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The function of Wtap in N6-adenosine methylation of mRNAs controls T cell receptor signaling and survival of T cells [m6A-CLIP]

ABSTRACT: The function of Wtap in N6-adenosine methylation of mRNAs controls T cell receptor signaling and survival of T cells [m6A-CLIP]

PROVIDER: PRJNA780524 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16949026.fastq.gz	Fastqsanger.gz
	SRR16949027.fastq.gz	Fastqsanger.gz
	SRR16949028.fastq.gz	Fastqsanger.gz
	SRR16949029.fastq.gz	Fastqsanger.gz
	SRR16949030.fastq.gz	Fastqsanger.gz

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Identification and Characterization of the Mammalian Nuclear RNA N6-Adenosine Methyltransferase Core Complex

Project description:N6-methyladenosine (m6A) is the most prevalent internal modification found in mammalian messenger and non-coding RNAs. The discoveries of functionally significant demethylases that reverse this methylation as well as the recently revealed m6A distributions in mammalian transcriptomes strongly indicate regulatory functions of this modification. Here we report the identification and characterization of the mammalian nuclear RNA N6-adenosine methyltransferase core (RNMTC) complex. Besides METTL3, a methyltransferase which was the only known component of RNMTC in the past, we discovered that a previously uncharacterized methyltransferase, METTL14, exhibits a N6-adenosine methyltransferase activity higher than METTL3. Together with WTAP, the third component that dramatically affects the cellular m6A level, these three proteins form the core complex that orchestrates m6A deposition on mammalian nuclear RNA. Biochemistry assays, imaging experiments, as well as transcriptome-wide analyses of the binding sites and their effects on m6A methylation support methylation function and reveal new insights of RNMTC. PAR-CLIP and m6A-seq in HeLa cells

2013-11-29 | E-GEOD-46705 | biostudies-arrayexpress

The function of Wtap in N6-adenosine methylation of mRNAs controls T cell receptor signaling and survival of T cells [m6A-CLIP]

Project description:T cell antigen receptor (TCR) signaling controls the development, activation and survival of T cells by involving several layers and numerous mechanisms of gene regulation. N6-methyladenosine (m6A) is the most prevalent mRNA modification affecting splicing, translation and stability of transcripts. Here, we describe the Wtap protein as essential for m6A methyltransferase complex function and reveal its crucial role in TCR signaling. Wtap and m6A methyltransferase functions were required for the differentiation of thymocytes, control of activation-induced death of peripheral T cells and prevention of colitis by enabling gut RORγt+ regulatory T cell function. Transcriptome and epitranscriptomic analyses reveal that m6A modification destabilizes Orai1 and Ripk1 mRNAs. Lack of post-transcriptional repression of the encoded proteins correlated with increased store-operated calcium entry (SOCE) activity and diminished survival of T cells. These findings uncover how m6A modification impacts on TCR signal transduction and determines activation and survival of T cells.

2022-06-03 | GSE188853 | GEO

The function of Wtap in N6-adenosine methylation of mRNAs controls T cell receptor signaling and survival of T cells [RNA-seq]

2022-06-03 | GSE188814 | GEO

The function of Wtap in N6-adenosine methylation of mRNAs controls T cell receptor signaling and survival of T cells [YTHDF2-iCLIP]

2022-06-03 | GSE188846 | GEO

The function of Wtap in N6-adenosine methylation of mRNAs controls T cell receptor signaling and survival of T cells

Project description:The function of Wtap in N6-adenosine methylation of mRNAs controls T cell receptor signaling and survival of T cells

| PRJNA780510 | ENA

N6-adenosine methylation in miRNAs

Project description:Methylation of N6-adenosine (me6A) has been observed in rRNA, tRNA, snoRNA, lncRNA and mRNA (ref.), but not yet miRNA. Interestingly, many mRNAs contain miRNA-binding sites and me6A in their 3'-UTR, although they do not appear to overlap (Mayer). We have investigated whether adenosine methylation affects miRNA levels and whether miRNAs are methylated. Indeed, we have obtained evidence suggesting that miRNA can be methylated and that the steady state level of certain miRNAs is affected by the level of the 6meA demethylase FTO.

2015-07-20 | GSE59767 | GEO

The function of Wtap in N6-adenosine methylation of mRNAs controls T cell receptor signaling and survival of T cells [YTHDF2-iCLIP]

Project description:The function of Wtap in N6-adenosine methylation of mRNAs controls T cell receptor signaling and survival of T cells [YTHDF2-iCLIP]

| PRJNA780503 | ENA

The function of Wtap in N6-adenosine methylation of mRNAs controls T cell receptor signaling and survival of T cells [RNA-seq]

Project description:The function of Wtap in N6-adenosine methylation of mRNAs controls T cell receptor signaling and survival of T cells [RNA-seq]

| PRJNA780461 | ENA

Identification and Characterization of the Mammalian Nuclear RNA N6-Adenosine Methyltransferase Core Complex

2013-11-29 | GSE46705 | GEO

N6-adenosine methylation enhances nuclear mRNA export through METTL3 and NUP93

Project description:Nuclear export of messenger RNAs (mRNAs) through nuclear pore complexes (NPCs) is a critical step in gene expression. Although N6-adenosine methylation (m6A) has been implicated in this process, the underlying mechanism remains obscure. Here, using single-molecule imaging, we demonstrate that m6A markedly accelerates nuclear export of messenger ribonucleoproteins (mRNPs) by increasing export efficiency and shortening export time through NPCs. We further show that the m6A methyltransferase METTL3 localizes at NPCs and functionally associates with the nucleoporin NUP93 to promote efficient export of m6A-modified mRNPs. Disruption of this functional association between METTL3 and NUP93 substantially impairs overall mRNP export efficiency. Notably, a steroid-resistant nephrotic syndrome (SRNS)-associated NUP93 variant (c.1162C>T, p.Arg388Trp) fails to associate with METTL3, resulting in defective nuclear export of key methylated mRNAs required for kidney function. Together, our findings define an m6A-METTL3-NUP93 regulatory axis for nuclear mRNA export with broad implications for human disease.

2025-12-23 | MSV000100322 | MassIVE

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