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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE186863 | GEO | 2021/11/01

REPOSITORIES: GEO

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

2021-11-02 | GSE186699 | GEO

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

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

| PRJNA776519 | 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 [CHIP-seq]

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

| PRJNA776287 | ENA

BACH2 enforces the transcriptional and epigenetic programs of stem-like CD8+ T cells.

Project description:During chronic infection and cancer, a self-renewing CD8+ T cell subset maintains long-term immunity and is critical to the effectiveness of immunotherapy. These stem-like CD8+ T cells diverge from other CD8+ subsets early after chronic viral infection. However, pathways guarding stem-like CD8+ T cells against terminal exhaustion remain unclear. Here, we show that the gene encoding transcriptional repressor BACH2 is transcriptionally and epigenetically active in stem-like CD8+ T cells but not terminally exhausted cells early after infection. BACH2 overexpression enforced stem-like cell fate, whereas BACH2 deficiency impaired stem-like CD8+ T cell differentiation. Single-cell transcriptomic and epigenomic approaches revealed that BACH2 established the transcriptional and epigenetic programs of stem-like CD8+ T cells. In addition, BACH2 suppressed the molecular program driving terminal exhaustion through transcriptional repression and epigenetic silencing. Thus, our study reveals a new pathway that enforces commitment to stem-like CD8+ lineage and prevents an alternative terminally exhausted cell fate.

| S-EPMC7906956 | biostudies-literature

Distinct epigenetic signatures delineate transcriptional programs during virus-specific CD8(+) T cell differentiation.

Project description:The molecular mechanisms that regulate the rapid transcriptional changes that occur during cytotoxic T lymphocyte (CTL) proliferation and differentiation in response to infection are poorly understood. We have utilized ChIP-seq to assess histone H3 methylation dynamics within naive, effector, and memory virus-specific T cells isolated directly ex vivo after influenza A virus infection. Our results show that within naive T cells, codeposition of the permissive H3K4me3 and repressive H3K27me3 modifications is a signature of gene loci associated with gene transcription, replication, and cellular differentiation. Upon differentiation into effector and/or memory CTLs, the majority of these gene loci lose repressive H3K27me3 while retaining the permissive H3K4me3 modification. In contrast, immune-related effector gene promoters within naive T cells lacked the permissive H3K4me3 modification, with acquisition of this modification occurring upon differentiation into effector/memory CTLs. Thus, coordinate transcriptional regulation of CTL genes with related functions is achieved via distinct epigenetic mechanisms.

| S-EPMC4479393 | biostudies-literature

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

Project description:Protective immunity against pathogens depends on the efficient generation of functionally diverse effector and memory T lymphocytes. However, whether plasticity during effector-to-memory CD8+ T cell differentiation affects memory lineage specification and functional versatility remains unclear. Using genetic fate mapping analysis of highly cytotoxic KLRG1+ effector CD8+ T cells, we demonstrated that KLRG1+ cells receiving intermediate amounts of activating and inflammatory signals downregulated KLRG1 during the contraction phase in a Bach2-dependent manner and differentiated into all memory T cell linages, including CX3CR1int peripheral memory cells and tissue-resident memory cells. "ExKLRG1" memory cells retained high cytotoxic and proliferative capacity distinct from other populations, which contributed to effective anti-influenza and anti-tumor immunity. Our work demonstrates that developmental plasticity of KLRG1+ effector CD8+ T cells is important in promoting functionally versatile memory cells and long-term protective immunity.

| S-EPMC6465538 | biostudies-literature

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