Genetic and molecular studies of early embryogenesis in Drosophila
The Drosophila embryo is patterned by a complex interplay of zygotically expressed genes and maternally supplied components, a large number of which have been identified. However, many maternal components are encoded by essential zygotic genes whose maternal effects are not amenable to conventional genetic analysis. Investigation of such genes requires the generation of homozygous mutant germ cells in chimeric females, and analysis of their embryos. The recent development of techniques which allow the efficient generation of germline clones has made the screening of zygotic lethal mutations for maternal effects more feasible. I have generated a collection of X-linked zygotic lethal mutations and used FLP recombinase catalysed mitotic recombination to look for maternal effects affecting segmentation. Two mutations have been recovered which have maternal effect phenotypes similar to those of the pair-rule segmentation genes. The leprechaun mutation affects oogenesis, so fertile females are very rare, preventing straightforward phenotypic analysis of the segmentation phenotype. Attempts to generate a rescuing duplication are described. The second mutation, stunted (sun), initially gave rise to a segmentation cuticle phenotype. Subsequent attempts to reproduce the phenotype were unsuccessful as it was masked by a severe reduction in the amount of cuticle secreted, a phenotype characteristic of the neurogenic genes. Detailed analysis revealed that the primary lesion affects neither segmentation or neurogenesis. Rather, sun+ is required for cellularisation of the syncytial blastoderm and for the localisation of actin to 'caps' above the syncytial nuclei. Cloning of a candidate gene for stunted revealed a predicted protein product limited homology to cyclins. In addition to searching for novel segmentation genes, potential proteinprotein interactions of the segmentation gene hairy's protein product were also investigated, and a model is presented for its mode of action as a transcriptional repressor.