M6A-Seq in METTL14 R298P mutation knock-in cell clones
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA785880 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17118517_1.fastq.gz | Fastqsanger.gz | |||
| SRR17118517_2.fastq.gz | Fastqsanger.gz | |||
| SRR17118518_1.fastq.gz | Fastqsanger.gz | |||
| SRR17118518_2.fastq.gz | Fastqsanger.gz | |||
| SRR17118519_1.fastq.gz | Fastqsanger.gz |
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Project description:N6-methyladenosine (m6A) is the major type of RNA modification that regulates RNA stability and gene expression, characterized by a conserved motif including 5′-(m6A)C-3′. However, the functional significance of the specific motif for m6A modification is unclear. Here, we focused on a single amino acid substitution in the m6A “writer” complex, METTL14 R298P, and created mutation knock-in cells. m6A individual-nucleotide-resolution cross-linking and immunoprecipitation and methylated RNA immunoprecipitation with next-generation sequencing (MeRIP-Seq) revealed that METTL14R298P/R298P but not METTL14WT/R298P cells had an aberrant sequence motif, 5′-(m6A)[C/T]-3′. This study reveals a mechanism underlying sequence-specific m6A modification.
2021-12-06 | GSE190112 | GEO
Project description:N6-methyladenosine (m6A) is the major type of RNA modi'cation that regulates RNA stability and gene expression, characterized by a conserved motif including 5'-(m6A)C-3'. However, the functional significance of the specific motif for m6A modification is unclear. Here, we focused on a single amino acid substitution in the m6A 'writer' complex, METTL14 R298P, and created mutation knock-in cells. m6A individual-nucleotide-resolution cross-linking and immunoprecipitation and methylated RNA immunoprecipitation with next-generation sequencing (MeRIP-Seq) revealed that METTL14R298P/R298P but not METTL14WT/R298P cells had an aberrant sequence motif, 5'-(m6A)[C/T]-3'. This study reveals a mechanism underlying sequence-specific m6A modification.
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Project description:miCLIP in METTL14 R298P mutation knock-in cell clones
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Project description:Post-transcriptional m6A methylation on mRNA plays a key role in neural development. Here, we specifically depleted Mettl14 (a key component of m6A complex) in retina progenitor cells by crossing Mettl14 fl/fl mice with the Chx10-Egfp/Cre mouse line and investigated Mettl14 depletion-induced m6A alteration in developing retinas using m6A-seq.
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Project description:β-cell specific Mettl14 knock-out mice display reduced N6-methyladenosine (m6A) levels and recapitulate human Type II diabetes (T2D) islet phenotype with early diabetes onset and mortality secondary to decreased β-cell proliferation and insulin degranulation. To gain insights into the role of m6A in regulating the IGF1/insulin -> AKT - > PDX1 pathway and to dissect the signaling networks modulating AKT phosphorylation, we subjected freshly isolated islets from control and Mettl14 knock-out mice to phospho-antibody microarrays.
2019-08-09 | GSE132111 | GEO
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.
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Project description:Methyltransferase-like 3 (METTL3) and 14 (METTL14) are core subunits of the methyltransferase complex (MTC) that catalyzes mRNA N6-methyladenosine (m6A) modification. Despite the expanding list of m6A-dependent function of the MTC, m6A independent function of the METTL3 and METTL14 complex remains poorly understood. Here we show that genome-wide redistribution of METTL3 and METTL14 drives senescence-associated secretory phenotype (SASP) in a m6A-independent manner. METTL3 and METTL14 are necessary for SASP. However, SASP is not regulated by m6A mRNA modification. METTL14 is redistributed to the enhancers, while METTL3 is localized to the pre-existing NF-B sites within the promoters of the SASP genes during senescence. METTL3 interacts with NF-B and they are mutually dependent on their associations with the promoters of SASP genes. METTL14 but not METTL3 is necessary for function of SASP gene enhancers. METTL3 and METTL14 are required for both the tumor-promoting and immune surveillance functions of senescent cells mediated by SASP in vivo in mouse models. In summary, our results report a m6A independent function of the METTL3 and METTL14 complex in promoting SASP through regulating transcription by genome-wide redistribution of METTL14 to enhancers and METTL3 to promoters of SASP genes during senescence.
