Project description:To understand the function of Sox17 in the precursor cells of the mouse endocardium and the effect in the develoiping heart tube, single cell expression profiling of the Sox17-null endocardium and myocardium were performed.
Project description:To understand the function of Sox17 in the precursor cells of the mouse endocardium amd the effect in the develoiping heart tube, single cell expression profiling of the Sox17-null endocardium and myocardium were performed.
Project description:To identify genes that are differentially expressed in the developing mouse embryo as a result of SOX7 deficiency, we performed bulk RNA-seq on Sox7-null and wild-type embryos harvested at E8.5.
Project description:To determine the role of specific cis-regulatory elements within the Sox17 endoderm-preferential TSS2 promoter, we generated Sox17∆50 mutant animals, crossed them to a Sox17GFPCre (a Sox17 null allele), and surveyed how this mutation affected Sox17 expression. Livers were isolated from E12.5 Sox17∆50/GFPCRe compound heterozygous and Sox17+/+ embryos (n = 4 of each genotype), RNA isolated, and bulk RNA-Seq performed.
Project description:The endocardium is the endothelial component of the vertebrate heart and plays a key role in heart development. Where, when, and how the endocardium segregates during embryogenesis have remained largely unknown, however. We now show that Nkx2-5+ cardiac progenitor cells (CPCs) that express the Sry-type HMG box gene Sox17 from embryonic day (E) 7.5 to E8.5 specifically differentiate into the endocardium in mouse embryos. Although Sox17 is not essential or sufficient for endocardium fate, it can bias the fate of CPCs toward the endocardium. On the other hand, Sox17 expression in the endocardium is required for heart development. Deletion of Sox17 specifically in the mesoderm markedly impaired endocardium development with regard to cell proliferation and behavior. The proliferation of cardiomyocytes, ventricular trabeculation, and myocardium thickening were also impaired in a non-cell-autonomous manner in the Sox17 mutant, likely as a consequence of down-regulation of NOTCH signaling. An unknown signal, regulated by Sox17 and required for nurturing of the myocardium, is responsible for the reduction in NOTCH-related genes in the mutant embryos. Our results thus provide insight into differentiation of the endocardium and its role in heart development.
Project description:Gata4 is required for mouse endocardium development. To identify genes regulated by Gata4 in endocardium, we deleted Gata4 in endocardium with Cdh5(Pac)-CreERT2 and performed single cell RNA sequencing (scRNA-seq) to analyze all cells from the ventricles.