Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chromosome-wide profiling of X-inactivation status and epigenetic regulation in fetal brain

ABSTRACT: Evidence from a few genes of diverse species suggests that marsupial X-chromosome inactivation (XCI) is characterized by exclusive, but leaky, inactivation of the paternally derived X chromosome. To comprehensively study the mechanism of marsupial XCI, we profiled parent-of-origin-specific-allele expression, DNA methylation, and histone modifications in opossum fetal brain and extra-embryonic membranes. The majority (152/176) of X-linked genes exhibited paternally imprinted expression with nearly 100% maternal allele expression, whereas 24 loci (14%) escaped inactivation showing varying levels of biallelic expression. In addition to regulation by the non-coding RSX transcript, strong depletion of H3K27me3 at escaper gene loci indicates that histone states also influence opossum XCI. Notably, the opossum does not show an association between X-linked gene expression and promoter DNA methylation. Our study provides the first comprehensive catalogue of parent-of-origin expression status for X-linked genes in a marsupial and sheds light on the regulation and evolution of imprinted XCI in mammals.

ORGANISM(S): Monodelphis domestica

PROVIDER: GSE45186 | GEO | 2013/09/23

SECONDARY ACCESSION(S): PRJNA193185

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Chromosome-wide profiling of X-inactivation status and epigenetic regulation in fetal brain

Project description:Evidence from a few genes of diverse species suggests that marsupial X-chromosome inactivation (XCI) is characterized by exclusive, but leaky, inactivation of the paternally derived X chromosome. To comprehensively study the mechanism of marsupial XCI, we profiled parent-of-origin-specific-allele expression, DNA methylation, and histone modifications in opossum fetal brain and extra-embryonic membranes. The majority (152/176) of X-linked genes exhibited paternally imprinted expression with nearly 100% maternal allele expression, whereas 24 loci (14%) escaped inactivation showing varying levels of biallelic expression. In addition to regulation by the non-coding RSX transcript, strong depletion of H3K27me3 at escaper gene loci indicates that histone states also influence opossum XCI. Notably, the opossum does not show an association between X-linked gene expression and promoter DNA methylation. Our study provides the first comprehensive catalogue of parent-of-origin expression status for X-linked genes in a marsupial and sheds light on the regulation and evolution of imprinted XCI in mammals. Profiling of four histone modifications in embryonic day 13 opossum (Monodelphis domestica) fetal brain by Illumina ChIP-seq

2013-09-23 | E-GEOD-45186 | biostudies-arrayexpress

Chromosome-wide profiling of X-inactivation status and epigenetic regulation in opossum fetal brain and placenta

Project description:Evidence from a few genes of diverse species suggests that marsupial X-chromosome inactivation (XCI) is characterized by exclusive, but leaky, inactivation of the paternally derived X chromosome. To comprehensively study the mechanism of marsupial XCI, we profiled parent-of-origin-specific-allele expression, DNA methylation, and histone modifications in opossum fetal brain and extra-embryonic membranes. The majority (152/176) of X-linked genes exhibited paternally imprinted expression with nearly 100% maternal allele expression, whereas 24 loci (14%) escaped inactivation showing varying levels of biallelic expression. In addition to regulation by the non-coding RSX transcript, strong depletion of H3K27me3 at escaper gene loci indicates that histone states also influence opossum XCI. Notably, the opossum does not show an association between X-linked gene expression and promoter DNA methylation. Our study provides the first comprehensive catalogue of parent-of-origin expression status for X-linked genes in a marsupial and sheds light on the regulation and evolution of imprinted XCI in mammals. Profiling of expression level and allele-specific expression ratios in embryonic day 13 opossum (Monodelphis domestica) fetal brain and extra-embyonic membranes by Illumina RNA-seq

2013-09-23 | E-GEOD-45211 | biostudies-arrayexpress

Chromosome-wide profiling of X-inactivation status and epigenetic regulation in opossum fetal brain and placenta

2013-09-23 | GSE45211 | GEO

Characterization of X Chromosome Inactivation by high-throughput sequencing

Project description:<p>This study of DNA and RNA sequencing of 5 parent-offspring trios is a single center study. The goal of this study is to characterize X chromosome inactivation (XCI) ratio in females using phased genomic variations obtained through whole genome or exome sequencing in trios, followed by allele-specific expression analysis of the phased, heterozygous alleles in the mRNA of the female offspring, and to apply this method to clinical diagnosis. The distribution of allele ratios across X obtained from mRNA sequencing allows for the estimation of X inactivation status of inherited X chromosomes, and the parameters of each parental allele distributions in the offspring's mRNA data can be used as determinants for XCI ratio. This approach was used to evaluate the contribution of skewed XCI ratio to phenotypic heterogeneity in an undiagnosed, mild neurological condition.</p>

| phs000816 | dbGaP

Xist-dependent imprinted X inactivation and the early developmental consequences of its failure

