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Mus musculus

ABSTRACT: Analysis of transcriptome changes in Kmt2d deletion in cardiac mesoderm, anterior heart field precursors and cardiomyocytes

PROVIDER: PRJNA301146 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2927460_1.fastq.gz	Fastqsanger.gz
	SRR2927460_2.fastq.gz	Fastqsanger.gz
	SRR2927470_1.fastq.gz	Fastqsanger.gz
	SRR2927470_2.fastq.gz	Fastqsanger.gz
	SRR2927461_1.fastq.gz	Fastqsanger.gz

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Analysis of transcriptome changes in Kmt2d deletion in cardiac mesoderm, anterior heart field precursors and cardiomyocytes

Project description:KMT2D is required in the cardiac mesoderm, anterior heart field precursors and cardiomyocytes. Kmt2d deletion in cardiac mesoderm (Mesp1Cre) is embryonic lethal at E10.5 and mutants have hypoplastic hearts; Kmt2d deletion in anterior heart field precursors (Mef2cAHF::Cre) deletion is embryonic lethal at E13.5 and mutants have defects in septation of outflow tract and interventricular septum (IVS); Kmt2d deletion in cardiomyocytes (Tnnt2::Cre) deletion is embryonic lethal at E14.5 and mutants have defects in IVS septation and compact myocardium. The goal of this study is to compare changes in gene expression in these Kmt2d conditional deletion mutants and understand common or distinct pathways dysregulated in absence of KMT2D. Whole genome gene expression analysis was performed on RNA isolated from control and mutant embryonic hearts (or right ventricles and outflow tract for anterior heart field deletion samples). Libraries were prepared using Illumina TruSeq Paired-End Cluster Kit v3, and sequenced with the Illumina HiSeq 2500 system for pair-ended 100 base pairs (PE 100 bp).

2015-11-04 | E-GEOD-74679 | biostudies-arrayexpress

Analysis of transcriptome changes in Kmt2d deletion in cardiac mesoderm, anterior heart field precursors and cardiomyocytes

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KMT2D regulates specific programs in heart development via histone H3 lysine 4 dimethylation

Project description:Histone modifying genes involved in histone H3 lysine 4 (H3K4) methylation are critical for heart development, but the roles of these genes are not well understood. Here, we demonstrate a requirement for the H3K4 methyltransferase KMT2D in cardiac precursors and cardiomyocytes during cardiogenesis. Gene expression analysis revealed upregulation of hypoxia response genes, as well as downregulation of ion transport and cell cycle genes, leading to altered calcium handling and cell cycle defects. We further determined that myocardial Kmt2d deletion led to decreased H3K4me2 at promoters and enhancers. Finally, we identified KMT2D binding regions in cardiomyocytes, of which a subset was associated with decreased gene expression and decreased H3K4me2 in mutant hearts. This subset included genes related to ion transport, hypoxia-reoxygenation and cell cycle regulation, suggesting that KMT2D is important for these processes. Our findings indicate that KMT2D is essential for regulating cardiac gene expression during heart development via H3K4 dimethylation.

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Temporal single-cell transcriptomic profiling of cardiac differentiation in human induced pluripotent stem cells with NOTCH1 mutations

Project description:Pathological variants in NOTCH1 have been implicated in multiple types of congenital heart defects including bicuspid aortic valve and hypoplastic left heart syndrome (HLHS). To probe how NOTCH1 deficiency affects cardiac development, we generated homozygous NOTCH1 knockout (N1KO) human induced pluripotent stem cells (iPSCs). We then ran single-cell RNA-seq to temporally profile transcriptomic changes during cardiac differentiation in wild type (WT) and N1KO iPSCs. We collected differentiating cells at multiple time points corresponding to different development stages, i.e., Day 0 (D0: pluripotent stem cell), D2 (mesoderm), D5 (cardiac mesoderm), D10 (cardiac progenitor), D14 (early cardiomyocyte), and D30 (fetal cardiomyocyte). Single-cell transcriptomics analysis reveals that NOTCH1 disruption impairs human ventricular cardiomyocyte differentiation and proliferation through balancing cell fate determination of cardiac mesoderm toward the first heart field, second heart field, and epicardial lineages.

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Project description:Self-organisation and coordinated morphogenesis of multiple cardiac lineages is essential for the development and function of the heart1-3. However, the absence of a human in vitro model that mimics the basic lineage architecture of the heart hinders research into developmental mechanisms and congenital defects4. Here, we describe the establishment of a reliable, lineage-controlled and high-throughput cardiac organoid platform. We show that cardiac mesoderm derived from human pluripotent stem cells robustly self-organises and differentiates into cardiomyocytes forming a cavity. Co-differentiation of cardiomyocytes and endothelial cells from cardiac mesoderm within these structures is required to form a separate endothelial layer. As in vivo, the epicardium engulfs these cardiac organoids, migrates into the cardiomyocyte layer and differentiates. We use this model to demonstrate that cardiac cavity formation is controlled by a mesodermal WNT-BMP signalling axis. Disruption of one of the key BMP targets in cardiac mesoderm, the transcription factor HAND1, interferes with cavity formation, which is consistent with its role in early heart tube and left chamber development5. Thus, the cardiac organoid platform represents a powerful resource for the quantitative and mechanistic analysis of early human cardiogenesis and defects that are otherwise inaccessible. Beyond understanding congenital heart disease, cardiac organoids provide a foundation for future translational research into human cardiac disorders.

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Project description:Differentiation into diverse cell lineages requires orchestration of gene regulatory networks guiding cell fate choices. Genetic factors acting through changes in transcriptional levels can contribute to cardiovascular disease risk by impacting early stages of development and have cell type-specific effects. We set out to characterize lineage trajectory progression of subpopulations and identify potential disease-related genes by examining their expression changes in single cells during early stages of cardiac lineage specification. Using 43,168 single-cell transcriptomes, we developed novel classification and trajectory analysis methods to dissect cellular composition and gene networks across five discrete time points underlying lineage derivation of mesoderm, definitive endoderm, vascular endothelium, cardiac precursors, and definitive cell types that comprise cardiomyocytes and a previously unrecognized cardiac outflow tract population.

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