we show that different entities of JPX control the production of XIST at various steps depending on the species. Altogether, our study highlights the functional versatility of LRGs across evolution, and reveals that functional conservation of orthologous LRGs may involve diversified mechanisms of action. These findings represent a striking example of how the evolvability of LRGs can provide adaptative flexibility to constrained gene regulatory networks.

| S-EPMC10018341 | biostudies-literature

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