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Effect of loss of HNF4A in liver and effect of ectopic expression of HNF4A in mouse fibroblast cells

ABSTRACT: Effect of loss of HNF4A in liver and effect of ectopic expression of HNF4A in mouse fibroblast cells

PROVIDER: PRJNA867701 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20993100_1.fastq.gz	Fastqsanger.gz
	SRR20993100_2.fastq.gz	Fastqsanger.gz
	SRR20993101_1.fastq.gz	Fastqsanger.gz
	SRR20993101_2.fastq.gz	Fastqsanger.gz
	SRR20993102_1.fastq.gz	Fastqsanger.gz

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Effect of loss of HNF4A in liver and effect of ectopic expression of HNF4A in mouse fibroblast cells

Project description:To understand how HNF4A loss affects gene expression in mouse liver. We used control and HNF4A KO mouse livers for RNA sequencing. In addition, we also examined the effect of HNF4A gain in mouse fibroblast cells by ectropically expressing HNF4A in NIH3T3 cell to identify genes that are regulated by HNF4A.

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HNF4A

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Project description:The glucocorticoid receptor (GR) is a nuclear hormone receptor critical to the regulation of energy metabolism and the inflammatory response. The actions of GR are highly dependent on cell type and environmental context. Here, we demonstrate the necessity for liver lineage-determining factor hepatocyte nuclear factor 4A (HNF4A) in defining liver-specificity of GR action. In normal mouse liver, the HNF4 motif lies adjacent to the glucocorticoid response element (GRE) at GR binding sites found within regions of open chromatin. In the absence of HNF4A, the liver GR cistrome is remodelled, with both loss and gain of GR recruitment evident. Loss of chromatin accessibility at HNF4A-marked sites leads to loss of GR binding at weak GRE motifs. GR binding is gained at sites characterised by strong GRE motifs, which typically show GR recruitment in non-liver tissues. The functional importance of these HNF4A-regulated GR sites is further demonstrated by evidence of an altered transcriptional response to glucocorticoid treatment in the Hnf4a-null liver.

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