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M6A/m-Seq of mouse adult cortex of Mettl3 cKO or Fto cKO mice

ABSTRACT: m6A/m-Seq of mouse adult cortex of Mettl3 cKO or Fto cKO mice

PROVIDER: PRJNA454049 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7076570_1.fastq.gz	Fastqsanger.gz
	SRR7076570_2.fastq.gz	Fastqsanger.gz
	SRR7076580_1.fastq.gz	Fastqsanger.gz
	SRR7076580_2.fastq.gz	Fastqsanger.gz
	SRR7076571_1.fastq.gz	Fastqsanger.gz

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m6A/m-Seq of mouse adult cortex of Mettl3 cKO or Fto cKO mice

Project description:N6-Methyladenosine (m6A) and N6,2′-O-dimethyladenosine (m6Am) are abundant mRNA modifications that regulate transcript processing and translation. The role of both, here termed m6A/m, in the stress response in the adult brain in vivo are currently unknown. Here, we investigated the effect of gene deletion of Mettl3, a m6A methyltransferase, and Fto, a m6A and m6Am demethlyase, induced in adulthood in excitatory neurons of the neocortex and hippocampus (Camk2a-Cre Mettl3 or Fto cKO) on the cortical epitranscriptome. PolyA-RNA-fragments from 3-5 replicates per group were processed both as m6A/m-sample (RNA immunoprecipiation RIP with an m6A and m6Am antibody) and RNA-input sample.

2018-07-10 | GSE113793 | GEO

mRNA-Seq of mouse Mettl3 cKO and Fto cKO hippocampus after fear conditioning

Project description:N6-Methyladenosine (m6A) and N6,2′-O-dimethyladenosine (m6Am) are abundant mRNA modifications that regulate transcript processing and translation. The role of both, here termed m6A/m, in the stress response in the adult brain in vivo are currently unknown. Here, we investigated the effect of gene deletion of Mettl3, a m6A methyltransferase, and Fto, a m6A and m6Am demethlyase, induced in adulthood in excitatory neurons of the CA1 and CA3 in the hippocampus (Nex-CreERT2 Mettl3 or Fto cKO) on the transcriptome of CA1 and CA3 as well as the transcriptomic response of the CA1 and CA3 transcriptome to fear conditioning.

2018-07-10 | GSE113796 | GEO

mRNA-Seq of mouse Mettl3 cKO and Fto cKO hippocampus after fear conditioning

Project description:mRNA-Seq of mouse Mettl3 cKO and Fto cKO hippocampus after fear conditioning

| PRJNA454061 | ENA

Combined analysis of ribo-seq and rna-seq reveals that Mettl3 regulates embryonic cerebral cortex development in mice by controlling the proliferation and differentiation of neural progenitor cells

Project description:N6-methyladenosine (m6A) is the most important internal messenger RNA (mRNA) modification in mammals. The role of Mettl3, the core component of methyltransferase, and Fto, the demethylase, has not been revealed in the embryonic development of the cerebral cortex in mice. We constructed the conditional knockout of Mettl3 and Fto in the cerebral cortex of mice. We found that Mettl3 deletion causes cell cycle extension of progenitors and massive proliferation of intermediate progenitors at E15.5, which lead to a fold structure of cortex, while Fto deletion hardly altered cell numbers or morphology. Meanwhile, both transcriptome sequence (RNA-Seq) and ribosome profiling (Ribo-Seq) of Mettl3-deleted cortex mRNAs in E15.5 revealed that the differential genes were enriched in cell differentiation, neurogenesis, neuron differentiation, cell proliferation, and cell cycle. Moreover, deleted Mettl3 but not Fto significantly upregulated Ythdf1 and Ythdf2, which caused a substantial change in gene translation efficiency. Our findings indicate cortex m6A represents a novel layer of complexity in gene expression regulation and provide a new mechanism of precisely programmed RNA maturation.

2021-01-04 | GSE154992 | GEO

The m6A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis [m6A-RIP-seq]

Project description:m6A-RIP sequencing of primary hepatic stellate cells (HSCs) isolated from Control and HSC-specific Mettl3-knockout (Mettl3 cKO) mouse liver tissues.

