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Chromatin repression by PRC2 results in reduced gene expression driving key features of CD8 T cell exhaustion [Cut & Run]

ABSTRACT: Chromatin repression by PRC2 results in reduced gene expression driving key features of CD8 T cell exhaustion [Cut & Run]

PROVIDER: PRJNA1100421 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28681846_1.fastq.gz	Fastqsanger.gz
	SRR28681846_2.fastq.gz	Fastqsanger.gz
	SRR28681847_1.fastq.gz	Fastqsanger.gz
	SRR28681847_2.fastq.gz	Fastqsanger.gz
	SRR28681848_1.fastq.gz	Fastqsanger.gz

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Chromatin repression by PRC2 results in reduced gene expression driving key features of CD8 T cell exhaustion [Cut & Run]

Project description:Exhausted CD8 T cells result from chronic antigen stimulation and have reduced ability to clear disease. The epigenetic regulation of the dysfunctional phenotype of exhausted CD8 T cells is a promising avenue for therapies aimed at reversing or preventing CD8 T cell exhaustion. Here, utilizing an in vitro model, we show global increase of the repressive histone modification H3K27me3 in CD8 T cell exhaustion as well as increased gene expression of the subunits of PRC2, the complex responsible for H3K27me3 deposition. H3K27me3 correlated with decreased gene expression and localized to naïve/memory T cell genes in CD8 T cell exhaustion. PRC2 inhibition increased expression of many of these naïve/memory genes while reducing expression of key exhaustion genes. Further, we identified potential enhancers and transcription factors predicted to promote expression of the PRC2 subunits. Our study highlights the importance of the repressive epigenetic landscape of exhausted CD8 T cells as well as a novel role for PRC2 in T cell biology.

2024-10-31 | GSE263937 | GEO

Chromatin repression by PRC2 results in reduced gene expression driving key features of CD8 T cell exhaustion [RNA-seq]

2024-10-31 | GSE263885 | GEO

Chromatin repression by PRC2 results in reduced gene expression driving key features of CD8 T cell exhaustion

Project description:Chromatin repression by PRC2 results in reduced gene expression driving key features of CD8 T cell exhaustion

| PRJNA1100417 | ENA

Chromatin repression by PRC2 results in reduced gene expression driving key features of CD8 T cell exhaustion [RNA-seq]

Project description:Chromatin repression by PRC2 results in reduced gene expression driving key features of CD8 T cell exhaustion [RNA-seq]

| PRJNA1099680 | ENA

Chromatin repression by PRC2 results in reduced gene expression driving key features of CD8 T cell exhaustion

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

2024-10-31 | GSE263938 | GEO

PRC2

Project description:PRC2

| PRJNA761389 | ENA

Reduced PRC2 function alters male germline epigenetic programming and paternal inheritance.

Project description:Background: Defining the mechanisms that establish and regulate the transmission of epigenetic information from parent to offspring is critical for understanding disease heredity. Currently, the molecular pathways that regulate epigenetic information in the germline and its transmission to offspring are poorly understood. Results: Here we provide evidence that Polycomb Repressive Complex 2 (PRC2) regulates paternal inheritance, both at the phenotypic and molecular levels. Reduced PRC2 function in mice resulted in male sub-fertility and altered epigenetic and transcriptional control of retrotransposed elements in fetal male germ cells. Males with reduced PRC2 function produced offspring that over-expressed retrotransposed pseudogenes and had altered preimplantation embryo cleavage rates and cell cycle control. Conclusion: This study reveals a novel role for the histone modifying complex, PRC2, in epigenetic inheritance, with important implications for understanding disease inheritance.

2018-02-15 | GSE110529 | GEO

EZH2 inhibition results in genome-wide PRC2 redistribution in cancer cell models

Project description:Upon EZH2 inhibitor treatment, PRC2 components EZH2 and SUZ12 are redistributed across the genome towards a small number of genomic loci that are refractory to H3K27me3 loss. Focal PRC2 accumulation and H3K27me3 retention occur primarily at CpG islands and transcription start sites of genes, with enrichment at canonical PRC2 nucleation sites. EZH2 and SUZ12 are present at low levels at actively transcribed TSSs, and this signal is lost with EZH2 inhibition.

2019-08-09 | GSE134136 | GEO

PRC2-mediated repression is essential to maintain identity and function of differentiated dopaminergic and serotonergic neurons [snRNA-Seq]

Project description:Neurons of the CNS must maintain their distinct identity over an entire lifespan. Apart from instructive information provided by transcription factors driving neuron specific genes, other gene programs need to be permanently silenced. The mechanisms governing enduring gene-silencing in neurons are largely unknown, as are the consequences if they fail. Here we show that loss of the Polycomb repressive complex 2 (PRC2) obligate unit Eed in differentiated murine midbrain dopamine (mDA) neurons resulted in progressive loss of the H3K27me3 histone modification followed by upregulation of PRC2 targets, also highly enriched for the constitutive heterochromatin H3K9me3 modification. This was followed by reduced expression of mDA neuron-identity genes, particularly evident in the Substantia nigra pars compacta. Consequently, mDA-neuronal function was severely disrupted, causing parkinsonian-like motor skill deficits. Deletion of Eed in differentiated serotonergic (5HT) neurons resulted in a similar upregulation of PRC2-targets and reduced expression of genes defining 5HT neurons, which promoted loss of serotonergic identity followed by loss of function and altered behaviour. Overall, our results reveal that PRC2 inactivation leads to a selective and progressive loss of mDA or 5HT neuronal identity and function, but not to any loss of cells. Thus, our study shows that PRC2-dependent maintenance of neuronal identity is essential and safeguards against expression of other non-relevant gene programs and loss of neuronal function.

2022-07-11 | GSE189329 | GEO

PRC2-mediated repression is essential to maintain identity and function of differentiated dopaminergic and serotonergic neurons [ChIP-Seq]

2022-07-11 | GSE189017 | GEO