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Genome-wide transcriptomic profiling of cardiomyocyte differentiation from Wild-type and PERK-KO H1 hESCs [RNA-seq]

ABSTRACT: Genome-wide transcriptomic profiling of cardiomyocyte differentiation from Wild-type and PERK-KO H1 hESCs [RNA-seq]

PROVIDER: PRJNA777808 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16768631_1.fastq.gz	Fastqsanger.gz
	SRR16768631_2.fastq.gz	Fastqsanger.gz
	SRR16768632_1.fastq.gz	Fastqsanger.gz
	SRR16768632_2.fastq.gz	Fastqsanger.gz
	SRR16768633_1.fastq.gz	Fastqsanger.gz

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Genome-wide transcriptomic profiling of cardiomyocyte differentiation from Wild-type and PERK-KO H1 hESCs [RNA-seq]

Project description:Cardiac development involves large-scale rearrangements of the proteome. How the developing cardiac cells maintain the integrity of the proteome during the rapid lineage transition remains unclear. Here we show that proteotoxic stress visualized by the misfolded protein aggregates appears during early cardiac differentiation of human embryonic stem cells (hESCs) and is resolved by activation of the PERK branch of the unfolded protein response (UPR). PERK depletion increases misfolded protein accumulation, leading to pluripotency exit defect and impaired mesendoderm specification of hESCs. Mechanistically, we found that PERK safeguards cardiogenesis through its conserved downstream effector ATF4, which subsequently activates a novel transcriptional target WARS1, to cope with the differentiation-induced proteotoxic stress. Our results indicate that protein quality control represents a previously unrecognized core component of the cardiogenic regulatory network. Broadly, these findings provide a framework for understanding how UPR is integrated into the developmental program by activating the PERK-ATF4-WARS1 axis.

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