The Fragile X mental retardation protein regulates matrix metalloproteinase 9 mRNA at synapses.

Details

Serval ID
serval:BIB_79E7C1DFDEF3
Type
Article: article from journal or magazin.
Collection
Publications
Title
The Fragile X mental retardation protein regulates matrix metalloproteinase 9 mRNA at synapses.
Journal
The Journal of neuroscience : the official journal of the Society for Neuroscience
Author(s)
Janusz A., Milek J., Perycz M., Pacini L., Bagni C., Kaczmarek L., Dziembowska M.
ISSN
1529-2401 (Electronic)
ISSN-L
0270-6474
Publication state
Published
Issued date
13/11/2013
Volume
33
Number
46
Pages
18234-18241
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Abstract
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.

Keywords
Animals, Dendrites/enzymology, Dendrites/genetics, Female, Fragile X Mental Retardation Protein/physiology, Hippocampus/enzymology, Matrix Metalloproteinase 9/biosynthesis, Matrix Metalloproteinase 9/genetics, Mice, Mice, Knockout, RNA, Messenger/biosynthesis, RNA, Messenger/genetics, Rats, Synapses/enzymology, Synapses/genetics
Pubmed
Open Access
Yes
Create date
06/03/2017 18:23
Last modification date
08/05/2019 20:44
Usage data