M7G methylation by METTL1 regulates let-7 microRNAs [m7G-RIP-Seq Caco2]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA493087 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7903701.fastq.gz | Fastqsanger.gz | |||
| SRR7903702.fastq.gz | Fastqsanger.gz | |||
| SRR7903703.fastq.gz | Fastqsanger.gz | |||
| SRR7903704.fastq.gz | Fastqsanger.gz | |||
| SRR7903705.fastq.gz | Fastqsanger.gz |
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Project description:Methylation of N7-methylguanosine (m7G) is found at mRNA caps and at defined internal positions within abundant tRNAs and rRNAs. However, its detection within low abundance mRNAs and microRNAs (miRNAs) has been hampered by lack of sensitive detection strategies. Here, we adapt a chemical reactivity assay to detect internal m7G in RNA from eukaryotic cells. Using this approach, alongside a confirmational RNA immunoprecipitation assay, we identify m7G within miRNAs inhibiting cell migration, and show that METTL1 mediates this m7G methylation. Using Let-7 as an example we demonstrate that METTL1 activity is necessary for correct processing, is required for Let-7 dependent gene regulation and consequently has a negative effect on cell migration. These results identify m7G modification as a new pathway for the regulation of miRNAs.
2019-04-26 | GSE120454 | GEO
Project description:Methylation of N7-methylguanosine (m7G) is found at mRNA caps and at defined internal positions within abundant tRNAs and rRNAs. However, its detection within low abundance mRNAs and microRNAs (miRNAs) has been hampered by lack of sensitive detection strategies. Here, we adapt a chemical reactivity assay to detect internal m7G in RNA from eukaryotic cells. Using this approach, alongside a confirmational RNA immunoprecipitation assay, we identify m7G within miRNAs inhibiting cell migration, and show that METTL1 mediates this m7G methylation. Using Let-7 as an example we demonstrate that METTL1 activity is necessary for correct processing, is required for Let-7 dependent gene regulation and consequently has a negative effect on cell migration. These results identify m7G modification as a new pathway for the regulation of miRNAs.
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Project description:Methylation of N7-methylguanosine (m7G) is found at mRNA caps and at defined internal positions within abundant tRNAs and rRNAs. However, its detection within low abundance mRNAs and microRNAs (miRNAs) has been hampered by lack of sensitive detection strategies. Here, we adapt a chemical reactivity assay to detect internal m7G in RNA from eukaryotic cells. Using this approach, alongside a confirmational RNA immunoprecipitation assay, we identify m7G within miRNAs inhibiting cell migration, and show that METTL1 mediates this m7G methylation. Using Let-7 as an example we demonstrate that METTL1 activity is necessary for correct processing, is required for Let-7 dependent gene regulation and consequently has a negative effect on cell migration. These results identify m7G modification as a new pathway for the regulation of miRNAs.
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Project description:m7G methylation by METTL1 regulates let-7 microRNAs [m7G-RIP-Seq KD A549]
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Project description:m7G methylation by METTL1 regulates let-7 microRNAs [BoRed-Seq & m7G-RIP-Seq A549]
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Project description:Methylation of N7-methylguanosine (m7G) is found at mRNA caps and at defined internal positions within abundant tRNAs and rRNAs. However, its detection within low abundance mRNAs and microRNAs (miRNAs) has been hampered by lack of sensitive detection strategies. Here, we adapt a chemical reactivity assay to detect internal m7G in RNA from eukaryotic cells. Using this approach, alongside a confirmational RNA immunoprecipitation assay, we identify m7G within miRNAs inhibiting cell migration, and show that METTL1 mediates this m7G methylation. Using Let-7 as an example we demonstrate that METTL1 activity is necessary for correct processing, is required for Let-7 dependent gene regulation and consequently has a negative effect on cell migration. These results identify m7G modification as a new pathway for the regulation of miRNAs.
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Project description:m7G methylation by METTL1 regulates let-7 microRNAs
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Project description:N7-methylguanosine (m7G) modification is one of the most prevalent tRNA modifications in human. The precise function and molecular mechanism of m7G tRNA modification in regulation of cancer remain poorly understood. Here we showed that m7G tRNA modification, METTL1 and WDR4 are elevated in hepatocellular carcinoma (HCC) tissues and associated with HCC patient prognosis. Functionally, silencing METTL1 or WDR4 inhibits HCC cell proliferation, migration and invasion, while forced expression of wild type METTL1 but not its catalytic dead mutant promotes HCC progression. Knockdown of METTL1 reduces m7G tRNA modification and decreases m7G modified tRNA expression. Mechanistically, METTL1 depletion selectively decreases the mRNA translation of a subset of oncogenic genes, especially cell cycle and EGFR pathway genes, in m7G-related codon dependent manner. Moreover, in vivo studies using Mettl1 knock-in and knockout mice reveal a critical function of Mettl1 mediated m7G tRNA modifications in promoting hepatocarcinogenesis in the hydrodynamics transfection HCC model. Our work uncovers the critical functions of tRNA m7G modification in regulating cancer mRNA translation and promoting hepatocarcinogenesis, thus provides new insights into role of the mis-regulated tRNA modifications in cancers.
2021-06-26 | GSE174492 | GEO
Project description:The RNA methyltransferase METTL1 catalyzes the N7-methylguanosine (m7G) modification of certain tRNAs, mRNAs, and miRNA precursors. However, the role of METTL1 and its cofactor WDR4 in cancer remains largely unexplored. Here we reveal the oncogenic role of METTL1/WDR4. METTL1 is frequently amplified and overexpressed in cancers and correlates with poor patient survival. METTL1 depletion in human cancer cells causes decreased abundance of m7G-modified tRNAs, altered cell cycle, and inhibits oncogenicity. Strikingly, METTL1/WDR4 overexpression induces oncogenic transformation and carcinogenesis. Mechanistically, we find increased abundance of a subset of m7G-modified tRNAs including tRNA-Arg(TCT), and increased translation of mRNAs enriched in the corresponding AGA codon including cell cycle regulators. Accordingly, expression of tRNA-Arg(TCT) is significantly elevated in many cancer types, correlates with patient survival, and overexpression of this tRNA enhances reporter gene expression and cell transformation. Thus, METTL1/WDR4-mediated m7G tRNA modification drives oncogenic transformation, thereby highlighting METTL1 as a promising cancer therapeutic target.
2020-10-01 | GSE149989 | GEO
Project description:The RNA methyltransferase METTL1 catalyzes the N7-methylguanosine (m7G) modification of certain tRNAs, mRNAs, and miRNA precursors. However, the role of METTL1 and its cofactor WDR4 in cancer remains largely unexplored. Here we reveal the oncogenic role of METTL1/WDR4. METTL1 is frequently amplified and overexpressed in cancers and correlates with poor patient survival. METTL1 depletion in human cancer cells causes decreased abundance of m7G-modified tRNAs, altered cell cycle, and inhibits oncogenicity. Strikingly, METTL1/WDR4 overexpression induces oncogenic transformation and carcinogenesis. Mechanistically, we find increased abundance of a subset of m7G-modified tRNAs including tRNA-Arg(TCT), and increased translation of mRNAs enriched in the corresponding AGA codon including cell cycle regulators. Accordingly, expression of tRNA-Arg(TCT) is significantly elevated in many cancer types, correlates with patient survival, and overexpression of this tRNA enhances reporter gene expression and cell transformation. Thus, METTL1/WDR4-mediated m7G tRNA modification drives oncogenic transformation, thereby highlighting METTL1 as a promising cancer therapeutic target.
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