Abstract：
:MicroRNAs (miRNAs) are noncoding RNAs that suppress translation of specific mRNAs. The miRNA machinery interacts with fragile X mental retardation protein (FMRP), which functions as translational repressor. We show that miR-125b and miR-132, as well as several other miRNAs, are associated with FMRP in mouse brain. miR-125b and miR-132 had largely opposing effects on dendritic spine morphology and synaptic physiology in hippocampal neurons. FMRP knockdown ameliorates the effect of miRNA overexpression on spine morphology. We identified NMDA receptor subunit NR2A as a target of miR-125b and show that NR2A mRNA is specifically associated with FMRP in brain. In hippocampal neurons, NR2A expression is negatively regulated through its 3' UTR by FMRP, miR-125b, and Argonaute 1. Regulation of NR2A 3'UTR by FMRP depends in part on miR-125b. Because NMDA receptor subunit composition profoundly affects synaptic plasticity, these observations have implications for the pathophysiology of fragile X syndrome, in which plasticity is altered.
journal_name
Neuronjournal_title
Neuronauthors
Edbauer D,Neilson JR,Foster KA,Wang CF,Seeburg DP,Batterton MN,Tada T,Dolan BM,Sharp PA,Sheng Mdoi
10.1016/j.neuron.2010.01.005subject
Has Abstractpub_date
2010-02-11 00:00:00pages
373-84issue
3eissn
0896-6273issn
1097-4199pii
S0896-6273(10)00010-3journal_volume
65pub_type
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