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Transcriptome profile and Genome-wide chromatin accessibility profile of zebrafish cardiomyocytes throughout heart development

ABSTRACT: Transcriptome profile and Genome-wide chromatin accessibility profile of zebrafish cardiomyocytes throughout heart development

PROVIDER: PRJNA492279 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7882020_1.fastq.gz	Fastqsanger.gz
	SRR7882020_2.fastq.gz	Fastqsanger.gz
	SRR7882030_1.fastq.gz	Fastqsanger.gz
	SRR7882030_2.fastq.gz	Fastqsanger.gz
	SRR7882260_1.fastq.gz	Fastqsanger.gz

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Genome-wide chromatin accessibility profile of zebrafish cardiomyocytes throughout heart development

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Genome-wide chromatin accessibility profile of zebrafish cardiomyocytes throughout heart development

Project description:By using transgenic zebrafish lines Tg(nxk2.5:GFP) (Witzel et al. 2012) and Tg(myl7:EGFP) (D'Amico et al. 2007), we have characterized chromatin accessibility of FACS-isolated CM (GFP+) from developing zebrafish heart at 24, 48 and 72 hpf, corresponding to heart tube formation, chamber formation and differentiation and heart maturation, respectively. GFP- cells were used as a control. We have identified cardiac regulatory networks playing a crucial role in heart morphogenesis. To validate their importance in heart development, we employed zebrafish mutants of cardiac transciption factors Gata5, Hand2 and Tbx5a, the disruption of which were previously linked to impaired migration of the cardiac primordia to the embryonic midline, reduced number of myocardial precursors and failure of heart looping, respectively (Reiter et al. 1999; Yelon et al. 2000; Garrity et al. 2002). ATAC-seq was performed from homozygous gata5tm236a/tm236a, tbx5am21/ m21, hand2s6/s6 mutant 72 hpf embryos in Tg(myl7:EGFP) genetic background. Homozygous mutant embryos for analyses were selected on the basis of their phenotypes of cardia bifida (gata5tm236a/tm236a, hand2s6/s6) or heart-string (tbx5am21/ m21) .

2019-01-10 | GSE120237 | GEO

Transcriptomic profile of zebrafish cardiomyocytes throughout heart development

Project description:By using transgenic zebrafish lines Tg(nxk2.5:GFP) (Witzel et al. 2012) and Tg(myl7:EGFP) (D'Amico et al. 2007), we have characterized transcriptomic profile of FACS-isolated CM (GFP+) from developing zebrafish heart at 24, 48 and 72 hpf, corresponding to heart tube formation, chamber formation and differentiation and heart maturation, respectively. GFP- cells were used as a control. We have identified cardiac regulatory networks playing a crucial role in heart morphogenesis. To validate their importance in heart development, we employed zebrafish mutants of cardiac transciption factors Gata5, Hand2 and Tbx5a, the disruption of which were previously linked to impaired migration of the cardiac primordia to the embryonic midline, reduced number of myocardial precursors and failure of heart looping, respectively (Reiter et al. 1999; Yelon et al. 2000; Garrity et al. 2002). RNA-seq was performed from homozygous gata5tm236a/tm236a, tbx5am21/ m21, hand2s6/s6 mutant 72 hpf embryos in Tg(myl7:EGFP) genetic background. Homozygous mutant embryos for analyses were selected on the basis of their phenotypes of cardia bifida (gata5tm236a/tm236a, hand2s6/s6) or heart-string (tbx5am21/ m21) .

2019-01-10 | GSE120236 | GEO

Transcriptome profile and Genome-wide chromatin accessibility profile of zebrafish cardiomyocytes throughout heart development

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2019-01-10 | GSE120238 | GEO

m6A profile in cardiomyocytes

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Newborn apical resection preserves the proliferative capacity of cardiomyocytes located throughout the left ventricle

Project description:Background: When pigs underwent apical resection (AR) on postnatal day (P) 1 (ARP1) followed by myocardial infarction (MI) on P28, the hearts had little evidence of scarring; meanwhile, hearts underwent MI on P28 without ARP1 showed large infarcts on P56; and the improvement of ARP1 hearts was driven primarily by cardiomyocyte proliferation. AR and MI were performed ~5 mm (AR) and ~20 mm (MI) above the heart apex; thus, we hypothesize that ARP1 preserved the cardiomyocytes cell-cycle throughout the left ventricle, rather than only near the resection site. Methods: Sections of cardiac tissue were collected from the left ventricle of uninjured pigs and from both the border zone (BZ) of AR and uninjured regions (remote zone, [RZ]) in ARP1 hearts. Cardiomyocyte proliferation was evaluated via immunofluorescence analysis of phosphorylated histone 3 [PH3] and symmetric Aurora B (sAuB). Single nucleus RNA sequencing (snRNAseq) data collected from the hearts of fetal pigs, uninjured pigs, and the BZ and RZ of ARP1 pigs was evaluated via our cell-cycle-specific Autoencoder to identify proliferating cardiomyocytes. Results: Cardiomyocyte PH3 and sAuB expression, and percentage of proliferating cardiomyocytes in snRNA data was significantly more common in both BZ and RZ of ARP1 than uninjured hearts but did not differ significantly between the ARP1-BZ and ARP1-RZ at any time point. Heat shock protein HSPA5 and HSP90B1 were overexpressed at both ARP1-BZ and ARP1-RZ. In AC16 cell, overexpression (and knockdown) of HSPA5-HSP90B1 increased (and decrease) cell-cycle activity. Conclusion: ARP1 preserved proliferative capacity of cardiomyocytes located throughout the left ventricle.

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AP-1 Regulates Chromatin Accessibility to Promote Sarcomere Disassembly and Cardiomyocyte Protrusion during Zebrafish Heart Regeneration

Project description:The zebrafish has emerged as a powerful model to study cardiac regeneration; however, the mechanisms by which cardiomyocytes respond to damage by disassembling sarcomeres, proliferating, and repopulating the injured area remain unclear. Here, we show that AP-1 transcription factors play an essential role in regulating the cardiomyocyte response. Using ATAC-Seq, we first find that the cardiomyocyte chromatin accessibility landscape is dynamic following cryoinjury, and that AP-1 motifs are the most highly enriched in regions that gain accessibility during regeneration. Using a cardiomyocyte-specific dominant-negative approach, we show that AP-1 promotes cardiomyocyte proliferation as well as chromatin accessibility at genes regulating sarcomere disassembly and cardiomyocyte protrusion into the injured area. We further find distinct temporal requirements for AP-1 during cardiac regeneration. Altogether, these results indicate that AP-1 plays a key role in the cardiomyocyte response to injury by promoting chromatin accessibility changes, allowing the activation of gene expression programs that support regeneration.

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