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

ABSTRACT: 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/+).

ORGANISM(S): Mus musculus

PROVIDER: GSE246652 | GEO | 2023/12/31

REPOSITORIES: GEO

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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).

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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).

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Determine the methyltransferase activities of METTL3, METTL14, and METTL16 via MeRIP-seq (m6A-seq)

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

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

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Global N6-methyladenosine RNA profiling reveals CSF1R as a target of METTL14 in non-small cell lung cancer [meRIP-seq]

Project description:Non-small cell lung cancer (NSCLC) is a common type of lung cancer, characterized by a poor prognosis. N6-methyladenosine (m6A) emerges as one of the most important modification of RNA, and m6A modifier METTL14 were reported to play pivotal role in multiple cancer types. However, there are limited number of studies of METTL14 in lung cancer and there still lacks systematic investigation of the function, clinical significance and targets of METTL14 in NSCLC. Here, we first conducted comprehensive N6-methyladenosine profiling of non-small cell lung cancer patients, and acquired m6A RNA modification atlas and differentially methylated RNAs in non-small cell lung cancer patients. Then we focused on RNA methyl-transferase METTL14, and investigated its clinical significance and function in NSCLC. As a result, METTL14 was correlated with clinical pathological parameters of differentiation and M stage. Addionally, METTL14 promotes NSCLC growth, induces cell death, and enhances cell migration and invasion, in vitro. Finally, to identify potential targets of METTL14, RNA sequencing, METTL14 RIP-Sequencing, and METTL14 MeRIP-Sequencing were conducted. Five genes were commonly identified, including four protein coding genes (PPIEL, AKR1C1, SARS2 and CSF1R) and one lncRNA ASAP1-IT2. After validation with TCGA dataset, Colony Stimulating Factor 1 Receptor (CSF1R) showed significant positive coefficient with METTL14, and was presumed to be the target of METTl14 in lung cancer. In conclusion, this study, uncovered an m6A RNA modification atlas, and revealed the clinical significance, in vitro function and molecular targets CSF1R of METTL14 in NSCLC.

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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.

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Widespread N6-methyladenosine-dependent RNA Structural Switches Regulate RNA-Protein Interactions

Project description:We show that N6-methyladenosine (m6A), the most abundant internal modification in mRNA/lncRNA with still poorly characterized function, alters RNA structure to facilitate the access of RBM for heterogeneous nuclear ribonucleoprotein C (hnRNP C). We term this mechanism m6A-switch. Through combining PAR-CLIP with Me-RIP, we identify 39,060 m6A-switches among hnRNP C binding sites transcriptome-wide. We show that m6A-methyltransferases METTL3 or METTL14 knockdown decreases hnRNP C binding at 16,582 m6A-switches. Taken together, 2,798 m6A-switches of high confidence are identified to mediate RNA-hnRNP C interactions and affect diverse biological processes including cell cycle regulation. These findings reveal the biological importance of m6A and provide insights into the sophisticated regulation of RNA-RBP interactions through m6A-induced RNA structural remodeling. Measure the m6A methylated hnRNP C binding sites transcriptome-wide by PARCLIP-MeRIP; measure the differential hnRNP C occupancies upon METTL3/METTL14 knockdown by PAR-CLIP; measure RNA abundance and splicing level changes upon HNRNPC, METTL3 and METTL14 knockdown

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m6A independent genome-wide METTL3 and METTL14 redistribution drives senescence-associated secretory phenotype [MeRIP-seq]

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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