Expression data from E18.5 mouse dorsal telencephalon

Radial progenitors deficient in both Mek1 and Mek2 fail to transition to the gliogenic mode in late embryogenesis, and astrocyte and oligodendroglial precursors fail to appear. In exploring mechanisms, we found the Ets transcription family member Etv5/Erm is strongly regulated by MEK. Our microarray assay showed that Erm is specifically downregulated in Mek mutant brain. RNA was extracted from dorsal corticies of E18.5 WT or Mek1,2\NesCre conditional mutant embryos. There were totally 4 samples: 2 WT and 2 mutants. 200 ng of total RNA was prepared for microarray hybridization according to the GeneChip® Whole Transcript (WT) Sense Target Labeling Assay user manual.

同时缺失Mek1与Mek2的放射状前体细胞（radial progenitors）无法在胚胎发育晚期向胶质发生模式转换，且星形胶质细胞与少突胶质细胞前体无法正常生成。在探究其分子机制的过程中，我们发现Ets转录因子家族成员Etv5/Erm受到MEK的显著调控。我们的基因芯片（microarray）实验结果显示，Erm在Mek突变体小鼠脑组织中呈现特异性下调。我们从E18.5天野生型（WT）或Mek1/2联合NesCre的条件性突变胚胎的背侧大脑皮层中提取了总RNA，实验共包含4个样本：2个野生型样本与2个突变体样本。按照GeneChip®全转录组（WT）正义靶标标记分析用户手册的操作规范，我们制备了200 ng总RNA用于基因芯片杂交。