Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Adverse maternal environments perturb hepatic DNA methylome and transcriptome prior to the adult-onset non-alcoholic fatty liver disease in mouse offspring [RNA-seq]

ABSTRACT: Adverse maternal environments perturb hepatic DNA methylome and transcriptome prior to the adult-onset non-alcoholic fatty liver disease in mouse offspring [RNA-seq]

PROVIDER: PRJNA974009 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR24650832_1.fastq.gz	Fastqsanger.gz
	SRR24650832_2.fastq.gz	Fastqsanger.gz
	SRR24650833_1.fastq.gz	Fastqsanger.gz
	SRR24650833_2.fastq.gz	Fastqsanger.gz
	SRR24650834_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 40

Similar Datasets

Adverse maternal environments perturb hepatic DNA methylome and transcriptome prior to the adult-onset non-alcoholic fatty liver disease in mouse offspring

Project description:Adverse maternal environments perturb hepatic DNA methylome and transcriptome prior to the adult-onset non-alcoholic fatty liver disease in mouse offspring

| PRJNA974001 | ENA

Adverse maternal environments perturb hepatic DNA methylome and transcriptome prior to the adult-onset non-alcoholic fatty liver disease in mouse offspring [RRBS]

Project description:Exposure to adverse early-life environment (AME) increases the incidence of developing adult-onset non-alcoholic fatty liver disease (NAFLD). DNA methylation has been postulated to link AME and late-onset diseases. The objective was to investigate whether and to what extent hepatic DNA methylome was perturbed prior to the development of NAFLD in offspring exposed to AME in mice. AME constituted maternal western diet and late-gestational stress. Male offspring livers at birth (d0) and weaning (d21) were used for evaluating DNA methylome and transcriptome using reduced representation of bisulfite sequencing and RNA-seq, respectively. We found AME caused 5,879 differentially methylated regions (DMRs) and zero differentially expressed gene (DEG) at d0, and 2,970 and 123, respectively at d21. Majority of the DMRs were distal from gene transcription start sites and did not correlate with DEGs. The DEGs at d21 were significantly en-riched in GO biological processes characteristic of liver metabolic functions. In conclusion, AME drove changes in hepatic DNA methylome which preceded perturbations in the hepatic metabolic transcriptome, which preceded the onset of NAFLD. We speculate that subtle impacts in dynamic enhancers lead to long-range regulatory changes that manifest over time as gene network alter-nations to increase the incidence of NAFLD later in life.

2023-05-23 | GSE232810 | GEO

Adverse maternal environments perturb hepatic DNA methylome and transcriptome prior to the adult-onset non-alcoholic fatty liver disease in mouse offspring [RNA-seq]

2023-05-23 | GSE232811 | GEO

Adverse maternal environments perturb hepatic DNA methylome and transcriptome prior to the adult-onset non-alcoholic fatty liver disease in mouse offspring [RRBS]

Project description:Adverse maternal environments perturb hepatic DNA methylome and transcriptome prior to the adult-onset non-alcoholic fatty liver disease in mouse offspring [RRBS]

| PRJNA974008 | ENA

Adverse Maternal Environments Perturb Hepatic DNA Methylome and Transcriptome Prior to the Adult-Onset Non-Alcoholic Fatty Liver Disease in Mouse Offspring

Project description:Exposure to adverse early-life environments (AME) increases the incidence of developing adult-onset non-alcoholic fatty liver disease (NAFLD). DNA methylation has been postulated to link AME and late-onset diseases. This study aimed to investigate whether and to what extent the hepatic DNA methylome was perturbed prior to the development of NAFLD in offspring exposed to AME in mice. AME constituted maternal Western diet and late-gestational stress. Male offspring livers at birth (d0) and weaning (d21) were used for evaluating the DNA methylome and transcriptome using the reduced representation of bisulfite sequencing and RNA-seq, respectively. We found AME caused 5879 differentially methylated regions (DMRs) and zero differentially expressed genes (DEGs) at d0 and 2970 and 123, respectively, at d21. The majority of the DMRs were distal to gene transcription start sites and did not correlate with DEGs. The DEGs at d21 were significantly enriched in GO biological processes characteristic of liver metabolic functions. In conclusion, AME drove changes in the hepatic DNA methylome, which preceded perturbations in the hepatic metabolic transcriptome, which preceded the onset of NAFLD. We speculate that subtle impacts on dynamic enhancers lead to long-range regulatory changes that manifest over time as gene network alternations and increase the incidence of NAFLD later in life.

| S-EPMC10180730 | biostudies-literature

Adverse maternal environments perturb hepatic DNA methylome and transcriptome prior to the adult-onset non-alcoholic fatty liver disease in mouse offspring

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

2023-05-23 | GSE232812 | GEO

CRISPRai Perturb-seq [Series 1]

Project description:CRISPRai Perturb-seq [Series 1]

| PRJNA912208 | ENA

Perturb-Seq using T2D islets

Project description:Perturb-Seq using T2D islets

| PRJNA568200 | ENA

Perturb-Seq in pluripotent stem cells

Project description:CRISPRi Perturb-Seq of coding genes and lncRNAs in pluripotent stem cells

2025-06-01 | GSE176038 | GEO

Lineage recording in human cerebral organoids (iTracer-perturb)

Project description:Induced pluripotent stem cell (iPSC) derived organoid systems provide models to study human organ development. Single-cell transcriptome sequencing enables highly-resolved descriptions of cell state heterogeneity within these systems and computational methods can reconstruct developmental trajectories. However, new approaches are needed to directly measure lineage relationships in these systems. Here we establish an inducible dual channel lineage recorder, iTracer, that couples reporter barcodes, inducible CRISPR/Cas9 scarring, and single-cell transcriptomics to analyze state and lineage relationships in iPSC-derived systems. This data set include the iTracer-perturb data of one cerebral organoid with simultaneous TSC2 perturbation and lineage recording.

2021-11-03 | E-MTAB-10971 | biostudies-arrayexpress

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