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Genome-wide estrogen-related receptor gamma (ERRg) occupancy in human iPS cell-derived cardiomyocytes (hiPSC-CMs)

ABSTRACT: Genome-wide estrogen-related receptor gamma (ERRg) occupancy in human iPS cell-derived cardiomyocytes (hiPSC-CMs)

PROVIDER: PRJNA453931 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7073311.fastq.gz	Fastqsanger.gz
	SRR7073312.fastq.gz	Fastqsanger.gz
	SRR7073313.fastq.gz	Fastqsanger.gz
	SRR7073314.fastq.gz	Fastqsanger.gz
	SRR7073315.fastq.gz	Fastqsanger.gz

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RNA-Seq transcriptome profiling of human iPS cell-derived cardiomyocytes (hiPSC-CMs) following overexpression (OE) of estrogen-related receptor gamma (ERRg)

Project description:Transcriptional regulatory circuits that drive cardiomyocyte maturation are poorly understood. Human iPS cell-derived cardiomyocytes (hiPSC-CMs) have been shown to have fetal cardiomyocyte features in terms of metabolic gene expression profiles. Here we found that in hiPSC-CMs, overexpression of estrogen-related receptor gamma (ERRg) is sufficient to drive cardiomyocyte metabolic maturation programs including the induction of a number of oxidative mitochondrial metabolic genes.

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Project description:To determine the role of estrogen-related receptor alpha and gamma (ERRa/g) on chromatin accessibility, we performed ATAC-seq studies with WT control and ERRa/g KO hiPSC-CMs. We found that ERRa/g activates cardiac chromatin accessibilities in hiPSC-CMs. A subset of the decreased ATAC signals by loss of ERRa/g overlapped ERRg peaks (GSE113760) in hiPSC-CMs, suggesting that ERRg might be directly involved in the activation of cardiac chromatin accessibilities. The motif analysis with decreased ATAC signal by loss of ERRa/g revealed that cardiac-enriched transcription factors such as MEF2 and GATA could cooperate with ERR.

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