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

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

PROVIDER: PRJNA546526 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9202910_1.fastq.gz	Fastqsanger.gz
	SRR9202910_2.fastq.gz	Fastqsanger.gz
	SRR9202911_1.fastq.gz	Fastqsanger.gz
	SRR9202911_2.fastq.gz	Fastqsanger.gz
	SRR9202912_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

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

| PRJNA522968 | ENA

Epigenetic initiation of the TH17 differentiation program is promoted by Cxxc finger protein 1.

Project description:IL-6/STAT3 signaling is known to initiate the TH17 differentiation program, but the upstream regulatory mechanisms remain minimally explored. Here, we show that Cxxc finger protein 1 (Cxxc1) promoted the generation 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 deficiency decreased IL-6R? expression and impeded IL-6/STAT3 signaling, whereas the overexpression of IL-6R? could partially reverse the defects in Cxxc1-deficient TH17 cells in vitro and in vivo. Genome-wide occupancy analysis revealed that Cxxc1 bound to Il6r? gene loci 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-6R?, which affects IL-6/STAT3 signaling and has an impact on TH17-related autoimmune diseases.

| S-EPMC6785255 | biostudies-literature

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

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

Genome-wide mapping of the TET3 CXXC domain binding sites

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

Genome-wide mapping of the TET3 CXXC domain binding sites

2012-12-10 | GSE41551 | GEO

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 maintains homeostasis and function of intestinal group 3 innate lymphoid cells with aging

Project description:Cxxc finger protein 1 maintains homeostasis and function of intestinal group 3 innate lymphoid cells with aging

| PRJNA864756 | ENA

Cxxc finger protein 1 maintains homeostasis and function of intestinal group 3 innate lymphoid cells with aging

Project description:Cxxc finger protein 1 maintains homeostasis and function of intestinal group 3 innate lymphoid cells with aging

| PRJNA860836 | ENA