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Differentially expressed genes in Mettl3-deficient livers compared to control livers

ABSTRACT: Liver-specific deficiency of Mettl3 causes liver injury. By performing RNA sequencing (RNA-seq) analysis on the Mettl3-deficient versus control livers, we identified the potential target genes that were closely associated with the liver phenotype in liver-specific Mettl3 knockout mice. RNA-seq analysis revealed extensive metabolic reprogramming in Mettl3-deficient livers. These results demonstrated that Mettl3 coordinates metabolic homeostasis and functional maturation during postnatal liver development.

ORGANISM(S): Mus musculus

PROVIDER: GSE197800 | GEO | 2022/03/09

REPOSITORIES: GEO

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Mettl3-dependent m6A modification in postnatal liver

Project description:Liver-specific deficiency of Mettl3 causes liver injury. By performing RNA sequencing (RNA-seq) analysis on the Mettl3-deficient versus control livers, we identified the potential target genes that were closely associated with the liver phenotype in liver-specific Mettl3 knockout mice. RNA-seq analysis revealed extensive metabolic reprogramming in Mettl3-deficient livers. These results demonstrated that Mettl3 coordinates metabolic homeostasis and functional maturation during postnatal liver development.

2022-03-09 | GSE197799 | GEO

Differentially expressed genes in Mettl3-deficient livers compared to control livers

Project description:Differentially expressed genes in Mettl3-deficient livers compared to control livers

| PRJNA812058 | ENA

RNA-seq analysis of mRNA profiles in the livers of Mettl3 flox/flox and hepatocyte-specific Mettl3 knockout (HKO) mice

Project description:Purpose: The goal of this study is to compare transcriptome profilings of liver from Mettl3 flox/flox and hepatocyte-specific Mettl3 knockout (HKO) mice. Methods: Total RNA was extracted using Tripure Isolation Reagent (Roche, Mannheim, Germany) from livers of Mettl3 flox/flox and HKO mice at 8 weeks old. mRNA profiles were generated by deep sequencing using an Illumina HiSeq X Ten platform. Paired-end clean reads were aligned to the mouse reference genome(Ensemble_GRCm38.90) with Hisat2 (version 2.0.4), and the aligned reads were used to quantify mRNA expression by using HTSeq (version 0.9.1). Conclusion: The hepatic mRNA profiles in Mettl3 flox/flox and HKO mice were characterized.

2021-10-29 | GSE141216 | GEO

Transcriptome profiling of the livers from Mettl3 flox/flox and hepatocyte-specific Mettl3 knockout (HKO) mice

Project description:The goal of this study is to compare transcriptome profilings of liver from Mettl3 flox/flox and hepatocyte-specific Mettl3 knockout (HKO) mice. Gene ontology analysis showed that the dowregulated genes were associated with monocarboxylic acid metabolic process, small molecule catabolic process, fatty acid metabolic process, cofactor metabolic process, organic acid catabolic process, and lipid biosynthetic process, whereas the upregulated genes were associated with leukocyte migration, cell chemotaxis, leukocyte cell-cell adhesion, positive regulation of cytokine production and defense response to other organism. KEGG pathway analysis showed that the downregulated genes were associated with Steroid hormone biosynthesis, Peroxisome, Chemical carcinogenesis, proteasome, Oxidative phosphorylation and Non-alcoholic fatty liver disease (NAFLD), whereas the upregulated genes were associated with Cell adhesion molecules (CAMs), Staphylococcus aureus infection, Viral protein interaction with cytokine and cytokine receptor, and Chemokine signaling pathway.

