Role of CxxC-finger Protein 1 in the Establishment of Epigenetic Landscapes in Mouse Oocytes
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ABSTRACT:
PROVIDER: PRJNA669817 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12835300_1.fastq.gz | Fastqsanger.gz | |||
| SRR12835300_2.fastq.gz | Fastqsanger.gz | |||
| SRR12835301_1.fastq.gz | Fastqsanger.gz | |||
| SRR12835301_2.fastq.gz | Fastqsanger.gz | |||
| SRR12835302_1.fastq.gz | Fastqsanger.gz |
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Project description:During oogenesis, oocytes gain competence to accomplish meiotic maturation and prepare for embryonic development following fertilization. Trimethylated histone H3 on lysine-4 (H3K4me3) mediates a wide range of nuclear events during these processes. Oocyte-specific knockout of CxxC-finger protein 1 (CXXC1, also known as CFP1), the chromatin-binding subunit of SETD1 methyltransferase, impairs the H3K4me3 accumulation during murine oogenesis and caused changes in chromatin configurations. This study investigated the changes of genomic H3K4me3 landscapes in oocytes after Cxxc1 knockout, as well as the influences of H3K4me3 changes on other epigenetic marks including DNA methylation, H3K27me3, H2AK119ub1, and H3K36me3. Chromatin immunoprecipitation and sequencing results indicated that H3K4me3 is globally decreased after abolishing Cxxc1, including both the promoter region and the gene body. The results also demonstrate that CXXC1 and another histone H3 methyltransferase MLL2 have nonoverlapping roles in mediating H3K4 trimethylation during oogenesis. In addition, Cxxc1 deletion caused a significant decrease of DNA methylation level in oocytes, and affected H3K27me3 and H2AK119ub1 distributions in the maternal genome, particularly at the regions that have high DNA methylation levels. The changes of epigenetic networks caused by Cxxc1 deletion correlated with transcription changes of the genes in the corresponding genomic regions. Taken together, this study provided mechanistic explanations underlying the phenotypes and molecular defects in Cxxc1 deleted oocytes, and highlighted a role of CXXC1 in orchestrating multiple factors to build up the appropriate epigenetic states of maternal genome during oocyte maturation.
2021-02-04 | GSE159581 | GEO
Project description:CxxC-finger protein 1 regulates Treg fragility associated with H3K4me3 breadth
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Project description:During oogenesis, oocytes gain competence and subsequently undergo meiotic maturation and prepare for embryonic development; trimethylated histone H3 on lysine-4 (H3K4me3) mediates a wide range of nuclear events during these processes. Oocyte-specific knockout of CxxC-finger protein 1 (CXXC1, also known as CFP1) impairs H3K4me3 accumulation and causes changes in chromatin configurations. This study investigated the changes in genomic H3K4me3 landscapes in oocytes with Cxxc1 knockout and the effects on other epigenetic factors such as the DNA methylation, H3K27me3, H2AK119ub1 and H3K36me3. H3K4me3 is overall decreased after knocking out Cxxc1, including both the promoter region and the gene body. CXXC1 and MLL2, which is another histone H3 methyltransferase, have nonoverlapping roles in mediating H3K4 trimethylation during oogenesis. Cxxc1 deletion caused a decrease in DNA methylation levels and affected H3K27me3 and H2AK119ub1 distributions, particularly at regions with high DNA methylation levels. The changes in epigenetic networks implicated by Cxxc1 deletion were correlated with the transcriptional changes in genes in the corresponding genomic regions. This study elucidates the epigenetic changes underlying the phenotypes and molecular defects in oocytes with deleted Cxxc1 and highlights the role of CXXC1 in orchestrating multiple factors that are involved in establishing the appropriate epigenetic states of maternal genome.
| S-EPMC7969028 | biostudies-literature
Project description:A unique landscape of histone modifications is established during mouse oogenesis. For example, H3K4me3 forms noncanonically broad domains (ncH3K4me3) at intergenic regions in transcriptionally quiescent fully grown oocytes (FGOs), which are briefly transmitted to early embryos. How such a unique landscape of histone modification is established during oogenesis remains to be elucidated. Here we examine the distributions of histone H2A variants and the roles of H2A.Z in ncH3K4me3 establishment in mouse oocytes. We show that H2A.Z is broadly distributed at distal regions, along with ncH3K4me3, in FGOs, whereas H2A, H2A.X, and TH2A are evenly distributed throughout the genome. Temporal profiling of H2A.Z distributions during oocyte growth reveals that noncanonically broad H2A.Z (ncH2A.Z) is established at the end of oocyte growth, concomitantly with ncH3K4me3 establishment. Depletion of H2A.Z by oocyte-specific conditional double knockout of H2A.Z.1 and H2A.Z.2 impairs ncH3K4me3 establishment and meiotic progression, resembling Mll2 KO oocytes. Moreover, depletion of ncH3K4me3 also causes loss of ncH2A.Z in Mll2 KO FGOs, indicating that ncH2A.Z and ncH3K4me3 are mutually dependent. Thus, our study reveals the critical role of H2A.Z in proper establishment of the maternal epigenome and oocyte development.