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Project description:METTL3 and METTL14 are two components that form the core heterodimer of the main RNA m6A methyltransferase complex (MTC, also known as m6A writer) that installs m6A. Surprisingly, depletion of METTL3 or METTL14 displayed distinct effects on mouse embryonic stem cell (mESC) self-renewal. While comparable global hypo-methylation in RNA m6A was observed in Mettl3 or Mettl14 knockout mESCs, respectively. Mettl14 knockout led to a globally decreased nascent RNA synthesis, whereas Mettl3 depletion resulted in transcription upregulation, suggesting that METTL14 might possess an m6A-indenepent role in gene regulation. We found that METTL14 colocalizes with the repressive H3K27me3 modification and PRC2 complex. Mechanically, METTL14, but not METTL3, recognizes H3K27me3 and recruits KDM6B to induce H3K27me3 demethylation independent of METTL3. Depletion of METTL14 thus led to a global increase in H3K27me3 level along with a global gene suppression . The regulation of H3K27me3 by METTL14 is essential to the transition of mESCs from self-renewal to differentiation. This work reveals a regulation mechanism on heterochromatin by METTL14 in a manner distinct from METTL3 and independently of m6A, and critically impacts transcriptional regulation, stemness maintenance and differentiation of mESCs.
2024-08-16 | GSE183399 | GEO
Project description:Methyltransferase-like 3 (METTL3) and 14 (METTL14) are core subunits of the methyltransferase complex (MTC) that catalyzes mRNA N6-methyladenosine (m6A) modification. Despite the expanding list of m6A-dependent function of the MTC, m6A independent function of the METTL3 and METTL14 complex remains poorly understood. Here we show that genome-wide redistribution of METTL3 and METTL14 drives senescence-associated secretory phenotype (SASP) in a m6A-independent manner. METTL3 and METTL14 are necessary for SASP. However, SASP is not regulated by m6A mRNA modification. METTL14 is redistributed to the enhancers, while METTL3 is localized to the pre-existing NF-B sites within the promoters of the SASP genes during senescence. METTL3 interacts with NF-B and they are mutually dependent on their associations with the promoters of SASP genes. METTL14 but not METTL3 is necessary for function of SASP gene enhancers. METTL3 and METTL14 are required for both the tumor-promoting and immune surveillance functions of senescent cells mediated by SASP in vivo in mouse models. In summary, our results report a m6A independent function of the METTL3 and METTL14 complex in promoting SASP through regulating transcription by genome-wide redistribution of METTL14 to enhancers and METTL3 to promoters of SASP genes during senescence.
2020-12-10 | GSE159551 | GEO
Project description:Methyltransferase-like 3 (METTL3) and 14 (METTL14) are core subunits of the methyltransferase complex (MTC) that catalyzes mRNA N6-methyladenosine (m6A) modification. Despite the expanding list of m6A-dependent function of the MTC, m6A independent function of the METTL3 and METTL14 complex remains poorly understood. Here we show that genome-wide redistribution of METTL3 and METTL14 drives senescence-associated secretory phenotype (SASP) in a m6A-independent manner. METTL3 and METTL14 are necessary for SASP. However, SASP is not regulated by m6A mRNA modification. METTL14 is redistributed to the enhancers, while METTL3 is localized to the pre-existing NF-B sites within the promoters of the SASP genes during senescence. METTL3 interacts with NF-B and they are mutually dependent on their associations with the promoters of SASP genes. METTL14 but not METTL3 is necessary for function of SASP gene enhancers. METTL3 and METTL14 are required for both the tumor-promoting and immune surveillance functions of senescent cells mediated by SASP in vivo in mouse models. In summary, our results report a m6A independent function of the METTL3 and METTL14 complex in promoting SASP through regulating transcription by genome-wide redistribution of METTL14 to enhancers and METTL3 to promoters of SASP genes during senescence.
2020-12-10 | GSE141993 | GEO