2022-07-13 | GSE207908 | GEO

M6A-seq analysis of wild type and Mettl3-cKO liver tissues' transcriptomes

Project description:To investigate the role of METTL3-mediated m6A modification in liver, we performed m6A-sequencing to map the m6A modification in liver tissues of wild type (WT) and liver-sepcific Mettl3-KO mice.

2023-10-01 | GSE185142 | GEO

Exploring the Impact of m6A Methyltransferase Mettl3 on MASLD through Multi-Omics Analysis

Project description:Background: N6-methyladenosine (m6A) RNA modification plays a crucial role in various biological events and is implicated in various metabolic-related diseases. However, its role in MASLD remains unclear. This study aims to investigate the impact of Mettl3 on MASLD through multi-omics analysis, with a focus on exploring its potential mechanisms of action. Methods: MASLD mouse models were established by feeding a high-fat diet for 12 weeks, and Mettl3 stable overexpression AML12 cell models were constructed via lentiviral transfection. Subsequent transcriptomic and proteomic analyses, as well as integrated analysis between different omics datasets, were conducted. Results: Mettl3 expression significantly increased in MASLD mouse models. In the transcriptomic and proteomic analyses, we identified 848 genes with significant inconsistencies between transcriptomic and proteomic datasets. GO/KEGG enrichment terms may involve post-transcriptional modifications, particularly Mettl3-mediated m6A modification. Subsequently, through integrated proteomic analysis of Mettl3-overexpressed AML12 cell models and MASLD mouse models, we selected the top 20 co-upregulated and co-downregulated GO/KEGG terms as the main biological processes influenced by Mettl3 in MASLD. By intersecting with pathways obtained from previous integrated analyses, we identified GO/KEGG terms affected by Mettl3-induced m6A modification. Protein-protein interaction analysis of proteins involved in these pathways highlighted GAPDH, ENO1, and TPI1 as three key hub genes. Conclusion: In MASLD, Mettl3 regulates the glycolytic pathway through m6A modification, influencing the occurrence and development of the disease via the key hub genes GAPDH, ENO1, and TPI1. These findings expand our understanding of MASLD and provide strong evidence for potential therapeutic targets and drug development.

2024-09-20 | PXD050565 | Pride

Mettl3-m6A-YTHDF1 axis promotion of mitochondrial dysfunction in metabolic dysfunction–associated steatotic liver disease (MASLD)

Project description:The N6-methyladenosine (m6A) mRNA modification and the mitochondrial respiratory chain (MRC) hold paramount importance in the advancement of MASLD. This study thoroughly investigates the relationship and impact of m6A mRNA modification and mitochondrial function in the progression of MASLD. Here we report that the mRNA and protein levels of mitochondrial respiratory chain (MRC) subunits showed inconsistent trends in vivo experiments. Abnormal m6A modification and mitochondrial dysfunction in MASLD were attributed to the upregulation of methyltransferase like 3 (Mettl3) and the downregulation of YTH N6-methyladenosine RNA binding protein 1 (YTHDF1) induced by high-fat foods. Mettl3 promoted the MRC's function. However, knockout of the reader protein YTHDF1, which plays a crucial role in the m6A modification process, counteracted the effect of Mettl3 and suppressed MRC. In MASLD, damage to the MRC may be regulated by the Mettl3-m6A-YTHDF1 complex axis, especially by the role of YTHDF1. Our research has offered a novel perspective on the involvement of m6A mRNA methylation in the pathogenesis of MASLD.

2024-09-20 | PXD047819 | Pride

M6A-seq & RNA-seq analysis of wild type and Mettl3-cKO liver tissues' or hepatocytes' transcriptomes

Project description:To investigate the role of METTL3-mediated m6A modification in liver, we performed m6A-sequencing and RNA-seq to map the m6A modification and gene expression in liver tissues or hepatocytes of wild type (WT) and liver-sepcific Mettl3-KO mice.

2022-10-29 | GSE207566 | GEO

m6A-seq analysis of Mettl3fl/fl (WT) and Mettl3fl/fl,LyzM-cre (cKO) bone-marrow-derived macrophages(BMDMs) transcriptomes

Project description:To investigate the role of RNA methyltransferase METTL3-mediated m6A modification in macrophage, we performed m6A-sequencing to map the m6A modification in bone-marrow-derived macrophages (BMDMs) from Mettl3fl/fl (WT) and Mettl3fl/fl,LyzM-cre (cKO) mice

2021-10-01 | GSE184971 | GEO

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