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Essential and Opposite Roles of ARID1A in Coordinating Human Cardiogenesis and Neurogenesis from Pluripotent Stem Cells

ABSTRACT: Essential and Opposite Roles of ARID1A in Coordinating Human Cardiogenesis and Neurogenesis from Pluripotent Stem Cells

PROVIDER: PRJNA579345 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10341329_1.fastq.gz	Fastqsanger.gz
	SRR10341329_2.fastq.gz	Fastqsanger.gz
	SRR10341330_1.fastq.gz	Fastqsanger.gz
	SRR10341330_2.fastq.gz	Fastqsanger.gz
	SRR10341930_1.fastq.gz	Fastqsanger.gz

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Genome-wide maps of ARID1A binding genes in H9 human embryonic stem cells

Project description:We reported loss of ARID1A promoted neurogenesis and inhibited cardiogenesis. Here we used specific ARID1A antibody to pull down ARID1A binding genomic DNA in human embryonic stem cells, which let us know the potential genes regulated by ARID1A during neurogenesis and inhibited cardiogenesis. IgG was used as the control.

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Genome-wide maps of ARID1A binding genes in H9 human embryonic stem cells.

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Essential and Opposite Roles of ARID1A in Coordinating Human Cardiogenesis and Neurogenesis from Pluripotent Stem Cells

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Assay for Transposase Accessible Chromatin with high-throughput sequencing (ATAC-seq) revealed genomic chromatin accessibilities change induced by loss of ARID1A in differentiated (day 4) H9 hESCs

Project description:We reported loss of ARID1A promoted neurogenesis and inhibited cardiogenesis. Under microscopy, we observed that spontaneously differentiated cells were induced in ARID1A KO H9 hESCs cultured in mTesR medium. We did not know what cells types were. Here ATAC-seq were used to investigate chromatin accessibilities change in differentiated (day 4) WT H9 hESCs and ARID1A KO hESC cells.

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Single cell RNA-seq revealed different cell types induced by loss of ARID1A in undifferentiated and differentiation (day 10) H9 hESCs.

Project description:We reported loss of ARID1A promoted neurogenesis and inhibited cardiogenesis. Under microscopy, we observed that spontaneously differentiated cells were induced in ARID1A KO H9 hESCs cultured in mTesR medium. After cardiac differentiation for 10 days, we also observed the cell types were totally different between WT and ARID1A KO cells. We did not know what cells types were. Here scRNA-seq were used to identify the cell types in WT H9 hESCs and ARID1A KO H9 hESCs.

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Genome-wide studies reveal the essential and opposite roles of ARID1A in controlling human cardiogenesis and neurogenesis from pluripotent stem cells.

Project description:BackgroundEarly human heart and brain development simultaneously occur during embryogenesis. Notably, in human newborns, congenital heart defects strongly associate with neurodevelopmental abnormalities, suggesting a common gene or complex underlying both cardiogenesis and neurogenesis. However, due to lack of in vivo studies, the molecular mechanisms that govern both early human heart and brain development remain elusive.ResultsHere, we report ARID1A, a DNA-binding subunit of the SWI/SNF epigenetic complex, controls both neurogenesis and cardiogenesis from human embryonic stem cells (hESCs) through distinct mechanisms. Knockout-of-ARID1A (ARID1A-/-) leads to spontaneous differentiation of neural cells together with globally enhanced expression of neurogenic genes in undifferentiated hESCs. Additionally, when compared with WT hESCs, cardiac differentiation from ARID1A -/- hESCs is prominently suppressed, whereas neural differentiation is significantly promoted. Whole genome-wide scRNA-seq, ATAC-seq, and ChIP-seq analyses reveal that ARID1A is required to open chromatin accessibility on promoters of essential cardiogenic genes, and temporally associated with key cardiogenic transcriptional factors T and MEF2C during early cardiac development. However, during early neural development, transcription of most essential neurogenic genes is dependent on ARID1A, which can interact with a known neural restrictive silencer factor REST/NRSF.ConclusionsWe uncover the opposite roles by ARID1A to govern both early cardiac and neural development from pluripotent stem cells. Global chromatin accessibility on cardiogenic genes is dependent on ARID1A, whereas transcriptional activity of neurogenic genes is under control by ARID1A, possibly through ARID1A-REST/NRSF interaction.

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