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CTCF counter-regulates cardiomyocyte development and maturation programs in the embryonic heart

ABSTRACT: CTCF counter-regulates cardiomyocyte development and maturation programs in the embryonic heart

PROVIDER: PRJNA311079 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3148300.fastq.gz	Fastqsanger.gz
	SRR3148301.fastq.gz	Fastqsanger.gz
	SRR3148302.fastq.gz	Fastqsanger.gz
	SRR3148294.fastq.gz	Fastqsanger.gz
	SRR3148295.fastq.gz	Fastqsanger.gz

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Similar Datasets

CTCF counter-regulates cardiomyocyte development and maturation programs in the embryonic heart.

Project description:Cardiac progenitors are specified early in development and progressively differentiate and mature into fully functional cardiomyocytes. This process is controlled by an extensively studied transcriptional program. However, the regulatory events coordinating the progression of such program from development to maturation are largely unknown. Here, we show that the genome organizer CTCF is essential for cardiogenesis and that it mediates genomic interactions to coordinate cardiomyocyte differentiation and maturation in the developing heart. Inactivation of Ctcf in cardiac progenitor cells and their derivatives in vivo during development caused severe cardiac defects and death at embryonic day 12.5. Genome wide expression analysis in Ctcf mutant hearts revealed that genes controlling mitochondrial function and protein production, required for cardiomyocyte maturation, were upregulated. However, mitochondria from mutant cardiomyocytes do not mature properly. In contrast, multiple development regulatory genes near predicted heart enhancers, including genes in the IrxA cluster, were downregulated in Ctcf mutants, suggesting that CTCF promotes cardiomyocyte differentiation by facilitating enhancer-promoter interactions. Accordingly, loss of CTCF disrupts gene expression and chromatin interactions as shown by chromatin conformation capture followed by deep sequencing. Furthermore, CRISPR-mediated deletion of an intergenic CTCF site within the IrxA cluster alters gene expression in the developing heart. Thus, CTCF mediates local regulatory interactions to coordinate transcriptional programs controlling transitions in morphology and function during heart development.

| S-EPMC5591014 | biostudies-literature

CTCF counter-regulates cardiomyocyte development and maturation programs in the embryonic heart [4C-seq]

Project description:Analysis of chromatin architecture suggests that the 3D structure of the genome plays a major role in regulating gene expression, orchestrating the compartmentalization of chromatin and facilitating specific enhancer-promoter interactions. However, the mechanisms that control this structuring of the genome are not fully understood. We have addressed this issue by analyzing the role of CTCF, a major architectural factor in chromatin structure, in the embryonic heart. Loss of CTCF triggered an overall downregulation of the cardiac developmental program, suggesting that CTCF facilitates enhancer-promoter interactions in the developing heart. Detailed analysis of the IrxA gene cluster showed that CTCF loss leads to disruption of the heart-specific regulatory domain that surrounds Irx4, resulting in changes in expression of IrxA cluster genes and neighboring genes. In contrast to the critical role proposed for CTCF in organizing large-scale chromatin domains, our results show that CTCF preferentially mediates local regulatory interactions.

2017-08-21 | GSE99118 | GEO

CTCF counter-regulates cardiomyocyte development and maturation programs in the embryonic heart [RNA-seq]

2017-08-21 | GSE77588 | GEO

AP-1 activation mediates postnatal cardiomyocyte maturation

Project description:Mammalian cardiomyocytes rapidly mature after birth, with hallmarks such as cell-cycle exit, binucleation, and metabolic switch to oxidative phosphorylation of lipids. The causes and transcriptional programs regulating cardiomyocyte maturation are not fully understood yet. Thus, we performed single cell RNA-seq of neonatal and postnatal day 7 rat hearts to identify the key factors for this process and found AP-1 as a key factor to regulate cardiomyocyte maturation. To find the mechanism of AP-1 during cardiomyocyte maturation, we performed RNA-seq analysis of neonatal rat ventricular cardiomyocytes and found Ap-1 promote cardiomyocyte maturation by regulating cardiomyocyte metabolism.

2021-12-01 | GSE182422 | GEO

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.

2022-05-21 | E-MTAB-11719 | biostudies-arrayexpress

CTCF counter-regulates cardiomyocyte development and maturation programs in the embryonic heart

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-08-21 | GSE77644 | GEO

Mus musculus

Project description:CTCF counter-regulates cardiomyocyte development and maturation programs in the embryonic heart [4C-seq]

| PRJNA387343 | ENA

Mus musculus

Project description:CTCF counter-regulates cardiomyocyte development and maturation programs in the embryonic heart [RNA-seq]

| PRJNA311076 | ENA

AP-1 activation mediates postnatal cardiomyocyte maturation

Project description:AP-1 activation mediates postnatal cardiomyocyte maturation

| PRJNA756241 | ENA

Single cell analysis of murine fibroblasts identifies neonatal to adult switching that regulates cardiomyocyte maturation

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.

2020-04-20 | GSE122706 | GEO

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