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Gene expression profiling of E12.5 wildtype- and Sp3 null hearts

ABSTRACT: Mice lacking the zinc finger transcription factor Specificity protein 3 (Sp3) die prenatally in the C57Bl/6 background. To elucidate the cause of mortality we analyzed the potential role of Sp3 in embryonic heart development. Sp3 null hearts display defective looping at E10.5, and at E14.5 the Sp3 null mutants have developed a range of severe cardiac malformations. In an attempt to position Sp3 in the cardiac developmental hierarchy, we analysed the expression patterns of >15 marker genes in Sp3 null hearts. Expression of Cardiac ankyrin repeat protein (Carp) was downregulated prematurely after E12.5, while expression of the other marker genes was not affected. ChIP analysis revealed that Sp3 is bound to the Carp promoter region in vivo. Microarray analysis indicates that small molecule metabolism and cell-cell interactions are the most significantly affected biological processes in E12.5 Sp3 null myocardium. Since the epicardium showed distension from the myocardium, we studied expression of Wt1, a marker for epicardial cells. Wt1 expression was diminished in epicardium-derived cells in the myocardium of Sp3 null hearts. We conclude that Sp3 is required for normal cardiac development, and suggest that it has a crucial role in myocardial differentiation. ( Keywords: Transcription factors, Sp3, knockout mice, cardiac malformations, E12.5

ORGANISM(S): Mus musculus

PROVIDER: GSE9124 | GEO | 2007/11/01

SECONDARY ACCESSION(S): PRJNA102663

REPOSITORIES: GEO

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Transcription profiling of mouse heart from E12.5 wildtype- and Sp3 animals

Project description:Mice lacking the zinc finger transcription factor Specificity protein 3 (Sp3) die prenatally in the C57Bl/6 background. To elucidate the cause of mortality we analyzed the potential role of Sp3 in embryonic heart development. Sp3 null hearts display defective looping at E10.5, and at E14.5 the Sp3 null mutants have developed a range of severe cardiac malformations. In an attempt to position Sp3 in the cardiac developmental hierarchy, we analysed the expression patterns of >15 marker genes in Sp3 null hearts. Expression of Cardiac ankyrin repeat protein (Carp) was downregulated prematurely after E12.5, while expression of the other marker genes was not affected. ChIP analysis revealed that Sp3 is bound to the Carp promoter region in vivo. Microarray analysis indicates that small molecule metabolism and cell-cell interactions are the most significantly affected biological processes in E12.5 Sp3 null myocardium. Since the epicardium showed distension from the myocardium, we studied expression of Wt1, a marker for epicardial cells. Wt1 expression was diminished in epicardium-derived cells in the myocardium of Sp3 null hearts. We conclude that Sp3 is required for normal cardiac development, and suggest that it has a crucial role in myocardial differentiation. ( Experiment Overall Design: Hearts were dissected from E12.5 wildtype (n=3) and Sp3 knockout (n=3) fetuses. Total RNA was isolated from individual hearts; 5Î¼g was used for labelling and hybridization to 430 2.0 Gene Chips (a total of 6).

2008-06-17 | E-GEOD-9124 | biostudies-arrayexpress

Mus musculus

Project description:Gene expression profiling of E12.5 wildtype- and Sp3 null hearts

| PRJNA102663 | ENA

RNA sequencing data of Ing4;Ing5 double knock-out embryonic mouse hearts

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Single-cell sequencing of epicardial cells and fibroblasts within the infarcted heart

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2010-02-21 | E-GEOD-14906 | biostudies-arrayexpress

BNC1 is a master regulator of human epicardial cell heterogeneity and function

Project description:Single cell RNAseq of a model of epicardium derived from human pluripotent stem cell (hPSC-epi) reveals that distinct epicardial sub-populations are defined by high levels of expression for the transcription factors BNC1 and TCF21. Cells positive for the transcription factor WT1 are included in the BNC1 population, which confirms the heterogeneity observed in the mouse with TCF21 and WT1. Analysis of genes differentially expressed between the two populations suggests differences in their biological activities. We identified THY1 as a membrane marker of the TCF21 population and we show that THY1+ cells can differentiate into cardiac fibroblast and smooth muscle cells while THY1- cells mostly produce the latter. Knocking-down BNC1 during the establishment of the populations led to an homogeneous epicardium containing mostly the TCF21high populations and differentiating mainly into cardiac fibroblasts. Using network inference methods and transcriptomic data from the different epicardial lineages derived from the hPSC-epi, we identified a core transcriptional network organized around WT1, TCF21 and BNC1 and orchestrated by BNC1.

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The Gene Expression Analysis in E12.5 Mouse Hearts with GATA4-FOG2 Interaction Loss

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Downregulation of WT1 transcription factor gene expression is required to promote myocardial fate [RNA-seq]

Project description:During cardiac development, cells from the precardiac mesoderm fuse to form the primordial heart tube, which then grows by addition of further progenitors to the venous and arterial poles. In the zebrafish, wilms tumor 1 transcription factor a (wt1a) and b (wt1b) are expressed in the pericardial mesoderm at the venous pole of the forming heart tube. The pericardial mesoderm forms a single layered mesothelial sheet that contributes to further the growth of the myocardium, and forms the proepicardium. Proepicardial cells are subsequently transferred to the myocardial surface and give rise to the epicardium, the outer layer covering the myocardium in the adult heart. wt1a/b expression is downregulated during the transition from pericardium to myocardium, but remains high in proepicardial cells. Here we show that sustained wt1 expression impaired cardiomyocyte maturation including sarcomere assembly, ultimately affecting heart morphology and cardiac function. ATAC-seq data analysis of cardiomyocytes overexpressing wt1 revealed that chromatin regions associated with myocardial differentiation genes remain closed upon wt1b overexpression in cardiomyocytes, suggesting that wt1 represses a myocardial differentiation program. Indeed, a subset of wt1a/b-expressing cardiomyocytes changed their cell adhesion properties, delaminated from the myocardial epithelium, and upregulated the expression of epicardial genes, as confirmed by in vivo imaging. Thus, we conclude that wt1 acts as a break for cardiomyocyte differentiation by repressing chromatin opening at specific genomic loci and that sustained ectopic expression of wt1 in cardiomyocytes can lead to their transformation into epicardial cells.

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Downregulation of WT1 transcription factor gene expression is required to promote myocardial fate [ATAC-seq]

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