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Transcription Across the H19/Igf2 Imprinting Control Region Initiates Paternally Methylated Imprinting in Mouse Prospermatogonia

ABSTRACT: Transcription Across the H19/Igf2 Imprinting Control Region Initiates Paternally Methylated Imprinting in Mouse Prospermatogonia

PROVIDER: PRJNA990774 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19178585_1.fastq.gz	Fastqsanger.gz
	SRR19178585_2.fastq.gz	Fastqsanger.gz
	SRR19178586_1.fastq.gz	Fastqsanger.gz
	SRR19178586_2.fastq.gz	Fastqsanger.gz
	SRR19178587_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Transcription Across the H19/Igf2 Imprinting Control Region Initiates Paternally Methylated Imprinting in Mouse Prospermatogonia (ChIP-Seq)

Project description:The insulator model explains the workings of the H19 and Igf2 domain in the soma, where insulation of the Igf2 promoter from its enhancers occurs by CTCF in the maternally inherited unmethylated chromosome but not the paternally inherited methylated allele. The molecular mechanism that targets paternal methylation imprint establishment to the imprinting control region (ICR) in the male germline is unknown. We tested the function of a prospermatogonia-specific broad low-level transcription in this process using mouse genetics. Paternal imprint establishment was abnormal when transcription was stopped at the entry point to the ICR. The germline epimutation persisted into the paternal allele of the soma, resulting in reduced Igf2 in fetal organs, and reduced fetal growth, consistent with the insulator model and IGF2’s role as fetal growth factor. In summary, broad low-level transcription through the ICR initiates paternal imprint establishment at the H19/Igf2 ICR in the male germ line, with implications for Silver-Russell syndrome. The superseries contains RNAseq and ChIPseq data from 15.5 dpc fetal male germ cells that carry the RNA terminator cassette and also from control wild type mice.

2023-08-02 | GSE236416 | GEO

Transcription Across the H19/Igf2 Imprinting Control Region Initiates Paternally Methylated Imprinting in Mouse Prospermatogonia (RNA-Seq)

Project description:Silver-Russell syndrome(SRS, OMIM 180860) is an imprinting disordermanifesting in fetal and postnatal growth retardation. Loss of methylation (LOM) is detected in the imprinting control region 1 (ICR1) that controls the H19/IGF2 domain, in about 65% of SRS cases. The cause of this epigenetic deficiency is unknown. It may affect the process of imprint establishment --de novo methylation of ICR1 in the male germ line. In the paralogous mouse locus this process involves DNA methyltransferase DNMT3A and H3K36me2 histone methyltransferase NSD1, but the mechanism that targets these enzymes to this ICR is unknown. Based on our genome-wide deep-sequencing data of transcription and DNA methylation, we hypothesized that low-level transcription is required in prospermatogonia for targeting H3K36me2 and de novo methylation to ICR. We truncated this transcript at the entry point to ICR by gene-targeting. In response, the establishment of DNA methylation imprint was incomplete. The sporadic LOM persisted from the male germ line into the paternal allele of the soma, resulting in reduced Igf2, and increased, biallelic H19 RNA in the fetal organs, consistent with the insulator model. Fetus weight was also variably reduced upon paternal transmission of this mutation, consistent with the role of IGF2 as a fetal growth factor. We identify low-level transcription-through as the mechanism that initiates paternal imprint establishment at the H19/Igf2 ICR in the male germ line. The findings predict that RNA-dependent imprint establishment may be affected in human fetuses resulting in sporadic hypomethylation of the ICR1 in SRS.

2023-08-02 | GSE202875 | GEO

Transcription Across the H19/Igf2 Imprinting Control Region Initiates Paternally Methylated Imprinting in Mouse Prospermatogonia (RNA-Seq)

Project description:Transcription Across the H19/Igf2 Imprinting Control Region Initiates Paternally Methylated Imprinting in Mouse Prospermatogonia (RNA-Seq)

| PRJNA837578 | ENA

Transcription Across the H19/Igf2 Imprinting Control Region Initiates Paternally Methylated Imprinting in Mouse Prospermatogonia (ChIP-Seq)

Project description:Transcription Across the H19/Igf2 Imprinting Control Region Initiates Paternally Methylated Imprinting in Mouse Prospermatogonia (ChIP-Seq)

| PRJNA990775 | ENA

Transcription Across the H19/Igf2 Imprinting Control Region Initiates Paternally Methylated Imprinting in Mouse Prospermatogonia

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-08-01 | GSE236417 | GEO

Loss of imprinting mutations define both distinct and overlapping roles for misexpression of IGF2 and H19 lncRNA

