The regulation of gliogenesis is a fundamental process for nervous system development, as the appropriate glial number and identity is required for a functional nervous system. To investigate the molecular mechanisms involved in gliogenesis, we used C. elegans as a model and identified the function of the proneural gene lin-32/Atoh1 in gliogenesis. We found that lin-32 functions during embryonic development to negatively regulate the number of AMsh glia. The ectopic AMsh cells at least partially arise from cells originally fated to become CEPsh glia, suggesting that lin-32 is involved in the specification of specific glial subtypes. Moreover, we show that lin-32 acts in parallel with cnd-1/ NeuroD1 and ngn-1/ Neurog1 in negatively regulating an AMsh glia fate. Furthermore, expression of murine Atoh1 fully rescues lin-32 mutant phenotypes, suggesting lin-32/Atoh1 may have a conserved role in glial specification.

神经胶质生成的调节是神经系统发育的基本过程，因为功能性神经系统需要适当的神经胶质数量和身份。为了研究参与胶质发生的分子机制，我们使用秀丽隐杆线虫作为模型，并确定了原神经基因lin-32 / Atoh1 在胶质发生中的功能。我们发现lin-32在胚胎发育过程中发挥负调节 AMsh 胶质细胞数量的作用。异位 AMsh 细胞至少部分来自原本注定要成为 CEPsh 胶质细胞的细胞，这表明lin-32参与特定神经胶质亚型的规范。此外，我们表明lin-32与cnd-1/ NeuroD1 和ngn-1/ Neurog1 负调控 AMsh 神经胶质细胞的命运。此外，鼠 Atoh1 的表达完全拯救lin-32突变表型，表明lin-32 /Atoh1 可能在神经胶质规范中具有保守作用。