Brief Communication abstract


Nature Neuroscience 11, 1143 - 1145 (2008)
Published online: 7 September 2008 | doi:10.1038/nn.2175

Excess protein synthesis in Drosophila Fragile X mutants impairs long-term memory

François V Bolduc1,2,5, Kimberly Bell2, Hilary Cox2, Kendal S Broadie3 & Tim Tully1,2,4

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We used Drosophila olfactory memory as a model to study the molecular basis of cognitive defects in Fragile X syndrome in vivo. We observed that fragile X protein was acutely required and interacted with argonaute1 and staufen in the formation of long-term memory. Occlusion of long-term memory formation in Fragile X mutants could be rescued by protein synthesis inhibitors, suggesting that excess baseline protein synthesis could negatively affect cognition.

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  1. Watson School of Biological Sciences, 1 Bungtown Road, Cold Spring Harbor, New York 11724, USA.
  2. Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, New York 11724, USA.
  3. Vanderbilt University 1210 MRB III, VU Station B, Box 35-1634, Nashville, Tennessee 37235-1634, USA.
  4. Dart Neuroscience, LLC, 7374 Lusk Blvd., San Diego, California 92121, USA.
  5. Present address: Division of Pediatric Neuroscience, University of Alberta, Alberta T6G2J3, Canada.

Correspondence to: Tim Tully1,2,4 e-mail: Tim_Tully@dartneuroscience.com



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