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Transcriptome analysis and mapping histone acylations in fasted mouse livers

ABSTRACT: Transcriptome analysis and mapping histone acylations in fasted mouse livers

PROVIDER: PRJNA394910 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5838440.fastq.gz	Fastqsanger.gz
	SRR5838441.fastq.gz	Fastqsanger.gz
	SRR5838442.fastq.gz	Fastqsanger.gz
	SRR5838423.fastq.gz	Fastqsanger.gz
	SRR5838443.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of fasted mouse livers

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Transcriptome analysis and mapping histone acylations in fasted mouse livers

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Project description:Spatial heterogeneity and plasticity of the mammalian liver is critical for systemic metabolic homeostasis in response to fluctuating nutritional status. Here, we generated a high-resolution transcriptomic landscape of the livers from mice that were either fed chow (fed), fasted for 18 h (fasted), or fasted for 18 h and then refed for 6 h (refed) using spatial transcriptomics (ST) and quantified changes in gene expression. This work provides a critical foundation for future mechanistic studies of liver metabolic heterogeneity and plasticity, and will help to understand the zonated pathology during liver disease progression.

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Project description:RNAseq analysis was conducted to complement the targeted and untargeted metabolomics analysis of livers overexpressing the CoA-degrading enzyme Nudt7 or GFP (control). Lipid metabolism requires coenzyme A (CoA), which is found in multiple subcellular compartments including the peroxisomes. In the liver, CoA levels are dynamically adjusted between the fed and fasted states. The elevation in CoA levels that occurs during fasting is driven by increased synthesis but also correlates with decreased expression of Nudt7, the major CoA-degrading enzyme in the liver. Nudt7 resides in the peroxisomes and we overexpressed this enzyme in mouse livers to determine its effect on the size and composition of the hepatic CoA pool in the fed and fasted states. Nudt7 overexpression did not change total CoA levels but decreased the concentration of short-chain acyl-CoAs and choloyl-CoA in fasted livers, when endogenous Nudt7 activity was lowest. The effect on these acyl-CoAs correlated with a significant decrease in the hepatic bile acid content and in the rate of peroxisomal fatty acid oxidation, as estimated by targeted and untargeted metabolomics, combined with the measurement of fatty acid oxidation in intact hepatocytes. Identification of the CoA species and metabolic pathways affected the overexpression on Nudt7 in vivo supports the conclusion that the nutritionally-driven modulation of Nudt7 activity could contribute to the regulation of the peroxisomal CoA pool and peroxisomal lipid metabolism.

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