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Mettl3-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network

ABSTRACT: Mettl3-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network

PROVIDER: PRJNA815660 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18312828_1.fastq.gz	Fastqsanger.gz
	SRR18312828_2.fastq.gz	Fastqsanger.gz
	SRR18312829_1.fastq.gz	Fastqsanger.gz
	SRR18312829_2.fastq.gz	Fastqsanger.gz
	SRR18312830_1.fastq.gz	Fastqsanger.gz

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

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

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

Project description:Mettl3-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network [Primary hepatocyte RNA-seq]

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

Project description:Mettl3-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network [m6A-RIP-RNA-seq]

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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

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

Project description:RNA sequencing of primary hepatocytes from Control and and hepatocyte-specific Mettl3 knockout with ALB-Cre (Mettl3 cKO) mice after Actinomycin D treatment.

2022-05-26 | GSE198513 | GEO

Mettl3-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-05-25 | GSE197564 | GEO

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

Project description:m6A-RIP sequencing of mouse liver tissues at different time points after birth.

2022-05-26 | GSE198511 | GEO

Mettl3-mediated mRNA m<sup>6</sup>A modification controls postnatal liver development by modulating the transcription factor Hnf4a.

Project description:Hepatic specification and functional maturation are tightly controlled throughout development. N6-methyladenosine (m6A) is the most abundant RNA modification of eukaryotic mRNAs and is involved in various physiological and pathological processes. However, the function of m6A in liver development remains elusive. Here we dissect the role of Mettl3-mediated m6A modification in postnatal liver development and homeostasis. Knocking out Mettl3 perinatally with Alb-Cre (Mettl3 cKO) induces apoptosis and steatosis of hepatocytes, results in severe liver injury, and finally leads to postnatal lethality within 7 weeks. m6A-RIP sequencing and RNA-sequencing reveal that mRNAs of a series of crucial liver-enriched transcription factors are modified by m6A, including Hnf4a, a master regulator for hepatic parenchymal formation. Deleting Mettl3 reduces m6A modification on Hnf4a, decreases its transcript stability in an Igf2bp1-dependent manner, and down-regulates Hnf4a expression, while overexpressing Hnf4a with AAV8 alleviates the liver injury and prolongs the lifespan of Mettl3 cKO mice. However, knocking out Mettl3 in adults using Alb-CreERT2 does not affect liver homeostasis. Our study identifies a dynamic role of Mettl3-mediated RNA m6A modification in liver development.

| S-EPMC9355946 | biostudies-literature

HNF4A

Project description:HNF4A

| PRJNA940175 | ENA