Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA209038 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:A reporter transgene displayed parental imprinting in mouse embryos when positioned into the Itga6 gene. The strong lacZ pattern of expression scored in embryos inheriting the transgene from a male was not present when transmitted from a female. The transgene exhibited maternal allele-specific DNA hyper-methylation acquired in the germ-line and histone modifications corresponded to profiles described at known imprinted loci. Chromosome conformation analyzes revealed distinct, parent-of-origin interaction domains, with a more compact structure characterizing the maternally inherited repressed allele. The analysis of such transgene insertions with a selective potential to induce imprinting may help understanding the mechanisms identifying particular loci as targets for allele-specific repression.
2013-07-03 | GSE48148 | GEO
Project description:A reporter transgene displayed parental imprinting in mouse embryos when positioned into the Itga6 gene. The strong lacZ pattern of expression scored in embryos inheriting the transgene from a male was not present when transmitted from a female. The transgene exhibited maternal allele-specific DNA hyper-methylation acquired in the germ-line and histone modifications corresponded to profiles described at known imprinted loci. Chromosome conformation analyzes revealed distinct, parent-of-origin interaction domains, with a more compact structure characterizing the maternally inherited repressed allele. The analysis of such transgene insertions with a selective potential to induce imprinting may help understanding the mechanisms identifying particular loci as targets for allele-specific repression. Data were quantile normalized within 4C/input replicate groups and scaled to medial feature intensity of 100 using TAS software (Affymetrix), generating signal.bar files. For each genomic position, a data set was generated consisting of all (PM-MM) pairs mapping within a sliding window of 250 bp. For Inv(rel5-Itga6) tissues, two independent 4C experiments were performed and merged in the .bar file.
2013-07-03 | E-GEOD-48148 | biostudies-arrayexpress
Project description:Genomic imprinting and X chromosome inactivation (XCI) require epigenetic mechanisms to direct allele-specific expression. Despite their critical roles in embryonic development, how universal epigenetic regulators coordinate these specific tasks at single loci or across chromosome scales remains understudied. Here, we systematically disrupted essential epigenetic pathways within polymorphic F1 embryos to examine canonical and non-canonical genomic imprinting as well as X chromosome inactivation. We find that DNA methylation and Polycomb group repressors are both indispensable for autosomal imprinting, albeit at distinct gene sets. Moreover, the extraembryonic ectoderm relies on a broader spectrum of imprinting mechanisms, including non-canonical targeting of maternal endogenous retrovirus (ERV) driven promoters by the H3K9 methyltransferase G9a. We further utilize our data to identify Polycomb dependent and independent gene clusters on the imprinted X chromosome, which appears to reflect distinct domains of Xist-mediated suppression. From our data, we assemble a comprehensive inventory of the epigenetic mechanisms utilized in eutherian mammals to maintain parent-specific imprinting, including an expanded view of the placental lineage that comprises multiple unique pathways.
2021-11-12 | GSE171206 | GEO
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
Project description:We report locus-specific disintegration of megabase-scale chromosomal conformations after Kmt1e/Setdb1 histone H3-lysine 9 methyltransferase ablation in mouse brian. Histone modification, CCCTC-binding factor (CTCF), transcriptome and ‘3D genome’ (in situ Hi-C) mappings each identified a uniquely affected ~1Mb domain on chromosome 18 in cortical and striatal neurons, encompassing the Protocadherin cell adhesion gene clusters (cPcdh). Setdb1-deficient neuronal genomes showed de novo CTCF occupancies at thousands of cryptic binding sites and locus-specific disintegration of 1Mb cPcdh higher order chromatin. Loss of long-range repressive chromosomal conformations triggered massively increased proportions of neurons expressing specific cPcdh genes due to relaxation of stochastic constraint. Setdb1, shielding mature neuronal genomes from excess CTCF binding, maintains TAD integrity essential for mouse brain function.
2017-07-01 | GSE99363 | GEO
Project description:Genomic imprinting results in the preferential expression of the paternal, or maternal allele of certain genes. We have performed a genome-wide characterization of imprinting in the mouse embryonic and adult brain using F1 hybrid mice generated from reciprocal crosses of CASTEiJ and C57BL/6J mice. We also uncovered genes associated with sex specific parental effects in the adult mouse brain. Our study identified preferential selection of the maternally inherited X chromosome in glutamatergic neurons of the female cortex. Examination of allele specific expression in the brains of reciprocal crosses of F1 hybrid mice from CASTEiJ and C57BL/6J crosses. Processed data files (GenomicAligned, SNP_calls, TranscriptomeAligned, fRNAdbAligned) and README file linked below as supplementary files.
