Genetic screens forDrosophilamutants defective in pavlovian olfactory memory have provided unique insight into the molecular basis of memory storage. Occasionally, these singular genetic lesions have been assembled into meaningful molecular pathways and neural circuitries. For the most part, however, these genes and their expression patterns in the CNS remain fragmented, demanding new clues from continued mutant screens. From a behavioral screen for long-term memory (LTM) mutants, we have identifiedben(CG32594), which encodes a novel protein. Mutations ofbenspecifically disrupt LTM, leaving earlier memory phases intact. The role ofbenappears physiological rather than developmental, because acutely induced expression of aben+transgene in adults rescues the mutant's LTM defect. More interestingly, induced expression ofben+specifically in mushroom bodies (MBs), but not in the ellipsoid body of the central complex, is sufficient to rescue the mutant LTM defect. This suggests a role forbenin the MB during olfactory memory formation. We also provide evidence that BEN interacts genetically in both synaptic transmission and LTM formation with SCAMP, a synaptic protein known to be involved in vesicle recycling.