2025-03-01 | GSE262044 | GEO
Project description:A unique landscape of histone modifications is established during mouse oogenesis. For example, H3K4me3 forms noncanonically broad domains (ncH3K4me3) at intergenic regions in transcriptionally quiescent fully grown oocytes (FGOs), which are briefly transmitted to early embryos. How such a unique landscape of histone modification is established during oogenesis remains to be elucidated. Here we examine the distributions of histone H2A variants and the roles of H2A.Z in ncH3K4me3 establishment in mouse oocytes. We show that H2A.Z is broadly distributed at distal regions, along with ncH3K4me3, in FGOs, whereas H2A, H2A.X, and TH2A are evenly distributed throughout the genome. Temporal profiling of H2A.Z distributions during oocyte growth reveals that noncanonically broad H2A.Z (ncH2A.Z) is established at the end of oocyte growth, concomitantly with ncH3K4me3 establishment. Depletion of H2A.Z by oocyte-specific conditional double knockout of H2A.Z.1 and H2A.Z.2 impairs ncH3K4me3 establishment and meiotic progression, resembling Mll2 KO oocytes. Moreover, depletion of ncH3K4me3 also causes loss of ncH2A.Z in Mll2 KO FGOs, indicating that ncH2A.Z and ncH3K4me3 are mutually dependent. Thus, our study reveals the critical role of H2A.Z in proper establishment of the maternal epigenome and oocyte development.
2025-03-01 | GSE262049 | GEO
Project description:Epigenetic initiation of the Th17 differentiation programme is promoted by Cxxc finger protein 1
| PRJNA546526 | ENA
Project description:IL-6/STAT3 signalling is known to initiate the Th17 differentiation programme, but the upstream regulatory mechanisms remain minimally explored. Here, we show that Cxxc finger protein 1 (Cxxc1) promoted the generation and stability of Th17 cells as an epigenetic regulator and prevented their differentiation into Treg cells. Mice with a T cell-specific deletion of Cxxc1 were protected from experimental autoimmune encephalomyelitis and were more susceptible to Citrobacter rodentium infection. Cxxc1-deficient T cells acquired a Treg cell-biased programme that dominantly suppressed Th17 cell generation via IL-6Rα production. Cxxc1 deficiency decreased IL-6Rα expression and impeded IL-6/STAT3 signalling, whereas the overexpression of IL-6Rα could reverse the defects seen in Cxxc1-deficient Th17 cells in vitro and in vivo. Genome-wide occupancy analysis revealed that Cxxc1 bound to Il6rα gene loci in the Th17 programme by maintaining the appropriate H3K4me3 modification of its promoter. Therefore, these data highlight that Cxxc1 as a key regulator governs the balance between Th17 and Treg cells by controlling the expression of IL-6Rα, which subsequently affects IL-6/STAT3 signalling and has a direct impact on Th17-related autoimmune diseases.
2020-04-10 | GSE132208 | GEO
Project description:CXXC finger protein 1 is critical for T cell intrathymic development through regulating H3K4 trimethylation
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Project description:The TET3 CXXC domain has unique DNA binding properties. It binds to DNA in a cytosine-dependent manner that prefers binding to CpG dinucleotides but is not restricted by the CpG-content, distinct from other well-characterized CXXC domains. To map the TET3 CXXC domain binding sites across the human genome, we purified the GST-tagged TET3 CXXC domain protein and performed the GST pull-down assay using the genomic DNA purified from HEK293T cells. The enriched DNA fragments were then sequenced and aligned to human genome(hg19). We used the GST pull-down assay followed by DNA deep sequencing to map the DNA bound by the TET3 CXXC domain in vitro.
2012-12-10 | E-GEOD-41551 | biostudies-arrayexpress
Project description:The TET3 CXXC domain has unique DNA binding properties. It binds to DNA in a cytosine-dependent manner that prefers binding to CpG dinucleotides but is not restricted by the CpG-content, distinct from other well-characterized CXXC domains. To map the TET3 CXXC domain binding sites across the human genome, we purified the GST-tagged TET3 CXXC domain protein and performed the GST pull-down assay using the genomic DNA purified from HEK293T cells. The enriched DNA fragments were then sequenced and aligned to human genome(hg19).
2012-12-10 | GSE41551 | GEO