Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1200796 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31784563_1.fastq.gz | Fastqsanger.gz | |||
| SRR31784563_2.fastq.gz | Fastqsanger.gz | |||
| SRR31784564_1.fastq.gz | Fastqsanger.gz | |||
| SRR31784564_2.fastq.gz | Fastqsanger.gz | |||
| SRR31784565_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
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Project description:Allele-specific chromosome conformations induced by a transgene- and locus-dependent imprinting
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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 is an epigenetic phenomenon in which genes exhibit restricted or biased expression from one allele according to parental origin. Imprinted gene expression plays a crucial role in the development, including the brain. Higher-order chromatin structure has long been associated with gene regulation, particularly in the context of spatial enhancer-promoter interactions. Given the characteristic parental allele-biased expression pattern of imprinted genes, a compelling question is whether the three-dimensional organization of parental genomes plays a role in imprinted gene regulation. Using a capture Hi-C approach, we identifiedparental allele-specific higher-order chromatin structures across multiple imprinted domains in the mouse brain. These allele-specific structural features largely stem from annotated imprinting control regions (ICRs), concomitant with allele-specific binding of CTCF. Detailed analysis suggests that transcriptional start sites (TSS) of active and inactive alleles of imprinted genes form distinct chromatin interactions, differing in degree and/or type. CRISPRi screeningrevealed a distal cis-regulatory element that modulates imprinted expression of the Mest-Copg2locus in neurons, and its regulatory mechanism is tightly associated with allele-specific chromatin interactions. Further investigation revealed that both a cis-acting long non-coding RNA and allele-specific enhancer-promoter architecture modulates Mest-Copg2 imprinted expression. Together, this study highlights the interplay between chromatin structure and regulatory landscapes that modulate allele-specific expression of imprinted genes.
2026-01-13 | GSE312069 | GEO
Project description:Genomic imprinting is an epigenetic phenomenon in which genes exhibit restricted or biased expression from one allele according to parental origin. Imprinted gene expression plays a crucial role in the development, including the brain. Higher-order chromatin structure has long been associated with gene regulation, particularly in the context of spatial enhancer-promoter interactions. Given the characteristic parental allele-biased expression pattern of imprinted genes, a compelling question is whether the three-dimensional organization of parental genomes plays a role in imprinted gene regulation. Using a capture Hi-C approach, we identifiedparental allele-specific higher-order chromatin structures across multiple imprinted domains in the mouse brain. These allele-specific structural features largely stem from annotated imprinting control regions (ICRs), concomitant with allele-specific binding of CTCF. Detailed analysis suggests that transcriptional start sites (TSS) of active and inactive alleles of imprinted genes form distinct chromatin interactions, differing in degree and/or type. CRISPRi screeningrevealed a distal cis-regulatory element that modulates imprinted expression of the Mest-Copg2locus in neurons, and its regulatory mechanism is tightly associated with allele-specific chromatin interactions. Further investigation revealed that both a cis-acting long non-coding RNA and allele-specific enhancer-promoter architecture modulates Mest-Copg2 imprinted expression. Together, this study highlights the interplay between chromatin structure and regulatory landscapes that modulate allele-specific expression of imprinted genes.
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Project description:Genomic imprinting is an epigenetic phenomenon in which genes exhibit restricted or biased expression from one allele according to parental origin. Imprinted gene expression plays a crucial role in the development, including the brain. Higher-order chromatin structure has long been associated with gene regulation, particularly in the context of spatial enhancer-promoter interactions. Given the characteristic parental allele-biased expression pattern of imprinted genes, a compelling question is whether the three-dimensional organization of parental genomes plays a role in imprinted gene regulation. Using a capture Hi-C approach, we identifiedparental allele-specific higher-order chromatin structures across multiple imprinted domains in the mouse brain. These allele-specific structural features largely stem from annotated imprinting control regions (ICRs), concomitant with allele-specific binding of CTCF. Detailed analysis suggests that transcriptional start sites (TSS) of active and inactive alleles of imprinted genes form distinct chromatin interactions, differing in degree and/or type. CRISPRi screeningrevealed a distal cis-regulatory element that modulates imprinted expression of the Mest-Copg2locus in neurons, and its regulatory mechanism is tightly associated with allele-specific chromatin interactions. Further investigation revealed that both a cis-acting long non-coding RNA and allele-specific enhancer-promoter architecture modulates Mest-Copg2 imprinted expression. Together, this study highlights the interplay between chromatin structure and regulatory landscapes that modulate allele-specific expression of imprinted genes.
