The regulatory roles of PAR-aPKC complex in the division patterns of neural stem cells

在哺乳动物大脑发育过程中，神经前体细胞（neural precursor cells, npc）首先扩大其数量并产生下一代神经元。然而，调控这种NPC分裂模式转变的分子机制尚不清楚。为了阐明调节这种转变的分子机制，我分析了进化上保守的极性蛋白PAR3在E10.5小鼠npc中的作用。我发现缺乏par3的npc明显偏向于自我更新分裂和几种转录因子的表达改变。这些观察结果表明，PAR3参与了小鼠鼻咽癌分裂模式转变的调控。

During mammalian cerebral development, neural precursor cells (NPCs) first expand their population and next generate neurons. However, the molecular mechanisms regulating this transition of NPC division modes have not been clarified yet. To elucidate the molecular mechanisms regulating this transition, I analyzed the roles of PAR3, the evolutionarily conserved polarity protein, in mouse NPCs at E10.5. I found that PAR3-deficient NPCs were significantly biased to self-renewal divisions and altered expression of several transcription factors. These observations suggest that PAR3 is involved in the regulation of the transition of NPC division modes in mice.