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

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

PROVIDER: PRJNA317542 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3341011.fastq.gz	Fastqsanger.gz
	SRR3341012.fastq.gz	Fastqsanger.gz
	SRR3341003.fastq.gz	Fastqsanger.gz
	SRR3341004.fastq.gz	Fastqsanger.gz
	SRR3341005.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

Project description:T-cell development in the thymus is largely controlled by an epigenetic program, involving in both DNA methylation and histone modifications. Previous studies have identified Cxxc1 as a regulator of both cytosine methylation and histone 3 lysine 4 trimethylation (H3K4me3). However, it is unknown whether Cxxc1 plays a role in thymocyte development. Here we show that T-cell development in the thymus is severely impaired in Cxxc1-deficient mice. Furthermore, we identify genome-wide Cxxc1-binding sites and H3K4me3 modification sites in wild-type and Cxxc1-deficient thymocytes. Our results demonstrate that Cxxc1 directly controls the expression of key genes important for thymocyte survival such as ROR?t and for T-cell receptor signalling including Zap70 and CD8, through maintaining the appropriate H3K4me3 on their promoters. Importantly, we show that ROR?t, a direct target of Cxxc1, can rescue the survival defects in Cxxc1-deficient thymocytes. Our data strongly support a critical role of Cxxc1 in thymocyte development.

| S-EPMC4879243 | biostudies-literature

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 [ChIP-Seq]

Project description:T cell development in the thymus is largely controlled by an epigenetic program involving in both DNA methylation and histone modifications. Previous studies have identified Cxxc1 as a regulator of both cytosine methylation and histone 3 lysine 4 trimethylation (H3K4me3). However, it is unknown whether Cxxc1 plays a role in thymocyte development. Here we show that T cell development in the thymus is severely impaired in Cxxc1-deficient mice. Furthermore, we identify genome-wide Cxxc1 binding sites and H3K4me3 modification sites in wild-type and Cxxc1-deficient thymocytes. Our results demonstrate that Cxxc1 directly controls the expression of key genes important for thymocyte survival such as RORγt and for TCR signaling including Zap70 and CD8, through maintaining the appropriate H3K4me3 on their promoters. Importantly, we show that RORγt, a direct target of Cxxc1, can rescue the survival defects in Cxxc1-deficient thymocytes. Our data strongly support a critical role of Cxxc1 in thymocyte development.

2016-04-14 | GSE79974 | GEO

CXXC finger protein 1 is critical for T cell intrathymic development through regulating H3K4 trimethylation [RNA-Seq]

2016-04-14 | GSE79975 | GEO

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

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-04-14 | E-GEOD-79976 | biostudies-arrayexpress

Mus musculus

Project description:CXXC finger protein 1 is critical for T cell intrathymic development through regulating H3K4 trimethylation [RNA-Seq]

| PRJNA317545 | ENA

Mus musculus

Project description:CXXC finger protein 1 is critical for T cell intrathymic development through regulating H3K4 trimethylation [ChIP-Seq]

| PRJNA317546 | ENA

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

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

2016-04-14 | GSE79976 | GEO

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

| PRJNA552071 | 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

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