The central nervous system (CNS) ofDrosophila develops from precursor cells called neuroblasts. Neuroblasts segregate in early embryogenesis from an apparantly undifferentiated ectoderm and move into the embryo, whereas most of the remaining ectodermal cells continue development as epidermal cell precursors. Segregation of neuroblasts occurs within a region called the neurogenic field. We are interested in understanding how the genome ofDrosophila controls the parcelling of the ectoderm into epidermal and neural territories. We describe here mutations belonging to seven complementation groups which effect an abnormal neurogenesis. The phenotypes produced by these mutations are similar. Essential features of these phenotypes are a conspicuous hypertrophy of the CNS accompanied by epidermal defects; the remaining organs and tissues of the mutants are apparently unaffected. The study of mutant phenotype development strongly suggests this phenotype to be due to misrouting into the neural pathway of development of ectodermal cells which in the wildtype would have given rise to epidermal cells, i.e. to an initial enlargement of the neurogenic region at the expense of the epidermogenic region. These observations indicate that the seven genetic loci revealed by the mutations described in this study contribute to control the neurogenic field. The present results suggest that in wildtype development neurogenic genes are supressed within all derivatives of the mesoderm and endoderm and some derivatives of the ectoderm, and conditionally expressed in the remaining ectoderm. The organisation of the neurogenic field in the wildtype is discussed.
Keywords: Drosophila; Early neurogenesis; Neurogenic mutants.