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Liver Homeostasis, Hepatocyte Ploidy, and Circadian Rhythm-controlled Gene Expression are Perturbed in Liver-Specific METTL3 Knockout Mice

ABSTRACT: Liver Homeostasis, Hepatocyte Ploidy, and Circadian Rhythm-controlled Gene Expression are Perturbed in Liver-Specific METTL3 Knockout Mice

PROVIDER: PRJNA734937 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14718160.fastq.gz	Fastqsanger.gz
	SRR14718161.fastq.gz	Fastqsanger.gz
	SRR14718162.fastq.gz	Fastqsanger.gz
	SRR14718163.fastq.gz	Fastqsanger.gz
	SRR14718164.fastq.gz	Fastqsanger.gz

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Liver Homeostasis, Hepatocyte Ploidy, and Circadian Rhythm-controlled Gene Expression are Perturbed in Liver-Specific METTL3 Knockout Mice

Project description:METTL3 is essential for ESC differentiation and embryonic development, and its dysregulation is linked to various diseases including metabolic disorders and cancer. However, the consequence of m6A perturbation in the mammalian liver is not understood. Here, we provide insight into this by generating mice M3LKO (Mettl3fl/fl; Alb-Cre) mice carrying a hepatocyte-specific deletion of Mettl3.

2021-09-15 | GSE176113 | GEO

METTL3 Regulates Liver Homeostasis, Hepatocyte Ploidy, and Circadian Rhythm-Controlled Gene Expression in Mice.

Project description:N6-methyladenosine (m6A), the most abundant internal modifier of mRNAs installed by the methyltransferase 13 (METTL3) at the (G/A)(m6A)C motif, plays a critical role in the regulation of gene expression. METTL3 is essential for embryonic development, and its dysregulation is linked to various diseases. However, the role of METTL3 in liver biology is largely unknown. In this study, METTL3 function was unraveled in mice depleted of Mettl3 in neonatal livers (Mettl3fl/fl; Alb-Cre). Liver-specific Mettl3 knockout (M3LKO) mice exhibited global decrease in m6A on polyadenylated RNAs and pathologic features associated with nonalcoholic fatty liver disease (eg, hepatocyte ballooning, ductular reaction, microsteatosis, pleomorphic nuclei, DNA damage, foci of altered hepatocytes, focal lobular and portal inflammation, and elevated serum alanine transaminase/alkaline phosphatase levels). Mettl3-depleted hepatocytes were highly proliferative, with decreased numbers of binucleate hepatocytes and increased nuclear polyploidy. M3LKO livers were characterized by reduced m6A and expression of several key metabolic transcripts regulated by circadian rhythm and decreased nuclear protein levels of the core clock transcription factors BMAL1 and CLOCK. A significant decrease in total Bmal1 and Clock mRNAs but an increase in their nuclear levels were observed in M3LKO livers, suggesting impaired nuclear export. Consistent with the phenotype, methylated (m6A) RNA immunoprecipitation coupled with sequencing and RNA sequencing revealed transcriptome-wide loss of m6A markers and alterations in abundance of mRNAs involved in metabolism in M3LKO. Collectively, METTL3 and m6A modifications are critical regulators of liver homeostasis and function.

| S-EPMC8759040 | biostudies-literature

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

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.

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Depletion of m6A methylation by conditional Mettl3 knockout in Ascl1-induced neurons

Project description:We have perturbed RNA methylation machinery and investigated the change in subcellular localization of mRNA in Ascl1-induced neurons (iNeurons). Mutant iNeuron line harbouring tagged endogenous Mettl3 was generated which allowed for the selective and targeted depletion of Mettl3 protein with the addition of dTAG. Cells were treated with dTAG for 40 hours then separated into compartments (neurites and soma) and then sequenced in parallel with samples which received no dTAG treatment.

2023-07-12 | E-MTAB-9643 | biostudies-arrayexpress

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Project description:This study investigated firstly, the impact of ploidy on growth performance and whole body composition of Atlantic salmon at different early freshwater stages (34 dph (days post-hatching) alevin; 109 dph; fry and 162 dph parr;) and secondly, whether phenotypic differences at these stages were reflected in the protein samples collectedproteome from whole fish, white muscle or liver tissue. Female diploid and triploid Atlantic salmon (n = 3) were first fed at 35 dph and then maintained by feeding to satiation on commercial feeds.

2017-12-14 | PXD005450 | Pride

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

NGS5413 - METTL3 and METTL14 KOs in hMDMs

Project description:human primay macrophages (hMDMs) were genetically perturbed for METTL3 and stimulated with IFNg for 18h

2024-08-14 | GSE268351 | GEO

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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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

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