ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
ben Functions with scamp during synaptic transmission and long-term memory formation in Drosophila.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Bendless-mediated K63 ubiquitination modulates cellular signalling to regulate Drosophila hematopoiesis.Cell communication and signaling : CCS · 2026Article
- Single-cell transcriptomics reveals the brain evolution of web-building spiders.Nature ecology & evolution · 2023Article
- Ubc13: the Lys63 ubiquitin chain building machine.Oncotarget · 2016Review
- Bendless modulates JNK-mediated cell death and migration in Drosophila.Cell death and differentiation · 2014Article
- Secretory Carrier Membrane Protein (SCAMP) deficiency influences behavior of adult flies.Frontiers in cell and developmental biology · 2014Article
- Proteomic and transcriptomic analysis of visual long-term memory in Drosophila melanogaster.Protein & cell · 2011Article
- Differential effects of three canonical Toxoplasma strains on gene expression in human neuroepithelial cells.Infection and immunity · 2011Article
- Epigenetic regulation of learning and memory by Drosophila EHMT/G9a.PLoS biology · 2011Article
- Equilibrative nucleoside transporter 2 regulates associative learning and synaptic function in Drosophila.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
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.
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Registered trials
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