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Mettl14-mediated m6A modification enhances the function of Foxp3+ regulatory T cells and promotes allograft acceptance

ABSTRACT: Mettl14-mediated m6A modification enhances the function of Foxp3+ regulatory T cells and promotes allograft acceptance

PROVIDER: PRJNA889928 | ENA |

REPOSITORIES: ENA

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Mettl14-mediated m6A modification enhances the function of Foxp3+ regulatory T cells and promotes allograft acceptance

Project description:The transcripts levels of 434 genes were upregulated and those of 277 genes were downregulated in Treg cells from Foxp3-Mettl14f/+ cKO mice compared to those genes in Treg cells from the littermate controls.

2022-11-09 | GSE215371 | GEO

METTL14 regulates neuroblastoma through the m6A modification

Project description:RNA methylation is involved in the regulation of cell response and cell fate, and is closely related to the development of tumors. METTL14 is considered to be a m6A methyltransferase. Studies have found that METTL14 is associated with the occurrence and development of a variety of tumors, but the mechanism in neuroblastoma is not clear. The expression of METTL14 in high risk patients was significantly higher than that in low risk patients. Interference with METTL14 expression in SK-N-BE(2) cells significantly interfered with cell cycle and inhibited cell proliferation, migration and invasion. In neuroblastoma, METTL14 activates the PI3K/AKT signaling pathway by targeting YWHAH by upregulating m6A levels in mRNA transcripts. In all findings, it was suggested that METTL14 has a cancer-promoting function in neuroblastoma.

2024-05-10 | GSE244350 | GEO

Alloantigen-Induced Regulatory T Cells Generated in Presence of Vitamin C Display Enhanced Stability of Foxp3 Expression and Promote Skin Allograft Acceptance

Project description:Regulatory T cells (Tregs) are critical for the maintenance of immune homeostasis and self‑tolerance, and can be therapeutically used for prevention of unwanted immune responses such as allotransplant rejection. Tregs are characterized by the expression of the transcription factor Foxp3, and recent work suggested that epigenetic imprinting of Foxp3 and other Treg‑specific epigenetic signatures genes is crucial for the stabilization of both Foxp3 expression and immunosuppressive properties within Tregs. Lately, Vitamin C was reported to enhance the activity of enzymes of the ten‑eleven‑translocation family, thereby fostering the demethylation of Foxp3 and other Treg‑specific epigenetic signatures genes in developing Tregs. Here, we in vitro generated alloantigen‑specific Foxp3+ Tregs (allo‑iTregs) in presence of vitamin C, and those Tregs showed a pronounced demethylation of Foxp3 and other Treg‑specific epigenetic signatures genes, accompanied with an enhanced stability of Foxp3 expression. However, RNA‑seq analysis revealed an only minor impact of Vitamin C on the transcriptome of allo‑iTregs. Importantly, when being tested in vivo in a highly immunogenic skin transplantation model vitamin C‑treated allo‑iTregs showed a superior suppressive capacity as compared to allo‑iTregs generated in absence of vitamin C. Together, our results might pave the way for the establishment of novel protocols for the in vitro generation of allo‑antigen specific Foxp3+ Tregs for therapeutic usage in transplantation medicine.

2017-06-22 | GSE96960 | GEO

Primarily Dissecting the Autonomous and Cooperative Functions of METTL3 and METTL14 in mRNA Modification and Tumor Progression

Project description:METTL3 and METTL14 are considered to faithfully form the m6A writing complex in a 1:1 ratio, regulating the fate of mRNA by adding m6A modifications. However, recent studies have shown inconsistent expression and prognostic value of METTL3 and METTL14 in some tumors, suggesting that they may not be faithful in tumors. Pan-cancer analysis based on TCGA data reveals significant differences in expression, function, tumor burden correlation, and immune correlation between METTL3 and METTL14, especially in esophageal squamous cell carcinoma (ESCC). Knockdown of METTL3 significantly inhibits the cell proliferation in vitro and in vivo in ESCC EC109 cells, while the impact of METTL14 knockdown on proliferation is limited, and it cannot abolish the expression of METTL3 protein. mRNA-seq results indicate that METTL3 independently regulates the expression of 1615 genes, while only 776 genes are co-regulated by METTL3 and METTL14. Furthermore, through immunofluorescence co-localization, it is observed that METTL3 and METTL14 have certain inconsistencies in cellular localization. HPLC-MS results show that METTL3 independently binds to the Nop56p-associated pre-rRNA complex and mRNA splicing complex, separate from METTL14. Through bioinformatics and various omics studies, we have preliminarily discovered that METTL3 independently regulating tumor cell proliferation, and the participation in mRNA splicing may be a critical molecular mechanism. Our study provides an experimental basis and theoretical foundation for further understanding of the m6A writing complex and tumor therapy targeting METTL3.

