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Molecular and Cellular Biology, November 2006, p. 8586-8598, Vol. 26, No. 22
0270-7306/06/$08.00+0     doi:10.1128/MCB.00955-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Serotonin Increases Phosphorylation of Synaptic 4EBP through TOR, but Eukaryotic Initiation Factor 4E Levels Do Not Limit Somatic Cap-Dependent Translation in Aplysia Neurons{triangledown}

Matthew Carroll, John Dyer, and Wayne S. Sossin*

Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, 3801 University St., Montreal, Quebec H3A-2B4, Canada

Received 30 May 2006/ Returned for modification 10 July 2006/ Accepted 5 September 2006

The target of rapamycin (TOR) plays an important role in memory formation in Aplysia californica. Here, we characterize one of the downstream targets of TOR, the eukaryotic initiation factor 4E (eIF4E) binding protein (4EBP) from Aplysia. Aplysia 4EBP contains the four critical phosphorylation sites regulated by TOR as well as an N-terminal RAIP motif and a C-terminal TOS site. Aplysia 4EBP was hypophosphorylated in synaptosomes, and serotonin addition caused a rapamycin-sensitive increase in 4EBP phosphorylation both in synaptosomes and in isolated neurites. Aplysia 4EBP was regulated in a fashion similar to that of mammalian 4EBPs, binding to eIF4E when dephosphorylated and releasing eIF4E after phosphorylation. Overexpression of 4EBP in the soma of Aplysia neurons caused a specific decrease in cap-dependent translation that was rescued by concomitant overexpression of eIF4E. However, eIF4E overexpression by itself did not increase cap-dependent translation, suggesting that increasing levels of free eIF4E by phosphorylating 4EBP is not important in regulating cap-dependent translation in the cell soma. Total levels of eIF4E were also regulated by 4EBP, suggesting that 4EBP can also act as an eIF4E chaperone. These studies demonstrate the conserved nature of 4EBP regulation and its role in cap-dependent translation and suggest differential roles of 4EBP phosphorylation in the soma and synapse.

* Corresponding author. Mailing address: Department of Neurology and Neurosurgery, McGill University, Montreal Neurological Institute, BT 110, 3801 University Street, Montreal, Quebec H3A 2B4, Canada. Phone: (514) 398-1486. Fax: (514) 398-8106. E-mail: wayne.sossin{at}mcgill.ca.

{triangledown} Published ahead of print on 18 September 2006.

Molecular and Cellular Biology, November 2006, p. 8586-8598, Vol. 26, No. 22
0270-7306/06/$08.00+0     doi:10.1128/MCB.00955-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Farah, C. A., Weatherill, D., Dunn, T. W., Sossin, W. S. (2009). PKC Differentially Translocates during Spaced and Massed Training in Aplysia. J. Neurosci. 29: 10281-10286 [Abstract] [Full Text]  
  • Sangthong, P., Hughes, J., McCarthy, J. E. G. (2007). Distributed control for recruitment, scanning and subunit joining steps of translation initiation. Nucleic Acids Res 35: 3573-3580 [Abstract] [Full Text]  


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