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Project description:Genomic imprinting is an epigenetic phenomenon in which genes exhibit restricted or biased expression from one allele according to parental origin. Imprinted gene expression plays a crucial role in the development, including the brain. Higher-order chromatin structure has long been associated with gene regulation, particularly in the context of spatial enhancer-promoter interactions. Given the characteristic parental allele-biased expression pattern of imprinted genes, a compelling question is whether the three-dimensional organization of parental genomes plays a role in imprinted gene regulation. Using a capture Hi-C approach, we identifiedparental allele-specific higher-order chromatin structures across multiple imprinted domains in the mouse brain. These allele-specific structural features largely stem from annotated imprinting control regions (ICRs), concomitant with allele-specific binding of CTCF. Detailed analysis suggests that transcriptional start sites (TSS) of active and inactive alleles of imprinted genes form distinct chromatin interactions, differing in degree and/or type. CRISPRi screeningrevealed a distal cis-regulatory element that modulates imprinted expression of the Mest-Copg2locus in neurons, and its regulatory mechanism is tightly associated with allele-specific chromatin interactions. Further investigation revealed that both a cis-acting long non-coding RNA and allele-specific enhancer-promoter architecture modulates Mest-Copg2 imprinted expression. Together, this study highlights the interplay between chromatin structure and regulatory landscapes that modulate allele-specific expression of imprinted genes.
2026-01-13 | GSE312073 | GEO
Project description:Genomic imprinting is an epigenetic phenomenon in which genes exhibit restricted or biased expression from one allele according to parental origin. Imprinted gene expression plays a crucial role in the development, including the brain. Higher-order chromatin structure has long been associated with gene regulation, particularly in the context of spatial enhancer-promoter interactions. Given the characteristic parental allele-biased expression pattern of imprinted genes, a compelling question is whether the three-dimensional organization of parental genomes plays a role in imprinted gene regulation. Using a capture Hi-C approach, we identifiedparental allele-specific higher-order chromatin structures across multiple imprinted domains in the mouse brain. These allele-specific structural features largely stem from annotated imprinting control regions (ICRs), concomitant with allele-specific binding of CTCF. Detailed analysis suggests that transcriptional start sites (TSS) of active and inactive alleles of imprinted genes form distinct chromatin interactions, differing in degree and/or type. CRISPRi screeningrevealed a distal cis-regulatory element that modulates imprinted expression of the Mest-Copg2locus in neurons, and its regulatory mechanism is tightly associated with allele-specific chromatin interactions. Further investigation revealed that both a cis-acting long non-coding RNA and allele-specific enhancer-promoter architecture modulates Mest-Copg2 imprinted expression. Together, this study highlights the interplay between chromatin structure and regulatory landscapes that modulate allele-specific expression of imprinted genes.
2026-01-13 | GSE312072 | GEO
Project description:DNA methylation is essential for embryonic development and implicated in the regulation of genomic imprinting. Genomic imprinting is established in the germline through parent-specific methylation of distinct cis-regulatory DNA sequences, called imprinting control regions (ICRs). Which factors bind to the opposing chromatin states at ICRs within the same nuclear environment was not systematically addressed. By using a proximity labelling approach with the methylation sensitive transcription factor ZFP57, we identified ATF7IP and other major components of the epigenetic maintenance machinery at ICRs.
2023-03-10 | PXD034918 | Pride
Project description:Genetic variation and 3D chromatin structure have major roles in gene regulation. Structural differences between genotypically different chromosomes and their effects on gene expression remain ill understood, due to challenges in mapping 3D genome structure with allele-specific resolution. Here, we applied Genome Architecture Mapping (GAM) to a hybrid mouse embryonic stem cell (ESC) line with high SNP density. Given the high efficiency of GAM in haplotype phasing, we could resolve allele-specific 3D genome structures with high sensitivity. We discovered extensive genotype-specific folding of chromosomes in compartments, topologically associating domains (TADs), long-range enhancer-promoter contacts and CTCF loops, often coinciding with allele-specific gene expression in association with Polycomb repression. We show that histone genes are expressed with allelic imbalance in ESCs, and involved in allele-specific chromatin contacts marked by H3K27me3. Functional analysis through conditional Ezh2- or Ring1b-knockdown shows a role for Polycomb repression in tuning histone protein levels. Our work reveals that the homologous chromosomes have highly distinct 3D folding structures, and their intricate relationships with gene-specific mechanisms of allelic expression imbalance.
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Project description:How constitutive allelic methylation at imprinting control regions (ICRs) interacts with other levels of regulation to drive timely parental allele-specific expression along large imprinted domains remains partially understood at most imprinted loci. To gain insight into the regulation of the Peg13-KcnK9 domain, an imprinted domain with important brain functions, during neural commitment, we performed a detailed integrative analysis of the epigenetic, transcriptomic and cis-spatial organisation in an allele-specific manner in a mouse stem cell-based model of corticogenesis that recapitulates the control of imprinted gene expression in the embryonic brain. We have evidence that despite an allelic higher order chromatin structure associated with the paternally CTCF-bound Peg13 ICR, enhancer-Kcnk9 promoter contacts can occur on both alleles, although they are only productive on the maternal allele. This observation challenges the canonical model in which CTCF binding isolates the enhancer and its target gene on either side, and suggests a more nuanced role for allelic CTCF binding at the ICR of this locus.
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