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

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

PROVIDER: PRJNA974008 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24650859_1.fastq.gz	Fastqsanger.gz
	SRR24650859_2.fastq.gz	Fastqsanger.gz
	SRR24650860_1.fastq.gz	Fastqsanger.gz
	SRR24650860_2.fastq.gz	Fastqsanger.gz
	SRR24650861_1.fastq.gz	Fastqsanger.gz

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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.

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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 [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 [RNA-seq]

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

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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.

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

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