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The Journal of Neuroscience, January 14, 2009, 29(2):414-424; doi:10.1523/JNEUROSCI.5036-07.2009

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Behavioral/Systems/Cognitive
ben Functions with Scamp during Synaptic Transmission and Long-Term Memory Formation in Drosophila

Hong Zhao,¹ Xingguo Zheng,¹ Xiaojing Yuan,¹ Lei Wang,¹ Xin Wang,² Yi Zhong,^1,2,3 Zuoping Xie,¹ and Tim Tully^3,4

¹State Key Laboratory of Biomembrane and Membrane Biotechnology, Department of Biological Sciences and Biotechnology, Tsinghua University, Beijing, China 100084, ²JoeKai Inc., Beijing, China 100084, ³Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, and ⁴Dart Neuroscience LLC, San Diego, California 92121

Correspondence should be addressed to either of the following: Dr. Tim Tully, Dart Neuroscience LLC, 7473 Lusk Boulevard, San Diego, CA 92075, Email: ttully{at}dartneuroscience.com; or Dr. Zuoping Xie, Department of Biological Sciences and Technology, Tsinghua University, Beijing, China 100084, Email: zuoping{at}tsinghua.edu.cn

Genetic screens for Drosophila mutants 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 identified ben (CG32594), which encodes a novel protein. Mutations of ben specifically disrupt LTM, leaving earlier memory phases intact. The role of ben appears physiological rather than developmental, because acutely induced expression of a ben⁺ transgene in adults rescues the mutant's LTM defect. More interestingly, induced expression of ben⁺ 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 for ben in 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.

Key words: olfactory learning; synaptic transmission mutants; larval neuromuscular junction; mutant; learning and memory; neurotransmission

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Received Aug. 20, 2008; revised Nov. 18, 2008; accepted Nov. 20, 2008.

Correspondence should be addressed to either of the following: Dr. Tim Tully, Dart Neuroscience LLC, 7473 Lusk Boulevard, San Diego, CA 92075, Email: ttully{at}dartneuroscience.com; or Dr. Zuoping Xie, Department of Biological Sciences and Technology, Tsinghua University, Beijing, China 100084, Email: zuoping{at}tsinghua.edu.cn

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