Previous genetic studies of intersegmental nerve b development have id
entified several cell-surface proteins required for correct axon guida
nce to appropriate target muscles. Here we provide evidence that the s
mall GTPase Drac1 also plays a key role in this guidance process. Neur
onal expression of the dominant negative mutation Drac1(N17) causes ax
ons to bypass and extend beyond normal synaptic partners. This phenoty
pe is consistently reproduced by pharmacological blockade of actin ass
embly. Genetic interactions between Drac1(N17) and the receptor-tyrosi
ne phosphatase Dlar suggest that intersegmental nerve b guidance requi
res the integration of multiple, convergent signals.