Jiménez F, Campos-Ortega J A
Centro de Biologia Molecular, Universidad Autonoma/CSIC, Canto Blanco, Madrid, Spain.
Neuron. 1990 Jul;5(1):81-9. doi: 10.1016/0896-6273(90)90036-f.
Loss of function mutations in genes of the achaete-scute complex (ASC) or in the gene vnd of D. melanogaster result in neural hypoplasia. Two types of defects contribute to the development of the neural hypoplasic phenotype: a lower than normal proportion of neuroblasts delaminate from the neuroectoderm, and there is abundant cell death in the neural primordium during later stages. In addition, we found that increasing the copy number of ASC wild-type alleles leads to effects opposite to those caused by their deletion. All of these results indicate that the function of these genes is required for the commitment of neuroectodermal cells as neuroblasts and that the loss of these genetic functions causes the cells either to take on an epidermal fate or to die.
果蝇achaete-scute复合体（ASC）基因或vnd基因功能丧失性突变会导致神经发育不全。两种类型的缺陷促成了神经发育不全表型的形成：从神经外胚层分层的神经母细胞比例低于正常水平，并且在后期神经原基中存在大量细胞死亡。此外，我们发现增加ASC野生型等位基因的拷贝数会产生与缺失这些等位基因所导致的效应相反的效果。所有这些结果表明，这些基因的功能对于神经外胚层细胞向神经母细胞的定向分化是必需的，并且这些基因功能的丧失会导致细胞要么转变为表皮细胞命运，要么死亡。
