RNAseq profiling of mouse wild-type and Uhrf1-/- E9.5 embryos
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE309704 | GEO | 2026/08/24
REPOSITORIES: GEO
Similar Datasets
Project description:UHRF1 is a chromatin-binding protein essential for maintaining DNA methylation and histone modification states, yet its integrated role in vivo remains incompletely understood. To define its function, we generated conditional Uhrf1 knockout embryonic stem cells (ESCs) and embryos. Uhrf1⁻/⁻ ESCs exhibited near-complete loss of 5mC and 5hmC but maintained pluripotency, whereas Uhrf1-null embryos developed normally until E8.5 and then failed to further develop by E9.5.
2026-08-24 | GSE309737 | GEO
Project description:UHRF1 is a chromatin-binding protein essential for maintaining DNA methylation and histone modification states, yet its integrated role in vivo remains incompletely understood. To define its function, we generated conditional Uhrf1 knockout embryonic stem cells (ESCs) and embryos. Uhrf1⁻/⁻ ESCs exhibited near-complete loss of 5mC and 5hmC but maintained pluripotency, whereas Uhrf1-null embryos developed normally until E8.5 and then failed to further develop by E9.5.
2026-03-21 | GSE312765 | GEO
Project description:UHRF1 is a chromatin-binding protein essential for maintaining DNA methylation and histone modification states, yet its integrated role in vivo remains incompletely understood. To define its function, we generated conditional Uhrf1 knockout embryonic stem cells (ESCs) and embryos. Uhrf1⁻/⁻ ESCs exhibited near-complete loss of 5mC and 5hmC but maintained pluripotency, whereas Uhrf1-null embryos developed normally until E8.5 and then failed to further develop by E9.5, phenocopying Dnmt1 loss. Single-cell multi-omic (ME-seq) profiling of E8.5 embryos revealed impaired lineage stabilization, widespread hypomethylation, and disrupted chromatin architecture. Uhrf1 loss predicted altered CTCF occupancy, accompanied with disorganized enhancer-promoter interactions, and defective Bmp signaling, particularly within neural crest populations. These findings identify Uhrf1 as a central regulator tightly coupling DNA methylation maintenance to 3D genome organization during gastrulation to direct early lineage specification, positioning Uhrf1 as a pivotal mediator of epigenetic information transfer during early embryogenesis.
2026-03-15 | GSE308175 | GEO
Project description:UHRF1 is a chromatin-binding protein essential for maintaining DNA methylation and histone modification states, yet its integrated role in vivo remains incompletely understood. To define its function, we generated conditional Uhrf1 knockout embryonic stem cells (ESCs) and embryos. Uhrf1⁻/⁻ ESCs exhibited near-complete loss of 5mC and 5hmC but maintained pluripotency, whereas Uhrf1-null embryos developed normally until E8.5 and then failed to further develop by E9.5, phenocopying Dnmt1 loss. Single-cell multi-omic (ME-seq) profiling of E8.5 embryos revealed impaired lineage stabilization, widespread hypomethylation, and disrupted chromatin architecture. Uhrf1 loss predicted altered CTCF occupancy, accompanied with disorganized enhancer-promoter interactions, and defective Bmp signaling, particularly within neural crest populations. These findings identify Uhrf1 as a central regulator tightly coupling DNA methylation maintenance to 3D genome organization during gastrulation to direct early lineage specification, positioning Uhrf1 as a pivotal mediator of epigenetic information transfer during early embryogenesis.
2026-08-25 | GSE337739 | GEO
Project description:RNAseq profiling of mouse wild-type and Uhrf1-/- E9.5 embryos
| PRJNA1336778 | ENA
Project description:RNAseq profiling of mouse wild-type and Uhrf1-/- E9.5 embryonic stem cells (ESCs)
| PRJNA1336819 | ENA
Project description:Tet enzymes (Tet1/2/3) convert 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC). Tet1 and Tet2 mediate 5hmC generation in mouse embryonic stem cells (ESCs) and various embryonic and adult tissues. To investigate the effects of combined deficiency of Tet1 and Tet2 on pluripotency and development, we have generated Tet1 and Tet2 double knockout (DKO) ESCs and mice. DKO ESCs were depleted of 5hmC, but remained pluripotent with subtle defects in differentiation and changes in gene expression. Double mutant embryos and chimeras exhibited mid-gestation defects and postnatal DKO mice displayed partially penetrant neonatal lethality and stochastic perturbation of imprinting. Viable DKO animals developed normally to adulthood but had reduced 5hmC level, increased 5mC level and lacked 5hmC in germ cells. Nevertheless, DKO mice of both sexes were fertile with females having smaller ovaries and reduced fertility. Our data suggest that both Tet1 and Tet2 contribute to 5hmC levels during development. Their combined loss does not block differentiation and embryogenesis, but leads to partially penetrant embryonic and perinatal abnormalities and compromised viability. Moreover, the presence of substantial levels of 5hmC in DKO embryos and adult mice suggests a significant contribution of Tet3 in hydroxylation of 5mC during development. Methylation patterns in tissue samples from a series of wt and Tet1/Tet2 DKO embryos, neonates and adults were generated using methylated DNA immunoprecipitation with antibodies against 5mC (MeDIP) and 5hmC (hMeDIP) followed by deep sequencing.
