Analysis of the regulation mechanism of the progenitor cell division pattern along developmental stages

我们发现细胞表面分子TAG-1的敲低导致祖细胞基底突的收缩，而TAG-1主要富集于早期小鼠脑壁。基底断连的茎样祖细胞不能发生向基底方向的INM和在心室周围空间过度拥挤。令人惊讶的是，过度拥挤的祖细胞离开顶端表面，迁移到基底神经元区域。尽管异位祖细胞出乎意料地保持干样，连续产生神经元直到胚胎后期，但组织发生严重中断。因此，祖细胞形态依赖的INM对于防止核/染色体过度拥挤至关重要，从而确保正常的脑组织发生。

We found that knockdown of the cell-surface molecule TAG-1, which is enriched basally in early mouse cerebral walls, causes retraction of progenitors’ basal processes. Basally disconnected stem-like progenitors failed to undergo basalward INM and overcrowded in the periventricular space. Surprisingly, the overcrowded progenitors left the apical surface and migrated into basal neuronal territories. Although the heterotopic progenitors unexpectedly remained stem-like, sequentially producing neurons until late embryonic period, histogenesis was severely disrupted. Thus, progenitors’ morphology-dependent INM is essential to prevent nuclear/somal overcrowding, thereby ensuring normal brain histogenesis.