Document Detail


Identification of small molecules rescuing fragile X syndrome phenotypes in Drosophila.
MedLine Citation:
PMID:  18327252     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Fragile X syndrome is caused by the functional loss of the fragile X mental retardation 1 (FMR1) gene. Deletion of the FMR1 ortholog in Drosophila melanogaster (Fmr1) recapitulates many phenotypes associated with fragile X syndrome. We have discovered that Fmr1 mutant Drosophila die during development when reared on food containing increased levels of glutamate, which is consistent with the theory that FMR1 loss results in excess glutamate signaling. Using this lethal phenotype, we screened a chemical library of 2,000 compounds and identified nine molecules that rescued the lethality, including three that implicate the GABAergic inhibitory pathway. Indeed, GABA treatment rescued several known Fmr1 mutant phenotypes in flies, including mushroom bodies defects, excess Futsch translation and abnormal male courtship behavior. These data are consistent with GABAergic inhibition of the enhanced excitatory pathway in fragile X syndrome. In addition, our screen reveals that the muscarinic cholinergic receptors may have a role in fragile X syndrome in parallel to the GABAergic pathway. These results point to potential therapeutic approaches for treating fragile X syndrome.
Authors:
Shuang Chang; Steven M Bray; Zigang Li; Daniela C Zarnescu; Chuan He; Peng Jin; Stephen T Warren
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2008-03-09
Journal Detail:
Title:  Nature chemical biology     Volume:  4     ISSN:  1552-4469     ISO Abbreviation:  Nat. Chem. Biol.     Publication Date:  2008 Apr 
Date Detail:
Created Date:  2008-03-18     Completed Date:  2008-09-15     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101231976     Medline TA:  Nat Chem Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  256-63     Citation Subset:  IM    
Affiliation:
Department of Human Genetics, Emory University School of Medicine, 615 Michael Street Suite 300, Atlanta, Georgia 30322, USA.
Data Bank Information
Bank Name/Acc. No.:
PubChem-Substance/47213189;  47213190;  47213191;  47213192;  47213193;  47213194;  47213195;  47213196;  47213197;  47213198;  47213199;  47213200;  47213201;  47213202;  47213203;  47213204;  47213205;  47213206;  47213207;  47213208;  47213209
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MeSH Terms
Descriptor/Qualifier:
Animals
Disease Models, Animal
Drosophila / genetics*
Drosophila Proteins / drug effects,  genetics*
Drug Evaluation, Preclinical / methods
Female
Fragile X Mental Retardation Protein / drug effects,  genetics*
Fragile X Syndrome / genetics*
Glutamic Acid / pharmacology
Male
Molecular Weight
Mutation
Phenotype
Pyridines / pharmacology
RNA, Messenger / drug effects,  genetics
Small Molecule Libraries / chemical synthesis,  chemistry*
gamma-Aminobutyric Acid / drug effects,  metabolism,  pharmacology
Grant Support
ID/Acronym/Agency:
HD020521/HD/NICHD NIH HHS; HD24064/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/6-methyl-2-(phenylethynyl)pyridine; 0/Drosophila Proteins; 0/FMR1 protein, Drosophila; 0/Pyridines; 0/RNA, Messenger; 0/Small Molecule Libraries; 139135-51-6/Fragile X Mental Retardation Protein; 56-12-2/gamma-Aminobutyric Acid; 56-86-0/Glutamic Acid

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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