RT Journal Article SR Electronic T1 The Steady-State Level of the Nervous-System-Specific MicroRNA-124a Is Regulated by dFMR1 in Drosophila JF The Journal of Neuroscience JO J. Neurosci. FD Society for Neuroscience SP 11883 OP 11889 DO 10.1523/JNEUROSCI.4114-08.2008 VO 28 IS 46 A1 Xu, Xia-Lian A1 Li, Yan A1 Wang, Fay A1 Gao, Fen-Biao YR 2008 UL http://www.jneurosci.org/content/28/46/11883.abstract 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.