Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE197564 | GEO | 2022/05/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

| PRJNA815660 | ENA

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]

| PRJNA815663 | ENA

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]

| PRJNA815662 | ENA

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

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]

| PRJNA815661 | ENA

METTL3-Mediated m6A Modification Controls Splicing Factor Abundance and Contributes to Aggressive CLL.

Project description:RNA splicing dysregulation underlies the onset and progression of cancers. In chronic lymphocytic leukemia (CLL), spliceosome mutations leading to aberrant splicing occur in ∼20% of patients. However, the mechanism for splicing defects in spliceosome-unmutated CLL cases remains elusive. Through an integrative transcriptomic and proteomic analysis, we discover that proteins involved in RNA splicing are posttranscriptionally upregulated in CLL cells, resulting in splicing dysregulation. The abundance of splicing complexes is an independent risk factor for poor prognosis. Moreover, increased splicing factor expression is highly correlated with the abundance of METTL3, an RNA methyltransferase that deposits N6-methyladenosine (m6A) on mRNA. METTL3 is essential for cell growth in vitro and in vivo and controls splicing factor protein expression in a methyltransferase-dependent manner through m6A modification-mediated ribosome recycling and decoding. Our results uncover METTL3-mediated m6A modification as a novel regulatory axis in driving splicing dysregulation and contributing to aggressive CLL.SignificanceMETTL3 controls widespread splicing factor abundance via translational control of m6A-modified mRNA, contributes to RNA splicing dysregulation and disease progression in CLL, and serves as a potential therapeutic target in aggressive CLL. See related commentary by Janin and Esteller, p. 176. This article is highlighted in the In This Issue feature, p. 171.

| S-EPMC10150290 | 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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data