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Sex-dependent RNA expression in opossum brain and liver.

ABSTRACT: To compensate for the increased dosage of X chromosomes in females one of the two X chromosomes is inactivated in eutherian mammals in an Xist-dependent manner. Xist is, however, not found in metatherians. Here we describe long non-coding RNA Rsx (RNA-on-the-silent X) that exhibits properties consistent with a role in X-inactivation in opossum. Rsx is abundantly expressed in females but not males and is transcribed from, and coats, the inactive X chromosome copy. Furthermore, when both X chromosomes are active, Rsx is silenced. We used RNA-Seq to determine exon-intron structure and expression level of Rsx in males and females. RNA sequencing was used to detect and characterize transcripts with strongly biased female expression.

ORGANISM(S): Monodelphis domestica

SUBMITTER: Pavel Khil

PROVIDER: E-GEOD-36861 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Rsx is a metatherian RNA with Xist-like properties in X-chromosome inactivation.

Grant Jennifer J Mahadevaiah Shantha K SK Khil Pavel P Sangrithi Mahesh N MN Royo Hélène H Duckworth Janine J McCarrey John R JR VandeBerg John L JL Renfree Marilyn B MB Taylor Willie W Elgar Greg G Camerini-Otero R Daniel RD Gilchrist Mike J MJ Turner James M A JM

Nature 20120701 7406

In female (XX) mammals, one of the two X chromosomes is inactivated to ensure an equal dose of X-linked genes with males (XY). X-chromosome inactivation in eutherian mammals is mediated by the non-coding RNA Xist. Xist is not found in metatherians (marsupials), and how X-chromosome inactivation is initiated in these mammals has been the subject of speculation for decades. Using the marsupial Monodelphis domestica, here we identify Rsx (RNA-on-the-silent X), an RNA that has properties consistent ...[more]

PMID: 22722828

Similar Datasets

Sex-dependent RNA expression in opossum brain and liver.

Project description:To compensate for the increased dosage of X chromosomes in females one of the two X chromosomes is inactivated in eutherian mammals in an Xist-dependent manner. Xist is, however, not found in metatherians. Here we describe long non-coding RNA Rsx (RNA-on-the-silent X) that exhibits properties consistent with a role in X-inactivation in opossum. Rsx is abundantly expressed in females but not males and is transcribed from, and coats, the inactive X chromosome copy. Furthermore, when both X chromosomes are active, Rsx is silenced. We used RNA-Seq to determine exon-intron structure and expression level of Rsx in males and females.

2012-06-11 | GSE36861 | GEO

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

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

2024-02-01 | GSE249827 | GEO

Males undergo a transient X-chromosome inactivation-like state at the onset of naïve cell differentiation

Project description:A hallmark of naïve cell identity is the presence of two active X-chromosomes in females. However, little is known if the naïve gene network prevents the initiation of X-chromosome-inactivation (XCI). Here, we demonstrate that robust naïve pluripotent stem cell (nPSC) self-renewal abolishes expression of Xist, the master regulator of XCI. Intriguingly, at the onset of differentiation when nPSCs become Nanog-negative they accumulate Xist on the male X-chromosome and on both female X-chromosomes. In fact, XCI occurs in males as characterised by appearance of a repressive chromatin signature and partial X-linked gene silencing, albeit transiently and rapidly. Likewise, in the embryo Xist is transiently expressed in males and in females from both X-chromosomes at the onset of epiblast differentiation. In conclusion, we propose that XCI initiation is gender independent and triggered by the destabilization of the naïve identity, which suggests that gender-specific mechanisms follow rather than precede XCI initiation.

2018-06-13 | GSE109173 | GEO

Incomplete X-inactivation initiated by a hypomorphic Xist allele in the mouse

2011-03-30 | GSE27373 | GEO

Incomplete X-inactivation initiated by a hypomorphic Xist allele in the mouse

Project description:Mammals have evolved a mechanism to compensate for the difference in the number of X chromosome genes between XX females and XY males by inactivating one of the two X chromosomes in females. This X chromosome inactivation phenomenon is triggered by Xist gene, which is essential for X-inactivation to occur in cis. We demonstrate that an Xist mutant, XistIVS, is unique in that it retains a partial function to silence the X chromosome, which would provide an opportunity to dissect the molecular mechanism of Xist RNA-mediated chromosome silencing. To study the effect of XistIVS mutation on silencing of X-linked genes, global expression levels of X-linked genes were measured in mutant and control cells. We used female trophoblast stem (TS) cells carrying XistIVS mutation and gene expression was assayed using microarray containing 572 probes corresponding most of the X-linked genes. Then the result was compared with that obtained from wild-type control cells.

