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The EJC factor eIF4AIII modulates synaptic strength and neuronal protein expression.

Authors: Giorgi, C  Yeo, GW  Stone, ME  Katz, DB  Burge, C  Turrigiano, G  Moore, MJ 
Citation: Giorgi C, etal., Cell. 2007 Jul 13;130(1):179-91.
Pubmed: (View Article at PubMed) PMID:17632064
DOI: Full-text: DOI:10.1016/j.cell.2007.05.028

Proper neuronal function and several forms of synaptic plasticity are highly dependent on precise control of mRNA translation, particularly in dendrites. We find that eIF4AIII, a core exon junction complex (EJC) component loaded onto mRNAs by pre-mRNA splicing, is associated with neuronal mRNA granules and dendritic mRNAs. eIF4AIII knockdown markedly increases both synaptic strength and GLUR1 AMPA receptor abundance at synapses. eIF4AIII depletion also increases ARC, a protein required for maintenance of long-term potentiation; arc mRNA, one of the most abundant in dendrites, is a natural target for nonsense-mediated decay (NMD). Numerous new NMD candidates, some with potential to affect synaptic activity, were also identified computationally. Two models are presented for how translation-dependent decay pathways such as NMD might advantageously function as critical brakes for protein synthesis in cells such as neurons that are highly dependent on spatially and temporally restricted protein expression.


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RGD Object Information
RGD ID: 10044262
Created: 2015-06-05
Species: All species
Last Modified: 2015-06-05
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.