The overall goal of this research is to determine the mechanisms governing the fidelity of neuronal connections in the Drosophila visual system. This project will test the proposition that the Drosophila bendless (ben) gene product regulates photoreceptor connectivity by mediating selected destruction of intracellular proteins via the ubiquitin pathway. Biochemical and genetic studies demonstrate that the ubiquitination pathway functions to target proteins for degradation, and it is suggested that the BEN protein functions to regulate neural development by targeting other specific proteins for degradation. The specific goals are to characterize the aberrant axonal projections in the visual system of the mutant and to identify the protein targets of BEN and the molecular mechanisms responsible for the abnormalities.