2011-03-30 | E-GEOD-27373 | biostudies-arrayexpress

Xi-reactivation: A mixed modality approach to MECP2 restoration for Rett Syndrome and other X-linked disorders

Project description:The X-chromosome harbors hundreds of disease genes whose associated diseases predominantly affect males. However, a subset — including neurodevelopmental disorders, Rett, Fragile X, and CDKL5 Syndromes — also affects females. These disorders lack disease-specific treatment. Because female cells carry two X-chromosomes, an emerging treatment strategy has been to reawaken the healthy allele on the inactive X (Xi). Here we focus on MECP2 restoration for Rett Syndrome and combinatorially target factors in the interactome of Xist, the noncoding RNA responsible for X-inactivation. We identify a mixed modality approach combining an Xist antisense oligonucleotide and a small molecule inhibitor of DNA methylation, which together achieve 30,000-fold MECP2 upregulation from the Xi in cultured cells. Combining a brain-specific genetic Xist ablation with short-term Aza treatment models the synergy in vivo without evident toxicity. The Xi is selectively reactivated. These experiments provide proof of concept for a mixed modality approach for treating X-linked disorders in females.

2018-01-04 | GSE97077 | GEO

ChIP-sequencing (ChIP-seq) experiments on female ESCs expressing V5-tagged REX1 and control wild-type Embryonic stem cells (ESCs)

Project description:Evolution of the mammalian sex chromosomes has resulted in a heterologous X and Y pair, where the Y chromosome has lost most of its genes. Hence, there is a need for X-linked gene dosage compensation between XY males and XX females. In placental mammals, this is achieved by random inactivation of one X chromosome (XCI) in all female somatic cells. Up-regulation of Xist transcription on the future inactive X chromosome (Xi) acts against Tsix antisense transcription, and spreading of Xist RNA in cis triggers epigenetic changes leading to XCI. Previously, we have shown that the X-encoded E3 ubiquitin ligase RNF12 is up-regulated in differentiating mouse embryonic stem cells (ESCs) and activates Xist transcription and XCI. Here, we have identified the pluripotency factor REX1 as a key target of RNF12 in the XCI mechanism. RNF12 causes ubiquitination and proteasomal degradation of REX1, and Rnf12 knockout mouse ESCs show an increased level of REX1. Using ChIP-seq, REX1 binding sites were detected in Xist and Tsix regulatory regions. Over-expression of REX1 in female ESCs was found to inhibit Xist transcription and XCI, whereas male Rex1+/- ESCs showed ectopic XCI. From this, we propose that RNF12 causes REX1 breakdown through dose-dependent catalysis, thereby representing an important pathway to initiate XCI. Rex1 and Xist are present only in placental mammals, which points to co-evolution of these two genes and XCI. 2 (one control one pulldown) samples

2012-06-12 | E-GEOD-36417 | biostudies-arrayexpress

Switching from Random to Imprinted X-inactivation by Maternal PRC2

Project description:Imprinted X-inactivation is a paradigm of transgenerational epigenetic inheritance in mammals and silences genes exclusively on the paternally-inherited X-chromosome. Here, we test the hypothesis that oocyte-derived maternal Polycomb repressive complex 2 (PRC2) protein EED orchestrates the selective inactivation of the paternal-X in mouse embryos. In maternal Eed null (Eedm-/-) but not zygotic Eed null female and male embryos, the maternal X-chromosome ectopically induced Xist lncRNA, which silences X-linked genes. Subsequently, Xist was silenced from one of the two X-chromosomes in females and from the sole maternal-X in males. As a result, later-stage female Eedm-/- embryos displayed random X-inactivation. The kinetics of Xist RNA induction in Eedm-/- embryos resemble that of early human embryos, which lack oocyte-derived PRC2 and only undergo random X-inactivation. Thus, expression of PRC2 genes in the oocyte and transmission of the gene products to the embryo may dictate the occurrence of imprinted X-inactivation in mammals.

2019-05-02 | GSE123173 | GEO

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