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 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 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: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
Project description:The craniofacial region encompassing rhombomere 2 and adjacent putative BA1 together with all more anterior tissues was collected from E8.5 mouse embryos, processed and analyzed by 10X Genomics Chromium scRNA-seq