School of Biological Sciences, University of Sussex, Brighton. BN1 9QG. U.K.,
The wingless signal is essential for a variety of patterning processes in the development of both embryonic and adult structures including those of the adult peripheral nervous system. Wingless is required for the formation of the sensory bristles on the margin of the wing and for a subset of the sensory organs on the notum. In addition, there is now evidence that the wingless signal interacts with Notch, a receptor in the lateral inhibition process which ensures that only a single sensory mother cell is selected within each proneural cluster. Another gene involved in these processes is shaggy, or zeste white 3 (sgg), a segment polarity gene which encodes a serine-threonine protein kinase that is ubiquitously expressed in embryos and imaginal discs. Shaggy is inactivated in response to the wingless signal and this inactivation is important for a number of developmental processes including sensory organ development. In the wing blade, clones of cells deficient for shaggy form dense tufts of margin-like bristles. Loss of shaggy function in the notum can cause formation of ectopic bristles. Sgg- clones in the wing ectopically express the proneural gene achaete and the panneural gene neuralised. One consequence of Shaggy inactivation is an accumulation of cytoplasmic Armadillo protein, but little else is known about the downstream targets of Shaggy.
We have screened for new mutations which suppress the sgg-phenotype and which are therefore likely to act downstream of shaggy. After EMS mutagenesis, the flp-frt recombination system was used to generate animals with clones which simultaneously lacked shaggy and were homozygous for new mutations on chromosome 2 right. We sought those where the sgg- phenotype of clusters of ectopic bristles in the wing blade was suppressed. In addition to screening for new mutations in this way, several mutations recently found in this laboratory in a separate 2R flp-frt screen for wing patterning defects, were put through this same test. 6 mutations capable of suppressing the sgg- phenotype in the wing have been identified. At least five of these also show some wingless-like mutant phenotypes in clones where the Sgg function is not removed. For example, when clones are induced in a Minute background, five of the mutations are capable of causing wing etching, whilst one causes loss of dorso-central bristles and microchaetes on the notum and gives rise to duplications and loss of ventral structures in the leg. All six mutations are incapable of supporting oocyte formation in homozygous germline clones. We are currently investigating neuralised and vestigial expression in these mutants and are analysing the mutations further. Little is known about genes acting downstream of sgg, other than armadillo, so that analysis of these mutations should yield exciting insights into this system.