This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by McPhillips, M. G. Articles by Graham, S. V. Search for Related Content PubMed PubMed Citation Articles by McPhillips, M. G. Articles by Graham, S. V.

SF2/ASF Binds the Human Papillomavirus Type 16 Late RNA Control Element and Is Regulated during Differentiation of Virus-Infected Epithelial Cells

Maria G. McPhillips ,^1,, Thanaporn Veerapraditsin,^1, Sarah A. Cumming,¹ Dimitra Karali,¹ Steven G. Milligan,¹ Winifred Boner,² Iain M. Morgan,² and Sheila V. Graham^1*

Institute of Biomedical and Life Sciences, Division of Virology,¹ Institute of Comparative Medicine, Department of Veterinary Pathology, University of Glasgow, Glasgow, Scotland, United Kingdom²

Received 2 February 2004/ Accepted 13 May 2004

Pre-mRNA splicing occurs in the spliceosome, which is composed of small ribonucleoprotein particles (snRNPs) and many non-snRNP components. SR proteins, so called because of their C-terminal arginine- and serine-rich domains (RS domains), are essential members of this class. Recruitment of snRNPs to 5' and 3' splice sites is mediated and promoted by SR proteins. SR proteins also bridge splicing factors across exons to help to define these units and have a central role in alternative and enhancer-dependent splicing. Here, we show that the SR protein SF2/ASF is part of a complex that forms upon the 79-nucleotide negative regulatory element (NRE) that is thought to be pivotal in posttranscriptional regulation of late gene expression in human papillomavirus type 16 (HPV-16). However, the NRE does not contain any active splice sites, is located in the viral late 3' untranslated region, and regulates RNA-processing events other than splicing. The level of expression and extent of phosphorylation of SF2/ASF are upregulated with epithelial differentiation, as is subcellular distribution, specifically in HPV-16-infected epithelial cells, and expression levels are controlled, at least in part, by the virus transcription regulator E2.

These authors contributed equally to the work.

Present address: DNA Tumor Virus Section, Laboratory of Viral Diseases, NIAID, NIH, Bethesda, Md.

This article has been cited by other articles:

• Goraczniak, R., Gunderson, S. I. (2008). The Regulatory Element in the 3'-Untranslated Region of Human Papillomavirus 16 Inhibits Expression by Binding CUG-binding Protein 1. J. Biol. Chem. 283: 2286-2296 [Abstract] [Full Text]  
• Bell, I., Martin, A., Roberts, S. (2007). The E1^E4 Protein of Human Papillomavirus Interacts with the Serine-Arginine-Specific Protein Kinase SRPK1. J. Virol. 81: 5437-5448 [Abstract] [Full Text]  
• Berro, R., Kehn, K., de la Fuente, C., Pumfery, A., Adair, R., Wade, J., Colberg-Poley, A. M., Hiscott, J., Kashanchi, F. (2006). Acetylated Tat Regulates Human Immunodeficiency Virus Type 1 Splicing through Its Interaction with the Splicing Regulator p32.. J. Virol. 80: 3189-3204 [Abstract] [Full Text]  
• Oberg, D., Fay, J., Lambkin, H., Schwartz, S. (2005). A Downstream Polyadenylation Element in Human Papillomavirus Type 16 L2 Encodes Multiple GGG Motifs and Interacts with hnRNP H. J. Virol. 79: 9254-9269 [Abstract] [Full Text]