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Journal of Virology, January 2009, p. 167-180, Vol. 83, No. 1
0022-538X/09/$08.00+0     doi:10.1128/JVI.01719-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Control of the Papillomavirus Early-to-Late Switch by Differentially Expressed SRp20{triangledown} ,{dagger}

Rong Jia,1 Xuefeng Liu,1 Mingfang Tao,1 Michael Kruhlak,2 Ming Guo,3 Craig Meyers,4 Carl C. Baker,5 and Zhi-Ming Zheng1*

HIV and AIDS Malignancy Branch,1 Experimental Immunology Branch,2 Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892,5 Department of Pathology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030,3 Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 170334

Received 7 August 2008/ Accepted 9 October 2008

The viral early-to-late switch of papillomavirus infection is tightly linked to keratinocyte differentiation and is mediated in part by alternative mRNA splicing. Here, we report that SRp20, a cellular splicing factor, controls the early-to-late switch via interactions with A/C-rich RNA elements. An A/C-rich SE4 element regulates the selection of a bovine papillomavirus type 1 (BPV-1) late-specific splice site, and binding of SRp20 to SE4 suppresses this selection. Expression of late BPV-1 L1 or human papillomavirus (HPV) L1, the major capsid protein, inversely correlates with SRp20 levels in the terminally differentiated keratinocytes. In HPV type 16, a similar SRp20-interacting element also controls the viral early-to-late switch. Keratinocytes in raft cultures, which support L1 expression, make considerably less SRp20 than keratinocytes in monolayer cultures, which do not support L1 expression. Conversely, abundant SRp20 in cancer cells or undifferentiated keratinocytes is important for the expression of the viral early E6 and E7 by promoting the expression of cellular transcription factor SP1 for transactivation of viral early promoters.

* Corresponding author. Mailing address: HIV and AIDS Malignancy Branch, National Cancer Institute, National Institutes of Health, 10 Center Dr. 6N106, Bethesda, MD 20892-1868. Phone: (301) 594-1382. Fax: (301) 480-8250. E-mail: zhengt{at}exchange.nih.gov

{triangledown} Published ahead of print on 22 October 2008.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

Journal of Virology, January 2009, p. 167-180, Vol. 83, No. 1
0022-538X/09/$08.00+0     doi:10.1128/JVI.01719-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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