Abstract
In Drosophila melanogaster the neuroblasts separate from epidermoblasts to give rise to the neural primordium. This process is under the control of several genes. The group of the so-called neurogenic genes is required for epidermal development; other genes, comprising those of the achaete-scute complex and daughterless, are required for neural development. We have studied the relationships between both groups of genes in two different ways. We have analyzed the phenotype of double-mutant embryos and our results show that the neural hyperplasia caused by neurogenic mutations can be partially prevented if a mutation in one of the other genes is present in the same genome. Only the neural cells that do not require the function of a particular gene of the achaete-scute complex in the wild-type seem to develop to a neural fate in the double mutant embryos. At least some of the genetic interactions affect the transcriptional level, as shown by in situ hybridization, since the territories of transcription of the achaetescute genes are expanded in neurogenic mutants. All cells of the neurogenic region of the double mutants apparently initiate neural development. However, during later development some of these cells switch their fate either to epidermogenesis or to cell death and this leads to the final phenotype of the double mutants. We discuss these results with respect to the events of early neurogenesis.
