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Journal of Virology, January 2006, p. 246-251, Vol. 80, No. 1
0022-538X/06/$08.00+0 doi:10.1128/JVI.80.1.246-251.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Isabel Alves-Rodrigues,1,
Amine Noueiry,2
Paul Ahlquist,3,4 and
Juana Díez1*
Departamento de Ciencias Experimentales y de la Salud, Universitat Pompeu Fabra, 08003 Barcelona, Spain,1 Division of Animal and Veterinary Sciences, West Virginia University, Morgantown, West Virginia,2 Institute for Molecular Virology,3 Howard Hughes Medical Institute, University of Wisconsin, Madison, Wisconsin 537064
Received 13 June 2005/ Accepted 2 October 2005
The genomes of positive-strand RNA [(+)RNA] viruses perform two mutually exclusive functions: they act as mRNAs for the translation of viral proteins and as templates for viral replication. A universal key step in the replication of (+)RNA viruses is the coordinated transition of the RNA genome from the cellular translation machinery to the viral replication complex. While host factors are involved in this step, their nature is largely unknown. By using the ability of the higher eukaryotic (+)RNA virus brome mosaic virus (BMV) to replicate in yeast, we previously showed that the host Lsm1p protein is required for efficient recruitment of BMV RNA from translation to replication. Here we show that in addition to Lsm1p, all tested components of the Lsm1p-7p/Pat1p/Dhh1p decapping activator complex, which functions in deadenylation-dependent decapping of cellular mRNAs, are required for BMV RNA recruitment for RNA replication. In contrast, other proteins of the decapping machinery, such as Edc1p and Edc2p from the deadenylation-dependent decapping pathway and Upf1p, Upf2p, and Upf3p from the deadenylation-independent decapping pathway, had no significant effects. The dependence of BMV RNA recruitment on the Lsm1p-7p/Pat1p/Dhh1p complex was linked exclusively to the 3' noncoding region of the BMV RNA. Collectively, our results suggest that the Lsm1p-7p/Pat1p/Dhh1p complex that transfers cellular mRNAs from translation to degradation might act as a key regulator in the switch from BMV RNA translation to replication.
Supplemental material for this article may be found at http://jvi.asm.org/.
Both authors contributed equally to this work.
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