PT  - JOURNAL ARTICLE
AU  - Xu, Xia-Lian
AU  - Li, Yan
AU  - Wang, Fay
AU  - Gao, Fen-Biao
TI  - The Steady-State Level of the Nervous-System-Specific MicroRNA-124a Is Regulated by dFMR1 in <em>Drosophila</em>
AID  - 10.1523/JNEUROSCI.4114-08.2008
DP  - 2008 Nov 12
TA  - The Journal of Neuroscience
PG  - 11883--11889
VI  - 28
IP  - 46
4099  - http://www.jneurosci.org/content/28/46/11883.short
4100  - http://www.jneurosci.org/content/28/46/11883.full
SO  - J. Neurosci.2008 Nov 12; 28
AB  - 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.