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Proc Natl Acad Sci U S A. 2010 Aug 31;107(35):15601-6. doi: 10.1073/pnas.1010564107. Epub 2010 Aug 16.

Altered mRNA transport, docking, and protein translation in neurons lacking fragile X mental retardation protein.

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  • 1Department of Cell and Developmental Biology, Beckman Institute, Neuroscience Program, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.


Fragile X syndrome is caused by the absence of functional fragile X mental retardation protein (FMRP), an RNA binding protein. The molecular mechanism of aberrant protein synthesis in fmr1 KO mice is closely associated with the role of FMRP in mRNA transport, delivery, and local protein synthesis. We show that GFP-labeled Fmr1 and CaMKIIalpha mRNAs undergo decelerated motion at 0-40 min after group I mGluR stimulation, and later recover at 40-60 min. Then we investigate targeting of mRNAs associated with FMRP after neuronal stimulation. We find that FMRP is synthesized closely adjacent to stimulated mGluR5 receptors. Moreover, in WT neurons, CaMKIIalpha mRNA can be delivered and translated in dendritic spines within 10 min in response to group I mGluR stimulation, whereas KO neurons fail to show this response. These data suggest that FMRP can mediate spatial mRNA delivery for local protein synthesis in response to synaptic stimulation.

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