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Disease Model of GATA4 Mutation Reveals Transcription Factor Cooperativity in Human Cardiogenesis

ABSTRACT: Disease Model of GATA4 Mutation Reveals Transcription Factor Cooperativity in Human Cardiogenesis

PROVIDER: PRJNA338963 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4032140.fastq.gz	Fastqsanger.gz
	SRR4032140_1.fastq.gz	Fastqsanger.gz
	SRR4032140_2.fastq.gz	Fastqsanger.gz
	SRR4032150.fastq.gz	Fastqsanger.gz
	SRR4032150_1.fastq.gz	Fastqsanger.gz

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Disease Model of GATA4 Mutation Reveals Transcription Factor Cooperativity in Human Cardiogenesis [ChIP-Seq]

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Disease Model of GATA4 Mutation Reveals Transcription Factor Cooperativity in Human Cardiogenesis.

Project description:Mutation of highly conserved residues in transcription factors may affect protein-protein or protein-DNA interactions, leading to gene network dysregulation and human disease. Human mutations in GATA4, a cardiogenic transcription factor, cause cardiac septal defects and cardiomyopathy. Here, iPS-derived cardiomyocytes from subjects with a heterozygous GATA4-G296S missense mutation showed impaired contractility, calcium handling, and metabolic activity. In human cardiomyocytes, GATA4 broadly co-occupied cardiac enhancers with TBX5, another transcription factor that causes septal defects when mutated. The GATA4-G296S mutation disrupted TBX5 recruitment, particularly to cardiac super-enhancers, concomitant with dysregulation of genes related to the phenotypic abnormalities, including cardiac septation. Conversely, the GATA4-G296S mutation led to failure of GATA4 and TBX5-mediated repression at non-cardiac genes and enhanced open chromatin states at endothelial/endocardial promoters. These results reveal how disease-causing missense mutations can disrupt transcriptional cooperativity, leading to aberrant chromatin states and cellular dysfunction, including those related to morphogenetic defects.

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Transcription profiling of Xenopus animal cap cardiogenesis model to examine immediate early targets of Gata4 and Gata5.

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