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Mettl3-dependent m6A modification is essential for effector differentiation and memory formation of CD8+ T cells

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

ORGANISM(S): Mus musculus

PROVIDER: GSE215762 | GEO | 2024/06/01

REPOSITORIES: GEO

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Mettl3-dependent m6A modification is essential for effector differentiation and memory formation of CD8+ T cells [miCLIP]

Project description:The goal of this study is to determine the critical requirement of N6-Methyladenosine (m6A) methyltransferase Mettl3 during CD8+ T cell responses upon acute viral infection. We demonstrate that conditional ablation of Mettl3 in CD8+ T cells impairs effector expansion and terminal differentiation in an m6A-dependent manner, which in turn affects memory formation and secondary response. Mechanism analysis indicates that Mettl3 deficiency broadly affects expression of cell cycle and transcriptional regulators. Based on these findings, our study reveals the important role of m6A modification in CD8+ T cell responses.

2024-06-01 | GSE215760 | GEO

Mettl3-dependent m6A modification is essential for effector differentiation and memory formation of CD8+ T cells [SLIM-seq]

2024-06-01 | GSE215761 | GEO

Mettl3-dependent m6A modification is essential for effector differentiation and memory formation of CD8+ T cells [RNA-seq]

2024-06-01 | GSE215759 | GEO

Mettl3-dependent m6A modification is essential for effector differentiation and memory formation of CD8+ T cells

Project description:Mettl3-dependent m6A modification is essential for effector differentiation and memory formation of CD8+ T cells

| PRJNA890571 | ENA

Mettl3-dependent m6A modification is essential for effector differentiation and memory formation of CD8+ T cells [miCLIP]

Project description:Mettl3-dependent m6A modification is essential for effector differentiation and memory formation of CD8+ T cells [miCLIP]

| PRJNA890578 | ENA

Mettl3-dependent m6A modification is essential for effector differentiation and memory formation of CD8+ T cells [RNA-seq]

Project description:Mettl3-dependent m6A modification is essential for effector differentiation and memory formation of CD8+ T cells [RNA-seq]

| PRJNA890575 | ENA

Mettl3-dependent m6A modification is essential for effector differentiation and memory formation of CD8+ T cells [SLIM-seq]

Project description:Mettl3-dependent m6A modification is essential for effector differentiation and memory formation of CD8+ T cells [SLIM-seq]

| PRJNA890581 | ENA

Autophagy is essential for effector CD8(+) T cell survival and memory formation.

Project description:The importance of autophagy in the generation of memory CD8(+) T cells in vivo is not well defined. We report here that autophagy was dynamically regulated in virus-specific CD8(+) T cells during acute infection of mice with lymphocytic choriomeningitis virus. In contrast to the current paradigm, autophagy decreased in activated proliferating effector CD8(+) T cells and was then upregulated when the cells stopped dividing just before the contraction phase. Consistent with those findings, deletion of the gene encoding either of the autophagy-related molecules Atg5 or Atg7 had little to no effect on the proliferation and function of effector cells, but these autophagy-deficient effector cells had survival defects that resulted in compromised formation of memory T cells. Our studies define when autophagy is needed during effector and memory differentiation and warrant reexamination of the relationship between T cell activation and autophagy.

| S-EPMC4232981 | biostudies-literature

piRNA-36741 regulates BMP2-mediated osteoblast differentiation via METTL3 controlled m6A modification.

Project description:The osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) is essential for bone formation, and its imbalance can lead to bone diseases such as osteoporosis. It is reported that PIWI-interacting RNA-36741 (piR-36741) is up-regulated during the osteogenic differentiation, but its role in regulating osteogenic differentiation remains unclear. Here, the primary human BMSCs were used to induce osteogenic differentiation, and the expression of piR-36741 and METTL3 (methyltransferase like 3) was up-regulated during the osteogenic differentiation of BMSCs. Moreover, interference with piR-36741 or METTL3 markedly hindered the osteogenic differentiation of BMSCs, which was manifested by a reduction in osteoblast marker expression (including RUNX2, COL1A1, OPN and OCN), osteogenic phenotype and matrix mineralization. Mechanistically, the piR-36741-PIWIL4 complex directly interacted with METTL3 and prevented METTL3-mediated m6A modification of BMP2 mRNA transcripts, thereby promoting BMP2 expression. And overexpression of BMP2 reversed the inhibitory effect of piR-36741 silence on osteogenic differentiation and the Smad pathway activity. In addition, administration with piR-36741 mimic alleviated ovariectomy-induced osteoporosis in mice. In conclusion, piRNA-36741 overexpression promoted osteogenic differentiation of BMSCs and mitigated ovariectomy-induced osteoporosis through METTL3-mediated m6A methylation of BMP2 transcripts.

| S-EPMC8544320 | biostudies-literature

METTL3-mediated m6A modification is required for cerebellar development.

Project description:N6-methyladenosine (m6A) RNA methylation is the most abundant modification on mRNAs and plays important roles in various biological processes. The formation of m6A is catalyzed by a methyltransferase complex including methyltransferase-like 3 (METTL3) as a key factor. However, the in vivo functions of METTL3 and m6A modification in mammalian development remain unclear. Here, we show that specific inactivation of Mettl3 in mouse nervous system causes severe developmental defects in the brain. Mettl3 conditional knockout (cKO) mice manifest cerebellar hypoplasia caused by drastically enhanced apoptosis of newborn cerebellar granule cells (CGCs) in the external granular layer (EGL). METTL3 depletion-induced loss of m6A modification causes extended RNA half-lives and aberrant splicing events, consequently leading to dysregulation of transcriptome-wide gene expression and premature CGC death. Our findings reveal a critical role of METTL3-mediated m6A in regulating the development of mammalian cerebellum.

| S-EPMC6021109 | biostudies-literature

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