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Quaking regulates lineage-specific splicing patterns between early progenitor cells and is required for cardiac cell fate specification

ABSTRACT: Quaking regulates lineage-specific splicing patterns between early progenitor cells and is required for cardiac cell fate specification

PROVIDER: PRJNA682547 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13197523_1.fastq.gz	Fastqsanger.gz
	SRR13197523_2.fastq.gz	Fastqsanger.gz
	SRR13197524_1.fastq.gz	Fastqsanger.gz
	SRR13197524_2.fastq.gz	Fastqsanger.gz
	SRR13197525_1.fastq.gz	Fastqsanger.gz

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Quaking regulates lineage-specific splicing patterns between early progenitor cells and is required for cardiac cell fate specification

Project description:Cell type-specific alternative splicing (AS) regulates tissue homeostasis, with several examples of AS promoting stem cell self-renewal or differentiation. However, the lineage-specific patterns of AS required for early progenitor cells of each of the three germ layers and the specific RNA binding proteins (RBPs) essential for early cell fate are unknown. To approach this question, we performed parallel RNA-seq on human embryonic stem cells (hESCs), hESC-derived definitive endoderm (DE), cardiac mesoderm (CM), and ectoderm (ECT) cells. Analysis of AS patterns in these datasets show that, unlike ECT cells, DE and CM cells display distinct and non-overlapping patterns of lineage-specific splicing.

2022-04-19 | GSE162649 | GEO

Definition of germ cell lineage alternative splicing programs reveals a critical role for Quaking in specifying cardiac cell fate

Project description:Alternative splicing is critical for development. However, its role in the specification of the three embryonic germ layers is poorly understood. By performing RNA-Seq on human embryonic stem cells (hESCs) and derived endoderm, cardiac mesoderm, and ectoderm cell lineages, we detect distinct alternative splicing programs associated with each lineage. The most prominent splicing program differences are observed between definitive endoderm and cardiac mesoderm. Integrative multi-omics analyses link each program with lineage-specific RNA binding protein regulators, and further suggest a widespread role for Quaking (QKI) in the specification of cardiac mesoderm. Remarkably, knockout of QKI disrupts the cardiac mesoderm-associated alternative splicing program and formation of myocytes. These changes likely arise in part through reduced expression of BIN1 splice variants linked to cardiac development. Collectively, our results thus uncover alternative splicing programs associated with the three germ lineages and demonstrate an important role for QKI in the formation of cardiac mesoderm.

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Definition of germ layer cell lineage alternative splicing programs reveals a critical role for Quaking in specifying cardiac cell fate.

Project description:Alternative splicing is critical for development; however, its role in the specification of the three embryonic germ layers is poorly understood. By performing RNA-Seq on human embryonic stem cells (hESCs) and derived definitive endoderm, cardiac mesoderm, and ectoderm cell lineages, we detect distinct alternative splicing programs associated with each lineage. The most prominent splicing program differences are observed between definitive endoderm and cardiac mesoderm. Integrative multi-omics analyses link each program with lineage-enriched RNA binding protein regulators, and further suggest a widespread role for Quaking (QKI) in the specification of cardiac mesoderm. Remarkably, knockout of QKI disrupts the cardiac mesoderm-associated alternative splicing program and formation of myocytes. These changes arise in part through reduced expression of BIN1 splice variants linked to cardiac development. Mechanistically, we find that QKI represses inclusion of exon 7 in BIN1 pre-mRNA via an exonic ACUAA motif, and this is concomitant with intron removal and cleavage from chromatin. Collectively, our results uncover alternative splicing programs associated with the three germ lineages and demonstrate an important role for QKI in the formation of cardiac mesoderm.

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