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

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

PROVIDER: PRJNA1079671 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28065714.fastq.gz	Fastqsanger.gz
	SRR28065715.fastq.gz	Fastqsanger.gz
	SRR28065716.fastq.gz	Fastqsanger.gz
	SRR28065717.fastq.gz	Fastqsanger.gz
	SRR28065718.fastq.gz	Fastqsanger.gz

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

Project description:Foxp3-expressing regulatory T cells (Treg cells) play a central role in maintaining immune homeostasis and tolerance. Activation of Treg cells prevents various types of inflammatory responses. However, it remains unclear how the epigenetic program in Treg cells is maintained during the dynamic activation process. Here we show that Cxxc1 is associated with Foxp3 and positively regulates the expression of target genes at H3K4me3-enriched sites. Treg cell-specific ablation of Cxxc1 in mice resulted in a lethal inflammatory disease characterized by spontaneous T-cell activation. Cxxc1-deficient Treg cells showed reduced immunosuppressive capacity in vivo but also induced aberrant expression of genes associated with Treg fragility. Mechanistically, Cxxc1 promotes the accumulation of H3K4me3 in the broad domain of Ikzf4, suppressing the expression of fragile genes including IFN-γ, and Ikzf4 expression partially restores Treg function.

2025-03-29 | GSE256436 | GEO

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

Interferon-γ drives T reg fragility to promote anti-tumor immunity

Project description:Regulatory T cells (Tregs) are a barrier to effective anti-tumor immunity. Neuropilin-1 (Nrp1) is required to maintain intratumoral Treg stability and function but is dispensable for peripheral immune homeostasis, Treg-restricted Nrp1 deletion in mice results in profound tumor resistant due to Treg functional fragility. Drivers of Treg fragility, the mechanistic basis of Nrp1 dependency, and the relevance of these processes for human cancer and immunotherapy remain unknown. NRP1 expression on human Tregs in melanoma and HNSCC was highly heterogeneous and correlated with prognosis. Using a mouse model of melanoma in which mutant Nrp1-deficient (Nrp1–/–) and wild type (WT) Tregs could be assessed in a competitive environment, we found that a high proportion of intratumoral Nrp1–/– Tregs produce interferon-γ (IFNγ), which in turn drove the fragility of surrounding WT Tregs, boosting anti-tumor immunity and facilitating tumor clearance. We also show that IFNγ-induced Treg fragility is required for an effective response to PD1 immunotherapy, suggesting that cancer therapies promoting Treg fragility may be efficacious .

2017-05-22 | GSE97939 | GEO

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 finger protein 1 maintains homeostasis and function of intestinal group 3 innate lymphoid cells with aging [H3K4me3]

Project description:Cxxc finger protein 1 maintains homeostasis and function of intestinal group 3 innate lymphoid cells with aging [H3K4me3]

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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

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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

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

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

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