The steady-state level of the nervous-system-specific microRNA-124a is regulated by dFMR1 in Drosophila. Export

@article{citeulike:3512905, abstract = {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.}, author = {Xu, X. L. and Li, Y. and Wang, F. and Gao, F. B.}, citeulike-article-id = {3512905}, citeulike-linkout-0 = {http://dx.doi.org/10.1523/JNEUROSCI.4114-08.2008}, citeulike-linkout-1 = {http://www.jneurosci.org/cgi/content/abstract/28/46/11883}, citeulike-linkout-2 = {http://view.ncbi.nlm.nih.gov/pubmed/19005053}, citeulike-linkout-3 = {http://www.hubmed.org/display.cgi?uids=19005053}, comment = {Article recommanded by Jan, proposing to check miR-124 in D1-miR-mGluR5 mice}, day = {12}, doi = {10.1523/JNEUROSCI.4114-08.2008}, issn = {1529-2401}, journal = {The Journal of neuroscience : the official journal of the Society for Neuroscience}, keywords = {fragilex, mglur5, mir-124}, month = {November}, number = {46}, pages = {11883--11889}, posted-at = {2008-11-14 12:19:47}, priority = {5}, title = {The steady-state level of the nervous-system-specific microRNA-124a is regulated by dFMR1 in Drosophila.}, url = {http://dx.doi.org/10.1523/JNEUROSCI.4114-08.2008}, volume = {28}, year = {2008} }

TY - JOUR ID - citeulike:3512905 L3 - citeulike-article-id:3512905 N2 - 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. IS - 46 JF - The Journal of neuroscience : the official journal of the Society for Neuroscience SN - 1529-2401 EP - 11889 TI - The steady-state level of the nervous-system-specific microRNA-124a is regulated by dFMR1 in Drosophila. VL - 28 SP - 11883 KW - fragilex KW - mglur5 KW - mir-124 N1 - Article recommanded by Jan, proposing to check miR-124 in D1-miR-mGluR5 mice AU - Xu, XL AU - Li, Y AU - Wang, F AU - Gao, FB PY - 2008/11/12/ UR - http://dx.doi.org/10.1523/JNEUROSCI.4114-08.2008 ER -