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PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells

ABSTRACT: PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells

PROVIDER: PRJNA776519 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16597300_1.fastq.gz	Fastqsanger.gz
	SRR16597300_2.fastq.gz	Fastqsanger.gz
	SRR16597301_1.fastq.gz	Fastqsanger.gz
	SRR16597301_2.fastq.gz	Fastqsanger.gz
	SRR16597302_1.fastq.gz	Fastqsanger.gz

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PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells [scRNA-seq]

Project description:Protein arginine methyltransferase 5 (PRMT5) participates in symmetric dimethylation of arginine residues of proteins and contributes to a wide range of biological processes. But how PRMT5 affects the transcriptional and epigenetic programs involved in the establishment and maintenance of T cell subsets differentiation and roles in antitumor immunity are still incompletely understood. Here, using the single cell RNA sequencing, CHIP-sequencing and bulk RNA sequencing, we found that mice T cell-specific deletion of PRMT5 had greater effects on CD8+ than CD4+ T cells development, enforcing CD8+ T cells differentiation into Klrg1+ terminal effector cells. Mechanically, T cells deficiency of PRMT5 activated Prdm1 by decreasing H4R3me2s and H3R8me2s deposition on its loci, which promote differentiation of Klrg1+CD8+ T cells. Furthermore, effector CD8+ T cells that transited into memory precursor cells were decreased in PRMT5 deficiency T cells thus caused dramatic CD8+ T cells death.

2021-11-02 | GSE186699 | GEO

PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells [RNA-seq]

2021-11-02 | GSE186851 | GEO

PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells [CHIP-seq]

2021-11-02 | GSE186850 | GEO

PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells [CHIP-seq]

Project description:PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells [CHIP-seq]

| PRJNA776287 | ENA

PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells [RNA-seq]

Project description:PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells [RNA-seq]

| PRJNA776290 | ENA

PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells [scRNA-seq]

Project description:PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells [scRNA-seq]

| PRJNA775082 | ENA

PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells

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

2021-11-01 | GSE186863 | GEO

RNA-sequencing of three murine memory CD8 T cell subsets: IL-7Rα+KLRG1- , IL-7Rα+KLRG1+, and IL-7Rα-KLRG1+

Project description:The goal of this study is to characterize the transcriptional profile of three memory CD8 T cell subsets: IL-7Rα+KLRG1- (memory precursors, MP), IL-7Rα+KLRG1+ (KLRG1+ MP) and IL-7Rα-KLRG1+ (terminal effectors, TE).

2022-12-12 | GSE218777 | GEO

KLRG1+ Memory CD8 T cells Combine Properties of Short-lived Effectors and Long-lived Memory

Project description:CD8 effector T cells with a CD127hi KLRG1- phenotype are considered precursors to the long-lived memory pool, while KLRG1+ CD127low cells are viewed as short-lived effectors. Nevertheless, we and others have shown that a KLRG1+ CD127low population persists into the memory phase and that these T cells (termed long-lived effector cells or LLEC) display robust protective function during acute re-challenge with bacteria or viruses. Whether these T cells represent a true memory population or are instead a remnant effector cell population that failed to undergo initial contraction has remained unclear. Here, we show that LLEC from mice express a distinct phenotypic and transcriptional signature that shares characteristics of both early effectors and long-lived memory cells. Furthermore, we find that LLEC are exclusively derived from day 12 KLRG1+ effector cells. Our work challenges the concept that the KLRG1+ CD127low population is dominated by short-lived cells and shows that KLRG1 downregulation is not a prerequisite to become a long-lived protective memory T cell.

2020-08-26 | GSE152841 | GEO

KLRG1+ Effector CD8+ T Cells Lose KLRG1, Differentiate Into All Memory T Cell Lineages, and Convey Enhanced Protective Immunity

Project description:KLRG1+ Effector CD8+ T Cells Lose KLRG1, Differentiate Into All Memory T Cell Lineages, and Convey Enhanced Protective Immunity

| PRJNA434329 | ENA

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