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

Nat Neurosci. 2008 Oct;11(10):1143-5. doi: 10.1038/nn.2175. Epub 2008 Sep 7.


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.

MeSH terms

  • Analysis of Variance
  • Animals
  • Animals, Genetically Modified
  • Behavior, Animal
  • Conditioning, Classical / physiology
  • Disease Models, Animal*
  • Drosophila
  • Drosophila Proteins / genetics
  • Electroshock
  • Fragile X Mental Retardation Protein / genetics
  • Fragile X Syndrome / complications*
  • Fragile X Syndrome / metabolism*
  • Memory Disorders / etiology*
  • Mutation
  • Olfactory Pathways / physiology
  • Protein Biosynthesis / drug effects
  • Protein Biosynthesis / physiology*
  • RNA Interference
  • Space Perception / physiology
  • Time Factors


  • Drosophila Proteins
  • Fragile X Mental Retardation Protein