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CxxC Finger Protein 1-mediated Histone H3 Lysine-4 Trimethylation is Essential for Proper Meiotic Crossover Formation in Mice

ABSTRACT: CxxC Finger Protein 1-mediated Histone H3 Lysine-4 Trimethylation is Essential for Proper Meiotic Crossover Formation in Mice

PROVIDER: PRJNA552071 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9624100_1.fastq.gz	Fastqsanger.gz
	SRR9624100_2.fastq.gz	Fastqsanger.gz
	SRR9624110_1.fastq.gz	Fastqsanger.gz
	SRR9624110_2.fastq.gz	Fastqsanger.gz
	SRR9624101_1.fastq.gz	Fastqsanger.gz

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CxxC Finger Protein 1-mediated Histone H3 Lysine-4 Trimethylation is Essential for Proper Meiotic Crossover Formation in Mice

Project description:CXXC finger protein 1 (Cfp1) is a DNA-binding component of the SETD1 methyltransferase complex, targets SETD1A/B to most CpG islands (CpGI), and mediates the generation of H3K4me3. Deficiency of CFP1 in mice leads to pre-implantation lethality. Previous data suggest an indispensable role of CFP1 in germ cell development and meiosis. However, it remains unclear if CFP1-mediated H3K4 trimethylation is also required for the earliest stages of meiosis in both male and female germ cells. Here, we revealed that Cxxc1 deletion caused a decrease of H3K4me3 levels in spermatocytes after the zygotene stage, impaired double strand breaks (DSBs) repairing, and crossover formation in meiotic prophase. As the results, Cxxc1-deleted spermatocytes failed to complete meiosis and were arrested at the meiosis II. ChIP-seq results revealed that H3K4me3 globally descreased at transcriptional start sites in Cxxc1-null spermatocytes at the leptotene/zygotene and pathytene stages.RNA-seq at different stages revealed an earlier expression of genes within the spermatogenesis pathway in Cxxc1-null spermatocytes. These results indicated that CFP1 is required for H3K4me3 accumulation at the gene promoters of male germ cells and play a key role in regulating programed gene expression that is essential for spermatogenesis.

2020-03-11 | GSE133636 | GEO

CXXC finger protein 1 is critical for T cell intrathymic development through regulating H3K4 trimethylation

Project description:CXXC finger protein 1 is critical for T cell intrathymic development through regulating H3K4 trimethylation

| PRJNA317542 | ENA

CxxC-finger protein 1 regulates Treg fragility associated with H3K4me3 breadth

Project description:CxxC-finger protein 1 regulates Treg fragility associated with H3K4me3 breadth

| PRJNA1079671 | ENA

Role of CxxC-finger Protein 1 in the Establishment of Epigenetic Landscapes in Mouse Oocytes

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

CXXC finger protein 1 is critical for T-cell intrathymic development through regulating H3K4 trimethylation.

Project description: Not available

| S-EPMC4879243 | biostudies-literature

Epigenetic initiation of the Th17 differentiation programme is promoted by Cxxc finger protein 1

Project description:Epigenetic initiation of the Th17 differentiation programme is promoted by Cxxc finger protein 1

| PRJNA546526 | ENA

CXXC zinc finger protein 1 (Cfp1) controls cardiomyocyte maturation by modifying histone H3K4me3 of structural, metabolic, and contractile related genes

Project description:Cardiomyocyte maturation is the final stage of heart development, and abnormal cardiomyocyte maturation will lead to serious heart diseases. CXXC zinc finger protein 1 (Cfp1) is an important epigenetic factor, which plays an essential role in the development and maturation of multi-lineage cells, while its effect on the maturation of cardiomyocyte remains unclear. This study was performed to explore the potential role of Cfp1 in cardiomyocyte maturation of heart and the underlying mechanisms. Cardiomyocyte-specific Cfp1 knockout (Cfp1-cKO) mice died within 4 weeks of birth. Cardiomyocytes from Cfp1-cKO mice showed an inhibited maturation phenotype in structure, metabolism, contractile function, and cell cycle, accompanied by down-regulation of adult genes and up-regulation of fetal genes. In contrast, cardiomyocyte-specific Cfp1 transgenic (Cfp1-TG) mice and human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) overexpressing Cfp1 showed a more mature phenotype. Mechanistically, deficiency of Cfp1 results in reduced trimethylation on lysine 4 of histone H3 (H3K4me3) modification and formation of ectopic H3K4me3. Moreover, Cfp1 deletion decreased the level of H3K4me3 modification in adult genes and increased the level of H3K4me3 modification in fetal genes. Collectively, Cfp1 modulates the expression of cardiomyocyte maturation related genes by modulating histone H3K4me3 modification, which in turn regulates cardiomyocyte maturation. This study implicates Cfp1 as an important molecule regulating cardiomyocyte maturation, and its dysfunction is strongly associated with cardiac disease.

2024-03-27 | GSE240852 | GEO

CXXC zinc finger protein 1 (Cfp1) controls cardiomyocyte maturation by modifying histone H3K4me3 of structural, metabolic, and contractile related genes (ChIP-Seq)

2024-03-27 | GSE241021 | GEO

Role of CxxC-finger Protein 1 in the Establishment of Epigenetic Landscapes in Mouse Oocytes

Project description:Role of CxxC-finger Protein 1 in the Establishment of Epigenetic Landscapes in Mouse Oocytes

| PRJNA669817 | ENA

Epigenetic initiation of the Th17 differentiation programme is promoted by Cxxc finger protein 1

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

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