Sex-dependent RNA expression in opossum brain and liver.
Ontology highlight
ABSTRACT:
ORGANISM(S): Monodelphis domestica
PROVIDER: GSE36861 | GEO | 2012/06/11
SECONDARY ACCESSION(S): PRJNA157033
REPOSITORIES: GEO
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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. RNA sequencing was used to detect and characterize transcripts with strongly biased female expression.
2012-06-11 | E-GEOD-36861 | biostudies-arrayexpress
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.
2011-03-30 | GSE27373 | GEO
Project description:Decades of work in placental (eutherian) species have constructed a paradigm of mammalian development, wherein the genome-wide erasure of parental DNA methylation is required for embryogenesis1-10. Whether such DNA methylation reprogramming is, in fact, conserved in other mammals is unknown. To resolve this point, we generated base-resolution DNA methylation maps in gametes, embryos and adult tissues of the opossum marsupial Monodelphis domestica, revealing extensive variations from the eutherian-derived model. In stark contrast with eutherians, the marsupial genome remains hypermethylated during the cleavage stages and in the embryo proper of the blastocyst. In the extra-embryonic trophectoderm DNA methylation is reduced, suggesting an important evolutionary conserved function for DNA hypomethylation in formation of the mammalian placenta. Furthermore, unlike in eutherians, the inactive X chromosome becomes globally DNA hypomethylated during embryogenesis. Using our DNA methylation profiles, we identify a candidate mechanism for imprinted X-inactivation in marsupials, via maternal promoter DNA methylation of the Xist-like non-coding RNA RSX11. How mammalian embryos employ DNA methylation to regulate their development is therefore more mechanistically diverse than current models can accommodate.
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Project description:Decades of work in placental (eutherian) species have constructed a paradigm of mammalian development, wherein the genome-wide erasure of parental DNA methylation is required for embryogenesis1-10. Whether such DNA methylation reprogramming is, in fact, conserved in other mammals is unknown. To resolve this point, we generated base-resolution DNA methylation maps in gametes, embryos and adult tissues of the opossum marsupial Monodelphis domestica, revealing extensive variations from the eutherian-derived model. In stark contrast with eutherians, the marsupial genome remains hypermethylated during the cleavage stages and in the embryo proper of the blastocyst. In the extra-embryonic trophectoderm DNA methylation is reduced, suggesting an important evolutionary conserved function for DNA hypomethylation in formation of the mammalian placenta. Furthermore, unlike in eutherians, the inactive X chromosome becomes globally DNA hypomethylated during embryogenesis. Using our DNA methylation profiles, we identify a candidate mechanism for imprinted X-inactivation in marsupials, via maternal promoter DNA methylation of the Xist-like non-coding RNA RSX11. How mammalian embryos employ DNA methylation to regulate their development is therefore more mechanistically diverse than current models can accommodate.
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Project description:Decades of work in placental (eutherian) species have constructed a paradigm of mammalian development, wherein the genome-wide erasure of parental DNA methylation is required for embryogenesis1-10. Whether such DNA methylation reprogramming is, in fact, conserved in other mammals is unknown. To resolve this point, we generated base-resolution DNA methylation maps in gametes, embryos and adult tissues of the opossum marsupial Monodelphis domestica, revealing extensive variations from the eutherian-derived model. In stark contrast with eutherians, the marsupial genome remains hypermethylated during the cleavage stages and in the embryo proper of the blastocyst. In the extra-embryonic trophectoderm DNA methylation is reduced, suggesting an important evolutionary conserved function for DNA hypomethylation in formation of the mammalian placenta. Furthermore, unlike in eutherians, the inactive X chromosome becomes globally DNA hypomethylated during embryogenesis. Using our DNA methylation profiles, we identify a candidate mechanism for imprinted X-inactivation in marsupials, via maternal promoter DNA methylation of the Xist-like non-coding RNA RSX11. How mammalian embryos employ DNA methylation to regulate their development is therefore more mechanistically diverse than current models can accommodate.
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Project description:Decades of work in placental (eutherian) species have constructed a paradigm of mammalian development, wherein the genome-wide erasure of parental DNA methylation is required for embryogenesis1-10. Whether such DNA methylation reprogramming is, in fact, conserved in other mammals is unknown. To resolve this point, we generated base-resolution DNA methylation maps in gametes, embryos and adult tissues of the opossum marsupial Monodelphis domestica, revealing extensive variations from the eutherian-derived model. In stark contrast with eutherians, the marsupial genome remains hypermethylated during the cleavage stages and in the embryo proper of the blastocyst. In the extra-embryonic trophectoderm DNA methylation is reduced, suggesting an important evolutionary conserved function for DNA hypomethylation in formation of the mammalian placenta. Furthermore, unlike in eutherians, the inactive X chromosome becomes globally DNA hypomethylated during embryogenesis. Using our DNA methylation profiles, we identify a candidate mechanism for imprinted X-inactivation in marsupials, via maternal promoter DNA methylation of the Xist-like non-coding RNA RSX11. How mammalian embryos employ DNA methylation to regulate their development is therefore more mechanistically diverse than current models can accommodate.
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Project description:Decades of work in placental (eutherian) species have constructed a paradigm of mammalian development, wherein the genome-wide erasure of parental DNA methylation is required for embryogenesis1-10. Whether such DNA methylation reprogramming is, in fact, conserved in other mammals is unknown. To resolve this point, we generated base-resolution DNA methylation maps in gametes, embryos and adult tissues of the opossum marsupial Monodelphis domestica, revealing extensive variations from the eutherian-derived model. In stark contrast with eutherians, the marsupial genome remains hypermethylated during the cleavage stages and in the embryo proper of the blastocyst. In the extra-embryonic trophectoderm DNA methylation is reduced, suggesting an important evolutionary conserved function for DNA hypomethylation in formation of the mammalian placenta. Furthermore, unlike in eutherians, the inactive X chromosome becomes globally DNA hypomethylated during embryogenesis. Using our DNA methylation profiles, we identify a candidate mechanism for imprinted X-inactivation in marsupials, via maternal promoter DNA methylation of the Xist-like non-coding RNA RSX11. How mammalian embryos employ DNA methylation to regulate their development is therefore more mechanistically diverse than current models can accommodate.
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Project description:Decades of work in placental (eutherian) species have constructed a paradigm of mammalian development, wherein the genome-wide erasure of parental DNA methylation is required for embryogenesis. Whether such DNA methylation reprogramming is, in fact, conserved in other mammals is unknown. To resolve this point, we generated base-resolution DNA methylation maps in gametes, embryos and adult tissues of the opossum marsupial Monodelphis domestica, revealing extensive variations from the eutherian-derived model. In stark contrast with eutherians, the marsupial genome remains hypermethylated during the cleavage stages and in the embryo proper of the blastocyst. In the extra-embryonic trophectoderm DNA methylation is reduced, suggesting an important evolutionary conserved function for DNA hypomethylation in formation of the mammalian placenta. Furthermore, unlike in eutherians, the inactive X chromosome becomes globally DNA hypomethylated during embryogenesis. Using our DNA methylation profiles, we identify a candidate mechanism for imprinted X-inactivation in marsupials, via maternal promoter DNA methylation of the Xist-like non-coding RNA RSX11. How mammalian embryos employ DNA methylation to regulate their development is therefore more mechanistically diverse than current models can accommodate.
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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
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.
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