WWW.JNEUROSCI.ORG
-
The Journal of Neuroscience
 QUICK SEARCH:   [advanced]


     
-


HOME
  |  
SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, November 12, 2008, 28(46):11883-11889; doi:10.1523/JNEUROSCI.4114-08.2008

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental Data
Right arrow Submit an eLetter
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (10)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Xu, X.-L.
Right arrow Articles by Gao, F.-B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Xu, X.-L.
Right arrow Articles by Gao, F.-B.

 Previous Article  |  Next Article 

Neurobiology of Disease
The Steady-State Level of the Nervous-System-Specific MicroRNA-124a Is Regulated by dFMR1 in Drosophila

Xia-Lian Xu, * Yan Li, * Fay Wang, and Fen-Biao Gao

Gladstone Institute of Neurological Disease and Department of Neurology, University of California, San Francisco, California 94158

Correspondence should be addressed to Fen-Biao Gao, Gladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158. Email: fgao{at}gladstone.ucsf.edu

Fragile X syndrome is the most common form of inherited mental retardation caused by loss of the fragile X mental retardation protein 1 (FMRP). The detailed molecular pathways underlying the pathogenesis of this disorder remain incompletely understood. Here, we show that miR-124a, a nervous-system-specific miRNA, is associated with the Drosophila homolog of FMRP (dFMR1) in vivo. Ectopic expression of wild-type but not mutant miR-124a precursors decreased dendritic branching of dendritic arborization sensory neurons, which was partially rescued by the loss of dFMR1 activity, suggesting that the biogenesis and/or function of miR-124a are partially dependent on dFMR1. Indeed, in contrast with the complete loss of mature miR-124a in Dicer-1 mutants, steady-state levels of endogenous or ectopically expressed mature miR-124a were partially reduced in dfmr1 mutants, whereas the level of pre-miR-124a increased. This effect could be explained in part by the reduced abundance of the Dicer-1-Ago1 complex in the absence of dFMR1. These findings suggest a modulatory role for dFMR1 to maintain proper levels of miRNAs during neuronal development.

Key words: miR-124a; processing; Drosophila; fragile X syndrome; dendrites; RNA


Received Aug. 28, 2008; revised Sept. 24, 2008; accepted Sept. 26, 2008.

Correspondence should be addressed to Fen-Biao Gao, Gladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158. Email: fgao{at}gladstone.ucsf.edu




This article has been cited by other articles:


Home page
Hum Mol GenetHome page
S. Chang, S. Wen, D. Chen, and P. Jin
Small regulatory RNAs in neurodevelopmental disorders
Hum. Mol. Genet., April 15, 2009; 18(R1): R18 - R26.
[Abstract] [Full Text] [PDF]



-
-

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help

-
Copyright 2009 by Society for Neuroscience ONLINE ISSN: 1529-2401
-