Journal
JOURNAL OF NEUROSCIENCE
Volume 33, Issue 46, Pages 18234-18241Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.2207-13.2013
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Funding
- NCN Harmonia [2013/08/M/NZ4/00650]
- Telethon [GGP10150]
- Compagnia San Paolo
- Associazione Italiana Sindrome X Fragile
- VIB
- Foundation for Polish Science, FNPTEAM
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Activity-dependent protein synthesis at synapses is dysregulated in the Fragile X syndrome (FXS). This process contributes to dendritic spine dysmorphogenesis and synaptic dysfunction in FXS. Matrix Metalloproteinase 9 (MMP-9) is an enzyme involved in activity-dependent reorganization of dendritic spine architecture and was shown to regulate spine morphology in a mouse model of FXS, the Fmr1 knock-out mice. Here we show that MMP-9 mRNA is part of the FMRP complex and colocalizes in dendrites. In the absence of FMRP MMP-9 mRNA translation is increased at synapses, suggesting that this mechanism contributes to the increased metalloproteinase level at synapses of Fmr1 knock-out mice. We propose that such a local effect can contribute to the aberrant dendritic spine morphology observed in the Fmr1 knock-out mice and in patients with FXS.
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