Gene expression profiling of rudhira null embryo and yolk sac at 9.5 dpc

Rudhira is essential for mouse developmental angiogenesis and tissue morphogenesis. Embryos lacking endothelial rudhira die at mid-gestation with vascular patterning defects. Rudhira mutant yolk sac endothelial cells show slow and random migration. So to identify key signaling pathways perturbed in the absence of rudhira, we undertook whole transcriptome based analysis of gene expression in rudhira null yolk sac and embryo. Transcriptome analysis shows that key mediators of angiogenesis, cell adhesion, migration and extracellular matrix degradation as well as several components of the TGFβ pathway are perturbed in rudhira null mutant yolk sacs at 9.5 dpc. We used two embryo samples ( 2E- wild type; 5E- rudhira mutant). Repetition was done on each sample. We used 4 yolk sac samples (3Y,4Y- wild type; 7Y,8Y-rudhira mutant) for the analysis. Repetition was done on each sample.

Rudhira对于小鼠发育性血管生成与组织形态发生至关重要。缺失内皮细胞中Rudhira的胚胎会在妊娠中期死亡，并伴随血管模式构建缺陷。Rudhira突变的卵黄囊内皮细胞表现出迁移缓慢且随机的表型。为了鉴定Rudhira缺失后发生紊乱的关键信号通路，我们对Rudhira纯合缺失的卵黄囊和胚胎开展了基于全转录组的基因表达分析。转录组分析结果显示，在胚胎发育第9.5天（9.5 dpc）的Rudhira纯合缺失突变卵黄囊中，血管生成、细胞黏附、细胞迁移以及细胞外基质降解的关键介导因子，以及转化生长因子β（TGFβ）通路的多种组分均出现表达异常。本研究共使用2份胚胎样本（2E-野生型；5E-Rudhira突变型），每份样本均设置生物学重复；另使用4份卵黄囊样本（3Y、4Y为野生型；7Y、8Y为Rudhira突变型）开展分析，每份样本同样设置生物学重复。