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

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

PROVIDER: PRJNA767803 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16148288_1.fastq.gz	Fastqsanger.gz
	SRR16148288_2.fastq.gz	Fastqsanger.gz
	SRR16148289_1.fastq.gz	Fastqsanger.gz
	SRR16148289_2.fastq.gz	Fastqsanger.gz
	SRR16148290_1.fastq.gz	Fastqsanger.gz

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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.

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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.

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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

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

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

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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.

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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.

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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

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m6A-seq analysis of Wild Type and Mettl3-/- BMDMs (bone-marrow-derived macrophages) Transcriptomes

Project description:To investigate the role of METTL3-mediated m6A modification in macrophage, we performed m6A-sequencing to map the m6A modification in bone-marrow-derived macrophages (BMDMs) in wild type (WT) and Mettl3-/- mice.

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

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

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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

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