Project description:In Mammals, the difference in sex-chromosome constitution between males (XY) and females (XX) has led to the evolution of dosage compensation strategies, including silencing of an entire X chromosome in females. In mice, X chromosome inactivation (XCI) first occurs in the pre-implantation embryo. Here the non-coding Xist RNA is expressed only from the paternal allele and the paternal X (Xp) becomes inactivated. The Xp is reactivated in the inner cell mass and this is followed by random XCI in the embryo proper, while in extra-embryonic tissues the Xp remains inactive. Although random XCI initiation is thought to be fully Xist-dependent in the mouse, initiation of imprinted XCI was reported to be Xist-independent. Furthermore, the chromosome-wide dynamics of XCI in early embryos of reciprocal inter-specific crosses, which better reflect a natural situation, have never been investigated. Here we report that the expression dynamics of X-linked genes depends both on strain and parent of origin, as well as on X chromosome location, using single-cell RNA-sequencing (scRNAseq) of early mouse embryos. We also demonstrate that initiation of imprinted XCI absolutely requires Xist and that its absence leads to genome-wide transcriptional misregulation in the early blastocyst, with massive over-expression of specific genes such as Rhox5 and failure to activate the extra-embryonic pathway essential for early post-implantation development. This study provides important insights into the transcriptional and allelic dynamics of the X chromosome and the first evidence of dosage compensation failure as early as the blastocyst stage.

2016-12-05 | GSE80810 | GEO

Genomic imprinting of Xist by maternal H3K27me3

Project description:Maternal imprinting at the Xist gene is essential to achieve paternal allele-specific imprinted X chromosome inactivation (XCI) in female mammals. However, the mechanism underlying the Xist imprinting is unclear. Here we show that the Xist gene is coated with H3K27me3 in mouse oocytes, which persists through preimplantation development. Ectopic removal of H3K27me3 induces maternal Xist expression and maternal XCI, indicating that maternal H3K27me3 is the imprinting mark of Xist.

2017-11-09 | GSE103714 | GEO

A Novel Approach Identifies New Differentially Methylated Regions (DMRs) Associated with Imprinted Genes

Project description:Imprinted genes are critical for normal human growth and neurodevelopment. We developed a strategy to identify new DNA differentially methylated regions (DMRs), a hallmark of imprinted genes. Using genome-wide methylation profiling, candidate DMRs were selected by identifying CpGs with putative allelic differential methylation in normal biparental tissues. In parallel, we looked for parent of origin-specific DNA methylation patterns in paternally derived human androgenetic complete hydatidiform mole (AnCHM), and maternally derived mature cystic ovarian teratoma (MCT). Using this approach, we found known DMRs associated with imprinted genomic regions as well as new DMRs for known imprinted genes, NAP1L5 and ZNF597. Most importantly, novel candidate imprinted genes were identified. The paternally methylated DMR for one candidate, AXL, a receptor tyrosine kinase, was validated by methylation analyses in humans. Further validation in mouse embryos showed that Axl was expressed preferentially from the maternal allele in a DNA methylation–dependent manner.

2011-01-26 | GSE22091 | GEO

A Novel Approach Identifies New Differentially Methylated Regions (DMRs) Associated with Imprinted Genes

2011-01-26 | E-GEOD-22091 | biostudies-arrayexpress

Discovery of novel imprinted genes by transcriptional analysis of parthenogenetic embryonic stem cells

Project description:Parthenogenetic embryonic stem cells (PESCs) may have future utility in cell replacement therapies. We examined genome-wide mRNA expression profiles of monkey PESCs relative to ESCs derived from fertilized embryos. Several known paternally-imprinted genes were in the highly down-regulated group in PESCs compared to ESCs. Allele specific expression analysis of paternally-imprinted genes, i.e., those genes whose expression is down-regulated in PESCs, led to the identification of one novel candidate that was exclusively expressed from a paternal allele. Our findings suggest that PESCs could be used as a model for studying genomic imprinting and in the discovery of novel imprinted genes. Keywords: gene expression

2010-06-21 | GSE17964 | GEO

Parent-of-origin effects on gene expression and DNA methylation in the maize endosperm

Project description:Imprinting describes the differential expression of alleles based upon their parent of origin. Deep sequencing of RNAs from maize endosperm and embryo tissue 14 days after pollination was used to identify imprinted genes among a set of ~12,000 genes that were expressed and contained sequence polymorphisms between the B73 and Mo17 genotypes. The analysis of parent-of-origin patterns of expression resulted in the identification of 100 putative imprinted genes in maize endosperm including 54 maternally expressed genes (MEGs) and 46 paternally expressed genes (PEGs). Three of these genes have been previously identified as imprinted while the remaining 97 genes represent novel imprinted maize genes. A genome-wide analysis of DNA methylation identified regions with reduced endosperm DNA methylation in, or near, 19 of the 100 imprinted genes. The reduced levels of DNA methylation in endosperm are caused by hypomethylation of the maternal allele for both MEGs and PEGs in all cases tested. Many of the imprinted genes with reduced DNA methylation levels also show endosperm-specific expression patterns. The imprinted maize genes were compared with imprinted genes identified in genome-wide screens of rice and Arabidopsis and at least 10 examples of conserved imprinting between maize and each of the other species were identified. Methylation profiles across endosperm tissue in B73 and Mo17 were assayed for three biological replications using a custom 2.1M gene-focused NimbleGen array.

2011-12-16 | E-GEOD-33730 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data