~ Department of Anatomy, Downing Street, Cambridge, UK., § Institute of Molecular Biology and Biotechnology GR 71110 Heraklion, Crete, Greece, # Institute fur Genetik, Universitat Hohenheim, Stuttgard,Germany.,
Cell fate aquisition is based on cell lineage and cell communication. The Notch signalling pathway mediates cell-cell communication in a number of developmental procceses in organisms as different as Drosophila, C. elegans and mammals. The pathway centers its activity on the transmembrane receptor Notch . Transduction of the Notch signal to the nucleus of the receiving cell results in activation of the E(spl) genes, which encode seven basic helix-loop-helix transcription factors and are implicated in repressing proneural gene function in the developing Drosophila CNS. The question arises whether E(spl) proteins mediate all the diverse effects of Notch or whether they are solely involved in neural suppression.
Using the GAL4/UAS system we ectopically expressed E(spl) mdelta and mgamma in various tissues. In a wild type background we observed loss of bristles in the notum, wing margin and abdomen, as well as loss of wing veins a cell type also known to be affected by Notch signalling. Using these phenotypes we documented genetic interactions between GAL4/UASmd combinations and genes involved in the Notch pathway. These lead to the conclusion that although ectopically expressed md can bypass partial loss of function of the Notch pathway, it is incapable of reproducing the effect of Notch signalling in a null background. Models to account for the findings will be discussed.