2023-03-12 | GSE214371 | GEO

METTL3 promotes translation in human cancer cells

Project description:we find METTL3 associates with polyribosomes and promotes translation. METTL3 depletion inhibits translation, and both wild-type and catalytically inactive METTL3 promote translation when tethered to the 3' untranslated region (UTR) of a reporter mRNA. Mechanistically, METTL3 enhances mRNA translation through an interaction with the translation initiation machinery. m6A seq in A549 and H1299 cells, RNA seq in METTL3 knockdown cells

2016-07-03 | E-GEOD-76367 | biostudies-arrayexpress

Binding motif analysis of METTL3，WTAP in METTL3，WTAP overexpressed Human 293T cells

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2014-01-16 | E-GEOD-50580 | biostudies-arrayexpress

ATAC-seq of liver samples in Mettl3 flox/flox and hepatocyte-specific Mettl3 knockout (HKO) mice

Project description:Purpose: The goal of this study is to determine whether hepatic deletion of Mettl3 affects chromatin accessibility. Methods: Liver samples were pooled from livers of Mettl3 HKO and Mettl3 flox/flox mice (n=4 for each group). Nuclei was extracted from liver samples, and the nuclei pellet was resuspended in the Tn5 transposase reaction mix. The transposition reaction was incubated at 37°C for 30 min. Equimolar Adapter1 and Adatper 2 were added after transposition, PCR was then performed to amplify the library. After the PCR reaction, libraries were purified with the AMPure beads and library quality was assessed with Qubit. The clustering of the index-coded samples was performed on a cBot Cluster Generation System using TruSeq PE Cluster Kit v3-cBot-HS (Illumina) according to the manufactuer’s instructions. After cluster generation, the library preparations were sequenced on an Illumina NovaSeq 6000 platform and 150 bp paired-end reads were generated. ATAC-seq analysis was performed using a standard protocol. Results: The hepatic chromatin accessibility in Mettl3 flox/flox and HKO mice were characterized.

2021-10-29 | GSE141245 | GEO

Mettl3-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network [Liver RNA-seq]

Project description:RNA sequencing of livers tissues from control and hepatocyte-specific Mettl3 knockout with ALB-Cre (Mettl3 cKO) mice at different time points after birth.

2022-05-26 | GSE198512 | GEO

RNA-seq analysis of mRNA profiles in the livers of Mettl3 flox/flox and hepatocyte-specific Mettl3 knockout (HKO) mice

Project description:RNA-seq analysis of mRNA profiles in the livers of Mettl3 flox/flox and hepatocyte-specific Mettl3 knockout (HKO) mice

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METTL3-mediated m6A mRNA modification was involved in cadmium-induced liver disease

Project description:Cadmium is an environmental pollutant that has extensive deleterious effects. However, the mechanisms underlying the hepatotoxicity induced by long-term exposure to cadmium remained undefined. In the present study, we explored the role of m6A methylation in the development of cadmium-induced liver disease. We showed a dynamic change of RNA methylation in liver tissue from mice administrated with cadmium chloride (CdCl2) for 3, 6 and 9 months, respectively. Particularly, the METTL3 expression was declined in a time-dependent manner, associated with the degree of liver injury, indicating the involvement of METTL3 in hepatotoxicity induced by CdCl2. Moreover, we established a mouse model with liver-specific over-expression of Mettl3 and administrated these mice with CdCl2 for 6 months. Notably, METTL3 highly expressed in hepatocytes attenuated CdCl2-induced steatosis and liver fibrosis in mice. In vitro assay also showed METTL3 overexpression ameliorated the CdCl2-induced cytotoxicity and activation of primary hepatic stellate cells. Furthermore, transcriptome analysis identified 268 differentially expressed genes both in mice liver tissue treated with CdCl2 for 3 months and 9 months. Among them, 115 genes were predicted to be regulated by METTL3 determined by m6A2Target database. Further analysis revealed the perturbation of metabolic pathway, glycerophospholipid metabolism, ErbB signaling pathway, Hippo signaling pathway, and choline metabolism in cancer, and circadian rhythm, led to hepatotoxicity induced by CdCl2. Collectively, our findings reveal new insight into the crucial role of epigenetic modifications in hepatic diseases caused by long-term exposure to cadmium.

2023-06-30 | GSE230188 | GEO

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