2013-02-01 | E-GEOD-42396 | biostudies-arrayexpress
Project description:Tet enzymes (Tet1/2/3) convert 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC). Tet1 and Tet2 mediate 5hmC generation in mouse embryonic stem cells (ESCs) and various embryonic and adult tissues. To investigate the effects of combined deficiency of Tet1 and Tet2 on pluripotency and development, we have generated Tet1 and Tet2 double knockout (DKO) ESCs and mice. DKO ESCs were depleted of 5hmC, but remained pluripotent with subtle defects in differentiation and changes in gene expression. Double mutant embryos and chimeras exhibited mid-gestation defects and postnatal DKO mice displayed partially penetrant neonatal lethality and stochastic perturbation of imprinting. Viable DKO animals developed normally to adulthood but had reduced 5hmC level, increased 5mC level and lacked 5hmC in germ cells. Nevertheless, DKO mice of both sexes were fertile with females having smaller ovaries and reduced fertility. Our data suggest that both Tet1 and Tet2 contribute to 5hmC levels during development. Their combined loss does not block differentiation and embryogenesis, but leads to partially penetrant embryonic and perinatal abnormalities and compromised viability. Moreover, the presence of substantial levels of 5hmC in DKO embryos and adult mice suggests a significant contribution of Tet3 in hydroxylation of 5mC during development.
2013-02-01 | GSE42396 | GEO
Project description:UHRF1 (Ubiquitin-like, containing PHD and RING finger domains, 1) recruits DNMT1 to hemimethylated DNA during replication, is essential for maintaining DNA methylation patterns during cell division and is suggested to direct additional repressive epigenetic marks. Uhrf1 mutation in zebrafish results in multiple embryonic defects including failed hepatic outgrowth, but the epigenetic basis of these phenotypes is not known. We find that DNA methylation is the only epigenetic mark that is depleted in uhrf1 mutants and make the surprising finding that despite the reduced organ size in uhrf1 mutants, genes regulating DNA replication and S-phase progression were highly upregulated. Further, there is a striking increase in BrdU incorporation in uhrf1 mutant cells, and they retained BrdU labeling over several days, indicating they are arrested in S-phase. Moreover, some of the label retaining nuclei co-localized with TUNEL positive nuclei, suggesting that arrested cells are responsible for apoptosis. Importantly, dnmt1 mutation phenocopies the S-phase arrest and hepatic outgrowth defects in uhrf1 mutants and Dnmt1 knock-down enhances the uhrf1 hepatic phenotype. Together, these data indicate that DNA hypomethylation is sufficient to generate the uhrf1 mutant phenotype by promoting an S-phase arrest. We thus propose that cell cycle arrest is a mechanism to restrict propagation of epigenetically deranged cells during embryogenesis. Genome-wide expression profiling was performed on 2 uhrf1 mutant and 2 wildtype zebrafish larvae (120 hours post fertilization) by using Zebrafish Genome Array (Affymetrix) according to manufacturer's instruction.
2015-02-09 | E-GEOD-55339 | biostudies-arrayexpress
Project description:Genomic imprinting is a important biological process, which leads to parental specific gene expressions. Improper gene imprinting results in several developmental abnormalities, cancer and other diseases. Studies in mice indicated genomic imprinting establishment relied on parental allele-specific DNA methylation during gametogenesis. Despite the fact that genomic imprinting is highly conserved in mammalian, the species specific pattern exists. Until now, except that of in mouse, informations about imprinting patterns is little, especially in primates. Through generation genome-wide 5mC and 5hmC profiles for two types of haploid genomes from rhesus monkeys, including parthenogenetic haploid ESCs ( PG ha ESCs) (derived from rhesus monkey parthenogenetic embryos) and sperms. We clearly characterized and distinguished methylome (5mC) from hydroxymethylome (5hmC)(which can not discriminate from methylome in traditional bisulfite (BS) sequencing) in haploid genomes. Based on these information, we determined distribution patterns of 5mC and 5hmC in ha ESCs and sperms. Interestingly, both 5hmC levels and distribution patterns were similar in ha ESCs and sperms, and 5hmC which is enriched in the regions with low 5mC frequency. Meanwhile through comparing DNA methylation and hydroxymethylation status between sperms and ha ESCs, we first provided a fundamental information of monkey imprinted differentially methylated regions (DMRs) distribution in monkey chromosomes. Second, we observed that DMRs did not overlap with hydroxymethylated regions (DMR or DhMR), suggesting that establishment of imprinted regions was not interfered by 5hmC. Our results demonstrate DNA methylation profiling of PG ha ESCs and sperms can be uesed as a powerful and effective method to map and characterize imprinted regions in non-human primates genome.
2016-12-08 | GSE75817 | GEO