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Liver-specific matrin-3 knockout regulates hepatic transcriptome and chromatin accessibility in mice

ABSTRACT: Liver-specific matrin-3 knockout regulates hepatic transcriptome and chromatin accessibility in mice

PROVIDER: PRJNA1034149 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26622665_1.fastq.gz	Fastqsanger.gz
	SRR26622665_2.fastq.gz	Fastqsanger.gz
	SRR26622666_1.fastq.gz	Fastqsanger.gz
	SRR26622666_2.fastq.gz	Fastqsanger.gz
	SRR26622667_1.fastq.gz	Fastqsanger.gz

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Liver-specific matrin-3 knockout alters the hepatic transcriptome of chow diet-fed mice [RNA-seq]

Project description:Matrin-3 is an RNA-binding protein involved in the pathogenesis of human diseases. Here we examined the hepatic transcriptome of chow-diet fed mice. Bulk RNA-seq and bioinformatics analysis identified 646 and 145 differentially expressed genes (Padj < 0.05), respectively in the livers of female and male matrin-3 LKO mice. Enrichr analysis of these DEGs revealed several common Hallmark terms including cholesterol homeostasis, fatty acid metabolism, xenobiotic metabolism, and epithelial mesenchymal transition between female and male mice. Our data demonstrated that liver-specific matrin-3 deficiency re-programs the hepatic transcriptome in the liver of chow diet-fed mice.

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Liver-specific matrin-3 knockout alters the hepatic transcriptome of high-fat diet-fed mice [RNA-seq]

Project description:Matrin-3 is an RNA-binding protein involved in the pathogenesis of human diseases. Here we examined its previously uncharacterized role in limiting hepatic steatosis and stress response via the constitutive androstane receptor. Matrin-3 expression was induced in the steatotic livers of mice and humans. Liver-specific matrin-3 knockout (LKO) exacerbated high-fat diet (HFD)-induced steatosis, acute phase response, and inflammation in the liver of mice. Bulk RNA-seq and bioinformatics analysis identified 1,333 and 239 differentially expressed genes (fold change > 1.5 & Padj < 0.05), respectively in the livers of female and male matrin-3 LKO mice. Gene Set Enrichment Analysis revealed that the top most enriched Gene Ontology Biological Process was the “Xenobiotic metabolic process” in female matrin-3 floxed mice that is downregulated. The top two enriched biological processes are “Acute inflammatory response” and “Acute phase response” in the liver of female LKO mice that are upregulated. Several GO terms related to lipid metabolism and xenobiotic metabolism were enriched in the livers of male mice. Real-time qPCR revealed that the expression of many genes involved in xenobiotic metabolism was reduced in the liver of female LKO mice and to a lesser extent in the liver of male LKO mice, while the expression of acute-phase response genes was induced in the liver of female but not male LKO mice. Our data demonstrated that liver-specific matrin-3 deficiency re-programs the hepatic transcriptome enriched for xenobiotic metabolism pathway, acute-phase and inflammatory response signaling in the liver of HFD-fed mice.

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Single-nucleus Multiome ATAC and Gene Expression analysis of the liver tissues from matrin-3 floxed and liver-specific knockout mice

Project description:Matrin-3 is an RNA-binding protein involved in the pathogenesis of human diseases. Here we examined the hepatic transcriptome and chromatin accessibility of high-fat-diet (Research Diets, Inc; D12492) fed mice. After quality control filtering and removal of putative doublets, single-nucleus RNA-seq clusters were assigned to five different cell types, including hepatocytes (Hep), Kupffer cells (KC), endothelial cells (EC), hepatic stellate cells (HSC), and leukocytes (Leuk). The total number of cells is 1,543. Differential analysis of single-nucleus RNA-seq data identified 492 DEGs (FDR < 0.05 & fold change > 1.5) in the hepatocyte cluster between matrin-3 floxed and liver-specific knockout (LKO) mice. GSEA revealed that KEGG terms such as “Drug metabolism cytochrome P450” and “Metabolism of xenobiotics by cytochrome P450” were enriched in hepatocytes

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Project description:Matrin-3 is an RNA-binding protein involved in the pathogenesis of human diseases. Here we examined its previously uncharacterized role in regulating chromatin accessibility in the liver of mice. Bulk ATAC-seq and bioinformatics analysis identified 523 and 829 differential peaks (FDR < 0.05), respectively, in the liver of female mice fed a chow diet or 60% HFD for 16 weeks. Peak annotation by HOMER and ChIPseeker identified 183 and 444 genes, respectively, that are associated with the differential peaks. Enrichr analysis of these genes revealed that Hallmark terms such as "Xenobiotic metabolism" was enriched in the liver of chow-fed and HFD-fed mice. TRRUST database analysis from Metascape uncovered that Hnf4α is the main transcription factor regulating these peak-associated genes in the liver of chow-fed mice, and Hnf4α and Nr1i3 are the main transcription factors regulating these peak-associated genes in the liver of HFD-fed mice. Our data demonstrated that liver-specific matrin-3 deficiency alters chromatin accessibility likely affecting the action of two transcription factors Hnf4α and Nr1i3 in the liver of mice.

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Liver-specific matrin-3 knockout regulates hepatic transcriptome and chromatin accessibility in mice

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

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Transcription profiling of HeLa cells expressing GFP-tagged chicken matrin 3

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