期刊
JOURNAL OF NEUROSCIENCE
卷 28, 期 46, 页码 11883-11889出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.4114-08.2008
关键词
miR-124a; processing; Drosophila; fragile X syndrome; dendrites; RNA
资金
- FRAXA Research Foundation
- National Institutes of Health
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.
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