In this proposal I will investigate signaling cascades that control branching at the nerve-terminal. The basis for this research will be three recently identified mutants that specifically alter nerve-terminal branching. Loss-of-function in the mutant cap ta in haddock (chad) leads to an increase in terminal branching, while loss-of-function in the mutant red rackham (rerak) leads to a decrease in terminal branching. Over- expression of the strung-out (stout) gene in muscle leads to an increase in nerve-terminal branching, indicating an alteration to a retrograde signaling pathway. chad and stout have been identified and are novel genes. I propose to identify the gene responsible for the rerak phenotype. I also propose to further characterize the phenotypes of these three mutations by analyzing their development live with GFP lines that specifically light up the synapse. In addition, I propose to do a series of electrophysiological experiments with these branching mutants that will test the importance of nerve-terminal branching for synaptic function and activity-dependent plasticity.
