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Journal of Virology, April 2002, p. 3292-3300, Vol. 76, No. 7
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.7.3292-3300.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Nuclear Interactions Are Necessary for Translational Enhancement by Spleen Necrosis Virus RU5

Andrew W. Dangel,1,2 Stacey Hull,1,3 Tiffiney M. Roberts,1,3 and Kathleen Boris-Lawrie1,2,3,4,5*

Center for Retrovirus Research,1 Departments of Veterinary Biosciences,2 Molecular Virology, Immunology and Medical Genetics,4 Molecular, Cellular and Developmental Biology Graduate Program,3 Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210-10935

Received 17 September 2001/ Accepted 4 January 2002

The 5' long terminal repeat of spleen necrosis virus (SNV) facilitates Rev/Rev-responsive element (RRE)-independent expression of intron-containing human immunodeficiency virus type 1 (HIV-1) gag. The SNV RU5 region, which corresponds to the 165-nucleotide 5' RNA terminus, functions in a position- and orientation-dependent manner to enhance polysome association of intron-containing HIV-1 gag RNA and also nonviral luc RNA. Evidence is mounting that association with nuclear factors during intron removal licenses mRNAs for nuclear export, efficient translation, and nonsense-mediated decay. This project addressed the relationship between the nuclear export pathway of SNV RU5-reporter RNA and translational enhancement. Results of RNA transfection experiments suggest that cytoplasmic proteins are insufficient for SNV RU5 translational enhancement of gag or luc RNA. Reporter gene assays, leptomycin B (LMB) sensitivity experiments, and RNase protection assays indicate that RU5 gag RNA accesses a nuclear export pathway that is distinct from the LMB-inhibited leucine-rich nuclear export sequence-dependent CRM1 pathway, which is used by the HIV-1 RRE. As a unique tool with which to investigate the relationship between different RNA trafficking routes and translational enhancement, SNV RU5 and Rev/RRE were combined on a single gag RNA. We observed a less-than-synergistic effect on cytoplasmic mRNA utilization. Instead, Rev/RRE diverts RU5 gag RNA to the CRM1-dependent, LMB-inhibited pathway and abrogates translational enhancement by SNV RU5. Our study is the first to show that a nuclear factor(s) directs SNV RU5-containing RNAs to a distinct export pathway that is not inhibited by LMB and programs the intron-containing transcript for translational enhancement.

* Corresponding author. Mailing address: Department of Veterinary Biosciences, The Ohio State University, 1925 Coffey Rd., Columbus, OH 43210-1093. Phone: (614) 292-1392. Fax: (614) 292-6473. E-mail: boris-lawrie.1{at}osu.edu.

Journal of Virology, April 2002, p. 3292-3300, Vol. 76, No. 7
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.7.3292-3300.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Groom, H. C. T., Anderson, E. C., Lever, A. M. L. (2009). Rev: beyond nuclear export. J. Gen. Virol. 90: 1303-1318 [Abstract] [Full Text]  
  • Bolinger, C., Yilmaz, A., Hartman, T. R., Kovacic, M. B., Fernandez, S., Ye, J., Forget, M., Green, P. L., Boris-Lawrie, K. (2007). RNA helicase A interacts with divergent lymphotropic retroviruses and promotes translation of human T-cell leukemia virus type 1. Nucleic Acids Res 0: gkm124v1-14 [Abstract] [Full Text]  
  • Roberts, T. M., Boris-Lawrie, K. (2003). Primary Sequence and Secondary Structure Motifs in Spleen Necrosis Virus RU5 Confer Translational Utilization of Unspliced Human Immunodeficiency Virus Type 1 Reporter RNA. J. Virol. 77: 11973-11984 [Abstract] [Full Text]  
  • Hull, S., Boris-Lawrie, K. (2002). RU5 of Mason-Pfizer Monkey Virus 5' Long Terminal Repeat Enhances Cytoplasmic Expression of Human Immunodeficiency Virus Type 1 gag-pol and Nonviral Reporter RNA. J. Virol. 76: 10211-10218 [Abstract] [Full Text]  


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