Excess protein synthesis in Drosophila fragile X mutants impairs long-term memory.
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.
Bolduc
François V
FV
Watson School of Biological Sciences, 1 Bungtown Road, Cold Spring Harbor, New York 11724, USA.
Bell
Kimberly
K
Cox
Hilary
H
Broadie
Kendal S
KS
Tully
Tim
T
D000704:Analysis of Variance; D000818:Animals; D030801:Animals, Genetically Modified; D001522:Behavior, Animal; D003214:Conditioning, Classical / Q000502:physiology; D004195:Disease Models, Animal; D004330:Drosophila; D029721:Drosophila Proteins / Q000235:genetics; D004597:Electroshock; D051860:Fragile X Messenger Ribonucleoprotein 1 / Q000235:genetics; D005600:Fragile X Syndrome / Q000150:complications* / Q000378:metabolism*; D008569:Memory Disorders / Q000209:etiology*; D009154:Mutation; D009833:Olfactory Pathways / Q000502:physiology; D014176:Protein Biosynthesis / Q000187:drug effects / Q000502:physiology*; D034622:RNA Interference; D013028:Space Perception / Q000502:physiology; D013997:Time Factors
D029721:Drosophila Proteins; D051860:Fragile X Messenger Ribonucleoprotein 1
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