2010-07-08 | E-GEOD-22131 | biostudies-arrayexpress
Project description:Faithful maintenance of genomic imprinting is essential for mammalian development. While germline DNA methylation-dependent (canonical) imprinting is relatively stable during development, the recently discovered oocyte-derived H3K27me3-mediated noncanonical imprinting is mostly transient in early embryos with only a few genes maintain imprinted expression in the extraembryonic lineage. How these few noncanonical imprinted genes maintain their extraembryonic-specific imprinting is unknown. Here we report that maintenance of extraembryonic-specific noncanonical imprinting requires maternal allele-specific de novo DNA methylation (secondary differentially methylation regions; DMRs) at implantation. The secondary DMRs are located at the gene promoters with paternal allele-specific H3K4me3 preformed during preimplantation development. Importantly, genetic ablation of Eed and DNA methyltransferases revealed that both maternal H3K27me3 and zygotic Dnmt3a/3b are required for establishing secondary DMRs and for maintaining noncanonical imprinting. Thus, our study not only reveals the mechanism underlying maintenance of noncanonical imprinting, but also sheds light on how histone modifications in oocytes and preimplantation embryos may shape the secondary DMRs in post-implantation embryos.
2019-12-26 | GSE130115 | GEO
Project description:Embryos generated with the use of assisted reproductive technologies (ART) can develop overgrowth syndromes. In ruminants, the condition is referred to as large offspring syndrome (LOS) and exhibits variable phenotypic abnormalities including overgrowth, enlarged tongue, and abdominal wall defects. These characteristics recapitulate those observed in the human loss-of-imprinting (LOI) overgrowth syndrome Beckwith-Wiedemann (BWS). We have recently shown LOI at the KCNQ1 locus in LOS, the most common epimutation in BWS. Although the first case of ART-induced LOS was reported in 1995, studies have not yet determined the extent of LOI in this condition. Here, we determined allele-specific expression of imprinted genes previously identified in human and/or mouse in day 105 Bos taurus indicus X Bos taurus taurus F1 hybrid control and LOS fetuses using RNAseq. Our analysis allowed us to determine the monoallelic expression of 20 genes in tissues of control fetuses. LOS fetuses displayed variable LOI when compared to controls. Biallelic expression of imprinted genes in LOS was associated with tissue-specific hypomethylation of the normally methylated parental allele. In addition, a positive correlation was observed between bodyweight and the number of biallelically expressed imprinted genes in LOS fetuses. Further, not only was there loss of allele-specific expression of imprinted genes in LOS, but we also observed differential transcript amounts of these genes between control and overgrown fetuses. In summary, we characterized previously unidentified imprinted genes in bovine and identified misregulation of imprinting at multiple loci in LOS. We concluded that LOS is a multi-locus loss-of-imprinting syndrome, as is BWS.
2015-03-06 | GSE63509 | GEO
Project description:Tlx (nr2e1) is an orphan nuclear receptor that is highly expressed in proliferating neural stem cells (NSCs) in the adult mouse forebrain. The goal was to identify Tlx-regulated genes in this specific cell population. Two populations of Tlx-positive neural stem cells were isolated from 2-month-old male mice based on a LacZ marker that was knocked into the Tlx locus. The first population, Tlx(f/Z;CreER), contains a floxed allele of Tlx (f), the LacZ marker (Z), and a CreER fusion transgene. Addition of tamoxifen (4OH-tamoxifen) into this NSC population leads to Cre-mediated deletion of the floxed allele of Tlx. The second NSC population, Tlx(f/Z), does not contain a CreER transgene; thus it does not respond to tamoxifen treatment and was used as a control. Keywords: Nuclear receptor-dependent gene expression
2008-12-01 | GSE9981 | GEO
Project description:Parental imprinting is a form of epigenetic regulation that results in parent-of-origin differential gene expression. To study Prader-Willi syndrome (PWS), a developmental imprinting disorder, we generated patient-derived induced pluripotent stem cells (iPSCs) harboring distinct deletions in the affected region on chromosome 15. Studying PWS-iPSCs and human parthenogenetic iPSCs unexpectedly revealed substantial upregulation of virtually all maternally expressed genes (MEGs) in the imprinted DLK1-DIO3 locus on chromosome 14. Subsequently, we identified IPW, a long noncoding RNA in the critical region of the PWS locus, as a regulator of the DLK1-DIO3 region, as its over-expression in PWS and parthenogenetic iPSCs results in downregulation of the MEGs in this locus. We further show that gene expression changes in the DLK1-DIO3 region coincide with chromatin modifications, rather than DNA methylation levels. Our results suggest that a subset of PWS phenotypes may arise from dysregulation of an imprinted locus distinct from the PWS region. Gene expression analysis was performed on a total of 4 human cell lines, including 3 Prader-Willi Syndrome indcued pluripotent stem cell lines - derived from 3 affected individuals and one of their parental fibroblast cell line.
2014-04-03 | E-GEOD-56136 | biostudies-arrayexpress