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Context-specific requirements of Tet enzymes in the modulation of CD8 effector and memory cell fates during acute viral infection [ATAC-seq]

ABSTRACT: Context-specific requirements of Tet enzymes in the modulation of CD8 effector and memory cell fates during acute viral infection [ATAC-seq]

PROVIDER: PRJNA1061311 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27432217_1.fastq.gz	Fastqsanger.gz
	SRR27432217_2.fastq.gz	Fastqsanger.gz
	SRR27432218_1.fastq.gz	Fastqsanger.gz
	SRR27432218_2.fastq.gz	Fastqsanger.gz
	SRR27432219_1.fastq.gz	Fastqsanger.gz

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Context-specific requirements of Tet enzymes in the modulation of CD8 effector and memory cell fates during acute viral infection

Project description:Context-specific requirements of Tet enzymes in the modulation of CD8 effector and memory cell fates during acute viral infection

| PRJNA1061307 | ENA

Context-specific requirements of Tet enzymes in the modulation of CD8 effector and memory cell fates during acute viral infection [EM-seq]

Project description:Context-specific requirements of Tet enzymes in the modulation of CD8 effector and memory cell fates during acute viral infection [EM-seq]

| PRJNA1061313 | ENA

Context-specific requirements of Tet enzymes in the modulation of CD8 effector and memory cell fates during acute viral infection [Cut&Tag]

Project description:Context-specific requirements of Tet enzymes in the modulation of CD8 effector and memory cell fates during acute viral infection [Cut&Tag]

| PRJNA1061310 | ENA

Context-specific requirements of Tet enzymes in the modulation of CD8 effector and memory cell fates during acute viral infection [Cut&Tag]

Project description:In response to infections, naïve CD8 T cells give rise effector and memory T cells. However, eliciting long-lived memory CD8T cells remains a challenge for many infections. DNA demethylation of cytosines within CpG dinucleotides by Tet enzymes is a key epigenetic mechanism that regulate transcriptional programs. However, their roles in CD8 T cell memory differentiation is unclear. We report that following viral infection, Tet1/3-deficient CD8 T cells preferentially differentiate into short-lived effectors and effector memory cells. Using genome-wide DNA methylation and mice, in which Tet1/3 were ablated during T cell development and in mature CD8 T cells, respectively, we established that Tet1/3 regulate these cell fates by licensing the chromatin landscape of genes downstream of T cell receptor signaling during thymic T cell maturation. These findings unveil the context-specific roles of DNA demethylation, which is essential for defining pathways that contribute to CD8 memory T cell generation against infectious diseases.

2025-04-01 | GSE252582 | GEO

Context-specific requirements of Tet enzymes in the modulation of CD8 effector and memory cell fates during acute viral infection [EM-seq]

2025-04-01 | GSE252581 | GEO

Context-specific requirements of Tet enzymes in the modulation of CD8 effector and memory cell fates during acute viral infection [ATAC-seq]

2025-04-01 | GSE252580 | GEO

Tet enzymes are essential for embryogenesis and completion of embryonic genome activation

Project description:Mammalian embryo development begins in transcriptional silence followed by activation of thousands of genes. Reprogramming of DNA methylation is integral to embryogenesis and linked to Tet enzymes; however, their function in early development is not fully understood. Here, we generated combined deficiencies of all three Tet enzymes in mouse oocytes and observed arrest at 2-cell stage with the most severe phenotype linked to Tet2. Gene expression analysis revealed that Tet enzymes are required for completion of embryonic genome activation. Our results demonstrate that Tet enzymes have non-redundant roles and are key components of EGA in mammalian embryos.

2021-11-22 | GSE57063 | GEO

Loss of Tet enzymes compromises proper differentiation of embryonic stem cells

Project description:Tet enzymes (Tet1/2/3) catalyze the conversion of 5-methylcytosine (5mC) to 5-hydroxy-methylcytosine (5hmC) and are dynamically expressed in various embryonic and adult cell types. While loss of individual Tet enzymes or combined deficiency of Tet1/2 allows for embryogenesis, the effect of complete loss of Tet activity and 5hmC marks in development has not been established. To define the role of Tet enzymes and 5hmC in development we have generated Tet1, Tet2 and Tet3 triple knockout (TKO) mouse embryonic stem cells (ESCs) and examined their developmental potential in vitro and in vivo. Combined deficiency of all three Tet enzymes led to complete depletion of 5hmC and impaired ESC differentiation as seen in poorly differentiated TKO embryoid bodies and teratomas. Consistent with impaired differentiation, TKO ES cells exhibited limited contribution to the chimeric embryos and could not support embryonic development in tetraploid complementation assays. Gene expression profiles and genome wide methylome analyses of TKO embryoid bodies revealed promoter hypermethylation and deregulation of genes implicated in embryonic development and differentiation. These findings suggest a requirement for Tet and 5hmC-mediated DNA demethylation in proper regulation of gene expression during differentiation of embryonic stem cells and development. Methylation patterns in tissue samples from a series of wt and Tet1/Tet2 DKO embryos, neonates and adults were generated using ethylated DNA immunoprecipitation with antibodies against 5mC (MeDIP) and 5hmC (hMeDIP) followed by deep sequencing.

2014-04-17 | E-GEOD-55049 | biostudies-arrayexpress

Loss of Tet enzymes compromises proper differentiation of embryonic stem cells

2014-04-17 | GSE55049 | GEO

Tet enzymes are required for mammalian embryonic hematopoiesis

Project description:In this study we have examined the role of Tet enzymes in regulation of embryonic Endothelial cells (ECs) and Hematopoietic stem and progenitor cells (HSPCs). We have performed transcriptomic and methylation analyses of Tet deficient and wild type ECs and HSPCs isolated from E11.5 embryonic aorta-gonad-mesonephros (AGM) to identify differentially expressed genes and differentially methylated regions.

2022-02-19 | GSE176391 | GEO

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