UMMS Affiliation

Department of Neurology

Publication Date


Document Type



Animals; Brain; Cells, Cultured; DEAD-box RNA Helicases; Female; *Fragile X Mental Retardation Protein; Fragile X Syndrome; HEK293 Cells; Humans; Male; Mice; Mice, Knockout; MicroRNAs; RNA-Binding Proteins; Ribonuclease III


Neurology | Neuroscience and Neurobiology


Mammalian brain-specific miR-9 and miR-124 have been implicated in several aspects of neuronal development and function. However, it is not known how their expression levels are regulated in vivo. We found that the levels of miR-9 and miR-124 are regulated by FXR1P but not by the loss of FXR2P or FMRP in vivo, a mouse model of fragile X syndrome. Surprisingly, the levels of miR-9 and miR-124 are elevated in fmr1/fxr2 double-knock-out mice, in part reflecting posttranscriptional upregulation of FXR1P. Indeed, FXR1P is required for efficient processing of pre-miR-9 and pre-miR-124 in vitro and forms a complex with Dicer and pre-miRNAs. These findings reveal differential roles of FMRP family proteins in controlling the expression levels of brain-specific miRNAs.

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Publisher PDF posted as allowed by the publisher's author rights policy at Copyright of all material published in The Journal of Neuroscience remains with the authors. The authors grant the Society for Neuroscience an exclusive license to publish their work for the first 6 months. After 6 months the work becomes available to the public to copy, distribute, or display under a Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported license.

DOI of Published Version



J Neurosci. 2011 Sep 28;31(39):13705-9. Link to article on publisher's site

Journal/Book/Conference Title

The Journal of neuroscience : the official journal of the Society for Neuroscience

Related Resources

Link to Article in PubMed

PubMed ID