Gene expression profiling of Tgfbr2 mutant mouse models of cleft palate

The overall goal of this project is to investigate the role of TGF-beta signaling in palate development in order to discover candidate therapeutics for preventing and treating congenital birth defects. Here, we conducted gene expression profiling of embryonic palatal tissue from wild type mice as well as those with a neural crest specific conditional inactivation of the Tgfbr2 gene. The latter mice provide a model of cleft palate formation. To investigate the mechanism of cleft palate resulting from mutations in TGFBR2, we analyzed neural crest specific conditional inactivation of Tgfbr2 in mice (Tgfbr2fl/fl;Wnt1-Cre). We performed microarray analyses using the palatal tissue of Tgfbr2fl/fl;Wnt1-Cre mice at embryonic day E13.5 (prior to palatal fusion, n=6 per genotype) and E14.5 (during palatal fusion, n=5 per genotype) to examine the genes regulated by Tgf-beta during palate formation.

本研究的总体目标是探究转化生长因子-β（TGF-beta）信号通路在腭发育中的作用，以期发掘用于预防和治疗先天性出生缺陷的候选治疗方案。为此，我们对野生型小鼠及携带神经嵴特异性条件性敲除Tgfbr2基因的小鼠的胚胎腭组织开展了基因表达谱分析。该类小鼠可作为腭裂形成的疾病模型。为阐明TGFBR2突变引发腭裂的分子机制，我们以神经嵴特异性条件性敲除Tgfbr2的小鼠模型（Tgfbr2fl/fl;Wnt1-Cre）为研究对象。我们分别采集胚胎发育第13.5天（腭融合前，每个基因型样本量n=6）与第14.5天（腭融合进程中，每个基因型样本量n=5）的Tgfbr2fl/fl;Wnt1-Cre小鼠腭组织进行微阵列分析，以检测腭发育过程中受Tgf-beta调控的基因。