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Nucleic Acids Research Advance Access published online on June 15, 2009
Nucleic Acids Research, doi:10.1093/nar/gkp497
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© 2009 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

RNA

Translation of intronless RNAs is strongly stimulated by the Epstein–Barr virus mRNA export factor EB2

Emiliano P. Ricci1,2,3, Fabrice Mure1,2,3, Henri Gruffat1,2,3, Didier Decimo1,2,3, Cahora Medina-Palazon1,2,3, Théophile Ohlmann1,2,3 and Evelyne Manet1,2,3,*

1INSERM U758, Unité de Virologie Humaine, 2Ecole Normale Supérieure de Lyon, Lyon F-69007 and 3IFR128 Biosciences Gerland-Lyon Sud, Lyon F-69364, France

*To whom correspondence should be addressed. Tel: +33 472 728 176; Fax: +33 472 728 137; Email: emanet{at}ens-lyon.fr

Received November 28, 2008. Revised May 18, 2009. Accepted May 21, 2009.

The Epstein–Barr virus protein (EB2) allows the nuclear export of a particular subset of early and late viral RNAs derived from intronless genes. EB2 is conserved among most herpesvirus members and its presence is essential for the production of infectious particles. Here we show that, besides its role as a nuclear export factor, EB2 strongly stimulates translation of unspliced mRNAs without affecting overall cellular translation. Interestingly, this effect can be reversed by the addition of an intron within the gene. The spliced mRNA is then efficiently exported and translated even in the absence of EB2. Moreover, we show that EB2 associates with translating ribosomes and increases the proportion of its target RNA in the polyribosomal fraction. Finally, testing of EB2 homolog proteins derived from EBV-related herpesviruses, shows that, even if they play similar roles within the replication cycle of their respective virus, their mechanisms of action are different.

Present address: Cahora Medina-Palazon, Westmead Institute for Cancer Research, University of Sydney, Westmead Millenium Institute, Westmead, New South Wales 2145, Australia.

The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors.


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