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:in vitro in various cell types and in vivo in placentae and blood Smchd1 removal results in loss of imprinting at the PWS cluster on mouse chromosome 7. Our aim was to assess whether CNS specific Smchd1 deletion after early development in vivo likewise resulted in activation of maternal PWS cluster genes - specifically the small nucleolar RNAs (snoRNAs) and long non-coding RNAs (lncRNAs) in the region, and what effects this deletion may have genome-wide. We found significant maternal gene activation at imprinted genes across the locus including snoRNAs and importantly activation of a lncRNA responsible for reciprocal imprinting on the paternal allele did not affect the imprinting status of paternally imprinted gene Ube3a. We also observed minimal genome-wide changes.
2026-08-30 | GSE329974 | 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:In recent years, long-read sequencing technologies have detected transcript isoforms with unprecedented accuracy and resolution. However, it remains unclear whether long-read sequencing can effectively disentangle the isoform landscape of complex allele-specific loci that arise from genetic or epigenetic differences between alleles. Here, we combine the PacBio Iso-Seq workflow with the established phasing approach WhatsHap to assign long reads to the corresponding allele in polymorphic F1 mouse hybrids. Upon comparing the long-read sequencing results with matched short reads, we observed general consistency in the allele-specific information and were able to confirm the imprinting status of known imprinted genes. We then explored the complex imprinted Gnas locus known for allele-specific non-coding and coding isoforms and were able to benchmark historical observations. This approach also allowed us to detect isoforms from both the active and inactive X chromosomes of genes that escape X chromosome inactivation. The described workflow offers a promising framework and demonstrates the power of long-read transcriptomic data to provide mechanistic insight into complex allele-specific loci.
2025-02-03 | GSE246857 | 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:Genomic imprinting secures parent-specific gene expression through differential DNA methylation at imprinted control regions (ICRs). However, how unmethylated alleles resist de novo methylation remains unclear. Using an allelic Dlk1-Dio3 ICR methylation reporter and genome-wide loss-of-function screening, we identify the zinc finger protein GZF1 that binds the unmethylated maternal ICR and protects it from de novo methylation via a regulatory element containing GZF1 and ZFP57 motifs that mediates mutually exclusive, methylation-dependent binding. Loss of either factor causes reciprocal imprinting failure: Gzf1 loss induces maternal allele methylation, H3K4me3 depletion, and silencing of maternal transcripts, whereas Zfp57 loss results in maternalization. Remarkably, GZF1 protects the unmethylated ICR from de novo methylation in both oocytes and embryos, and its loss leads to perinatal death consistent with paternalization of the maternal allele. Together, our findings establish a reciprocal mechanism that maintains parental epigenetic asymmetry across both imprint establishment and embryonic reprogramming.
2026-08-04 | PXD080456 | Pride