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Dynamic translational and proteasomal regulation of fragile X mental retardation protein controls mGluR-dependent long-term depression.

Abstract：

:Genetic deletion of fragile X mental retardation protein (FMRP) has been shown to enhance mGluR-dependent long-term depression (LTD). Herein, we demonstrate that mGluR-LTD induces a transient, translation-dependent increase in FMRP that is rapidly degraded by the ubiquitin-proteasome pathway. Moreover, proteasome inhibitors abolished mGluR-LTD, and LTD was absent in mice that overexpress human FMRP. Neither translation nor proteasome inhibitors blocked the augmentation of mGluR-LTD in FMRP-deficient mice. In addition, mGluR-LTD is associated with rapid increases in the protein levels of FMRP target mRNAs in wild-type mice. Interestingly, the basal levels of these proteins were elevated and their synthesis was improperly regulated during mGluR-LTD in FMRP-deficient mice. Our findings indicate that hippocampal mGluR-LTD requires the rapid synthesis and degradation of FMRP and that mGluR-LTD triggers the synthesis of FMRP binding mRNAs. These findings indicate that the translation, ubiquitination, and proteolysis of FMRP functions as a dynamic regulatory system for controlling synaptic plasticity.

journal_name

Neuron

journal_title

Neuron

authors

Hou L,Antion MD,Hu D,Spencer CM,Paylor R,Klann E

doi

10.1016/j.neuron.2006.07.005

subject

Has Abstract

pub_date

2006-08-17 00:00:00

pages

441-54

issue

4

eissn

0896-6273

issn

1097-4199

pii

S0896-6273(06)00545-9

journal_volume

51

pub_type

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