A Database of Drosophila Genes & Genomes

FB2008_06, released July 3, 2008
 

Reference Report

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Citation Zhang, Y.Q., Bailey, A.M., Matthies, H.J.G., Renden, R.B., Smith, M.A., Speese, S.D., Rubin, G.M., Broadie, K. (2001). Drosophila fragile X-related gene regulates the MAP1B homolog Futsch to control synaptic structure and function.  Cell 107(5): 591--603.
FlyBase ID FBrf0141416
Type of publication Research paper
Offprint Available Yes
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PubMed ID 11733059
PubMed Abstract Fragile X mental retardation gene (FMR1) encodes an RNA binding protein that acts as a negative translational regulator. We have developed a Drosophila fragile X syndrome model using loss-of-function mutants and overexpression of the FMR1 homolog (dfxr). dfxr nulls display enlarged synaptic terminals, whereas neuronal overexpression results in fewer and larger synaptic boutons. Synaptic structural defects are accompanied by altered neurotransmission, with synapse type-specific regulation in central and peripheral synapses. These phenotypes mimic those observed in mutants of microtubule-associated Futsch. Immunoprecipitation of dFXR shows association with futsch mRNA, and Western analyses demonstrate that dFXR inversely regulates Futsch expression. dfxr futsch double mutants restore normal synaptic structure and function. We propose that dFXR acts as a translational repressor of Futsch to regulate microtubule-dependent synaptic growth and function.
Biosis 2002.42664
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Language of publication English
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Abbreviation Cell
Title Cell
Authors
Volume range 1-
Year range 1974-
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Publisher Cell Press
Place of publication Cambridge, MA
Language of publication English
ISBN/ISSN 0092-8674
CODEN CELLB5
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