FXR1P but not FMRP regulates the levels of mammalian brain-specific microRNA-9 and microRNA-124
Authors
Xu, Xia-LianZong, Ruiting
Li, Zhaodong
Biswas, Md Helal Uddin
Fang, Zhe
Nelson, David L.
Gao, Fen-Biao
UMass Chan Affiliations
Department of NeurologyDocument Type
Journal ArticlePublication Date
2011-09-28Keywords
AnimalsBrain
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
Metadata
Show full item recordAbstract
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.Source
J Neurosci. 2011 Sep 28;31(39):13705-9. Link to article on publisher's siteDOI
10.1523/JNEUROSCI.2827-11.2011Permanent Link to this Item
http://hdl.handle.net/20.500.14038/37738PubMed ID
21957233Related Resources
Link to Article in PubMedRights
Publisher PDF posted as allowed by the publisher's author rights policy at http://www.jneurosci.org/site/misc/ifa_policies.xhtml#copyright. 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.
ae974a485f413a2113503eed53cd6c53
10.1523/JNEUROSCI.2827-11.2011