Drosophila Futsch regulates synaptic microtubule organization and is necessary for synaptic growth

We present evidence that Futsch, a novel protein with MAP1B homology, contr ols synaptic growth at the Drosophila neuromuscular junction through the re gulation of the synaptic microtubule cytoskeleton. Futsch colocalizes with microtubules and identifies cytoskeletal loops that traverse the lateral ma rgin of select synaptic boutons. An apparent rearrangement of microtubule l oop architecture occurs during bouton division, and a genetic analysis indi cates that Futsch is necessary for this process. futsch mutations disrupt s ynaptic microtubule organization, reduce bouton number, and increase bouton size. These deficits can be partially rescued by neuronal overexpression o f a futsch MAP1B homology domain. Finally, genetic manipulations that incre ase nerve-terminal branching correlate with increased synaptic microtubule loop formation, and both processes require normal Futsch function. These da ta suggest a common microtubule-based growth mechanism at the synapse and g rowth cone.