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Competitive regulation of HOPX transcription governs cardiomyocyte maturation

ABSTRACT: Competitive regulation of HOPX transcription governs cardiomyocyte maturation

PROVIDER: PRJEB52787 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR9717290.fastq.gz	Fastqsanger.gz
	ERR9717285.fastq.gz	Fastqsanger.gz
	ERR9717286.fastq.gz	Fastqsanger.gz
	ERR9717287.fastq.gz	Fastqsanger.gz
	ERR9717288.fastq.gz	Fastqsanger.gz

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Competitive regulation of HOPX transcription governs cardiomyocyte maturation

Project description:This study establishes the homeodomain only protein, HOPX, as a determinant controlling the molecular switch between cardiomyocyte progenitor and maturation gene programs. This dataset is about time-course CAGE (capped analysis of gene expression) data with genome-wide active transcription footprinting. HOPX CRISPRi cells were differentiated into cardiomyocytes ± DOX and analyzed by CAGE sequencing, among other methods. The study revealed that HOPX interacts with and controls core cardiac networks by regulating the activity of mutually exclusive developmental gene programs.

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Persistence of effector memory Th1 cells is regulated by the homeobox only protein Group1 Hopx-/-, Group2 Hopx+/-, Group3 Hopx+/+

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AP-1 activation mediates postnatal cardiomyocyte maturation

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Project description:Cardiac maturation lays the foundation for postnatal heart development and disease, yet little is known about the contributions of the microenvironment to cardiomyocyte maturation. By integrating single-cell RNA-sequencing data of mouse hearts at multiple postnatal stages, we construct cellular interactomes and regulatory signaling networks. Here we report switching of fibroblast subtypes from a neonatal to adult state and this drives cardiomyocyte maturation. Molecular and functional maturation of neonatal mouse cardiomyocytes and human embryonic stem cell-derived cardiomyocytes are considerably enhanced upon coculture with corresponding adult cardiac fibroblasts. Further, single-cell analysis of in vivo and in vitro cardiomyocyte maturation trajectories identify highly conserved signaling pathways, pharmacological targeting of which substantially delays cardiomyocyte maturation in postnatal hearts, and markedly enhances cardiomyocyte proliferation and improves cardiac function in infarcted hearts. Together, we identify cardiac fibroblasts as a key constituent in the microenvironment promoting cardiomyocyte maturation, providing insights into how the manipulation of cardiomyocyte maturity may impact on disease development and regeneration.

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