Gene expression profiling of the palate in Erk2 mutant mouse models

The overall goal of this project is to investigate the role of Erk2-mediated signaling in regulating the cellular metabolism of cranial neural crest (CNC) cells during palate development. Here, we conducted gene expression profiling of palate tissue from wild type mice as well as those with a neural crest specific conditional inactivation of the Erk2 gene. The latter mice exhibit micrognathia, tongue defects and cleft palate, which is among the most common congenital birth defects and observed in many syndromic conditions. To investigate the adverse effects of dysfunctional ERK signaling on the cellular metabolism of palatal mesenchyme during palatogenesis, we analyzed mice with a neural crest cell-specific conditional inactivation of Erk2 (Erk2fl/fl;Wnt1-Cre). We performed microarray analyses of primary mouse embryonic palatal mesenchymal cells of Erk2fl/fl;Wnt1-Cre mutant mice and Erk2fl/fl control mice, collected at embryonic day 13.5 (n=3 per genotype) and E14.5 (n=5 per genotype).本项目的总体目标为探究Erk2介导的信号通路在腭发育进程中对颅神经嵴（cranial neural crest, CNC）细胞代谢的调控作用。本研究对野生型小鼠，以及Erk2基因经神经嵴特异性条件性敲除的小鼠的腭组织进行了基因表达谱分析。该条件敲除小鼠表现出小颌畸形、舌部缺陷与腭裂；腭裂作为最常见的先天性出生缺陷之一，可在多种综合征性疾病中被观察到。为探究功能异常的ERK信号通路对腭发生过程中腭间充质细胞代谢的不良影响，本研究针对神经嵴细胞特异性Erk2条件性敲除小鼠（Erk2fl/fl;Wnt1-Cre）展开分析。我们分别在胚胎第13.5天（每个基因型组样本量为3）与胚胎第14.5天（每个基因型组样本量为5），采集Erk2fl/fl;Wnt1-Cre突变小鼠及Erk2fl/fl对照小鼠的原代小鼠胚胎腭间充质细胞，并完成了基因芯片分析。