Project description:Imprinted genes occur in discrete clusters that are coordinately regulated by shared DNA elements. H19 and Igf2 are linked imprinted genes that play critical roles in development. Loss of imprinting at the IGF2/H19 locus is associated with Beckwith Wiedemann Syndrome (BWS). Here we use comprehensive genetic and genomic analyses to follow muscle development in a mouse model of BWS to dissect the separate and shared roles for Igf2 and H19 in the disease phenotype. We show that LOI results in defects in muscle differentiation and hypertrophy and we identify primary downstream targets of Igf2 (MAPK signaling) and of H19 (AKT/mTOR signaling). Moreover, we demonstrate instances where H19 and Igf2 misexpression work separately, cooperatively, and also antagonistically to establish the disease phenotype. This study underscores the fact that LOI phenotypes are multigenic and complex interactions contribute to disease outcomes.

2017-09-25 | GSE89136 | GEO

Functional antagonism between Mir483 and its host gene Igf2 in the control of developmental growth

Project description:Many mammalian microRNAs are embedded within introns of protein-coding genes, yet their functional relationship with the host gene is poorly understood. Here we identify Mir483, as having opposing developmental and physiological roles to those of its host gene, the paternally-expressed Igf2. Mechanistically, Mir483 expression is dependent on Igf2 transcription and the epigenetic regulation of the Igf2/H19 imprinting control region. Mir483 deletion in vivo resulted in normal growth, but induced distinct molecular signatures. Transgenic Mir483 overexpression in utero caused fetal, but not placental, growth restriction and cardiovascular defects leading to fetal demise. Overexpression of Mir483 postnatally resulted in growth stunting through IGF1 repression, increased hepatic lipid production, and excessive adiposity. IGF1 infusion rescued the post-natal growth restriction. Our data highlight a novel functional antagonism between a growth-suppressor microRNA and its growth-promoting host gene. We suggest that Mir483 was evolutionary co-opted to provide exquisite control of IGF signalling activity.

2024-09-12 | PXD051516 | Pride

CTCF-dependent chromatin bias constitutes transient epigenetic memory of the mother at the H19-Igf2 imprinting control region in prospermatogonia.

Project description:Genomic imprints-parental allele-specific DNA methylation marks at the differentially methylated regions (DMRs) of imprinted genes-are erased and reestablished in germ cells according to the individual's sex. Imprint establishment at paternally methylated germ line DMRs occurs in fetal male germ cells. In prospermatogonia, the two unmethylated alleles exhibit different rates of de novo methylation at the H19/Igf2 imprinting control region (ICR) depending on parental origin. We investigated the nature of this epigenetic memory using bisulfite sequencing and allele-specific ChIP-SNuPE assays. We found that the chromatin composition in fetal germ cells was biased at the ICR between the two alleles with the maternally inherited allele exhibiting more H3K4me3 and less H3K9me3 than the paternally inherited allele. We determined genetically that the chromatin bias, and also the delayed methylation establishment in the maternal allele, depended on functional CTCF insulator binding sites in the ICR. Our data suggest that, in primordial germ cells, maternally inherited allele-specific CTCF binding sets up allele-specific chromatin differences at the ICR. The erasure of these allele-specific chromatin marks is not complete before the process of de novo methylation imprint establishment begins. CTCF-dependent allele-specific chromatin composition imposes a maternal allele-specific delay on de novo methylation imprint establishment at the H19/Igf2 ICR in prospermatogonia.

| S-EPMC2991272 | biostudies-literature

MicroRNA expression profiling of Igf2-p and H19-m mutant mouse embryos

Project description:Changes in microRNA expression in Igf2-p and H19-m mouse embryos (E9.5) were determined in order to assess whether perturbation of miR-483* and miR-675 in Igf2-p and H19-m mutants was likely to have contributed to a modification of tumour phenotype. The Igf2 gene contains miR-483* but the targeted deletion of Igf2-p in these mice spares the region encoding this microRNA. The H19 gene contains miR-675 and its expression was mono-allelelic in heterozygous H19-m mice as evidenced by a significant reduction in miR-675 in these mice relative to WT.

2011-12-01 | E-MTAB-873 | biostudies-arrayexpress

Imprinting Affy

Project description:Murine long-term hematopoietic stem cells (HSCs), short-term HSCs and multipotent progenitor cells (MPPs) were isolated from bone marrow and expression profiled on Affy chips. The behavior of maternal-specific imprinting genes, particularly in the H19-Igf2 locus, was focused on, to see if any might be involved in maintaining quiescence of long-term stem cells.

2013-08-12 | E-MTAB-1644 | biostudies-arrayexpress

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