2024-02-01 | PXD048886 | Pride

Arginine methylation of METTL14 promotes RNA N6-methyladenosine modification

Project description:Both mRNA and proteins can be modified through addition of methyl groups. For example, addition of N6-methyladenosine (m6A) to mRNAs is critical for human development and health. Post-translational methylation of proteins can impact the dynamic regulation of enzymatic activity. Here we sought to explore the nexus of transcriptional and post-translational methylation by studying the role of methylation of the core methyltransferase METTL3/METTL14 in m6A regulation. We found by mass spectrometry that METTL14 arginine 255 (R255) is methylated (R255me). Global mRNA m6A levels were greatly decreased in METTL14 R255K mutant mouse embryonic stem cells (mESCs). We further found that R255me greatly enhances the interaction of METTL3/METTL14 with WTAP and promotes the binding of the complex to substrate RNA.

2021-05-14 | GSE164047 | GEO

HRD1-mediated METTL14 degradation regulates m6A mRNA modification to suppress ER proteotoxic liver disease

Project description:Accumulation of unfolded or misfolded proteins in the endoplasmic reticulum (ER) lumen triggers unfolded protein response (UPR) for stress adaptation, the failure of which induces cell apoptosis and tissue/organ damage. The molecular switches underlying how the UPR selects for stress adaptation over apoptosis remain unknown. Here we discovered that accumulation of unfolded/misfolded proteins selectively induces N6-adenosine-methyltransferase-14 (METTL14) expression. METTL14 promotes CHOP mRNA decay through its 3’UTR N6-adenosine methylation (m6A) to inhibit its downstream pro-apoptotic target genes expression. UPR induces METTL14 expression through competing the HRD1-ERAD machinery to block METTL14 ubiquitination and degradation. Therefore, mice with liver-specific METTL14 deletion are highly susceptible to both acute pharmacological and alpha-1 antitrypsin (AAT) deficiency-induced ER proteotoxic stress and liver injury. Further hepatic CHOP deletion protects METTL14 knockout mice from ER stress-induced liver damage. Our study reveals a crosstalk between ER stress and mRNA m6A pathways, the ERm6A pathway, for ER stress adaptation to proteotoxicity.

2021-09-30 | GSE185109 | GEO

METTL14-mediated N6-methyladenosine modification of Col17a1/Itgα6/Itgβ4 governs epidermal homeostasis [MeRIP-seq]

Project description:To elucidate the role of METTL14-mediated m6A modification in epidermal development, we conditionally knocked out the m6A methyltransferase METTL14 in mouse epidermal keratinocytes. We then performed MeRIP-seq analysis of epidermal keratinosis from P0 control mice (K14Cre,Mettl14F/+).

2023-12-31 | GSE246652 | GEO

Resolvin D1 improves allograft osteointegration and directly enhances osteoblasts differentiation

Project description:Resolvin D1 improves allograft osteointegration and directly enhances osteoblasts differentiation

2023-02-08 | GSE224195 | GEO

METTL14-mediated N6-methyladenosine modification of Col17a1/Itgα6/Itgβ4 governs epidermal homeostasis [RNA-Seq]

Project description:To elucidate the role of METTL14-mediated m6A modification in epidermal development, we conditionally knocked out the m6A methyltransferase METTL14 in mouse epidermal keratinocytes. We then performed RNA-seq analysis of epidermal keratinosis from P0 control mice (K14Cre,Mettl14F/+) and cKO mice (K14CreMettl14F/F).

2023-12-31 | GSE246720 | GEO

METTL14-mediated N6-methyladenosine modification of Col17a1/Itgα6/Itgβ4 governs epidermal homeostasis [Ribo-Seq]

Project description:To elucidate the role of METTL14-mediated m6A modification in epidermal development, we conditionally knocked out the m6A methyltransferase METTL14 in mouse epidermal keratinocytes. We then performed ribosome-profiling analysis of epidermal keratinosis from P0 control mice (K14Cre,Mettl14F/+) and cKO mice (K14CreMettl14F/F).

2023-12-31 | GSE246653 | GEO

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