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Journal of Virology, November 2003, p. 11927-11932, Vol. 77, No. 22
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.22.11927-11932.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Oct-1 Is Posttranslationally Modified and Exhibits Reduced Capacity To Bind Cognate Sites at Late Times after Infection with Herpes Simplex Virus 1

Sunil J. Advani,1,2 Lizette O. Durand,1 Ralph R. Weichselbaum,2 and Bernard Roizman1*

The Marjorie B. Kovler Viral Oncology Laboratories,1 Department of Radiation and Cellular Oncology, The University of Chicago, Chicago, Illinois 606372

Received 17 June 2003/ Accepted 15 August 2003

In herpes simplex virus 1-infected cells, a high level of {alpha} gene expression requires the transactivation of the genes by a complex containing the viral {alpha} transinducing factor ({alpha}TIF) and two cellular proteins. The latter two, HCF-1 and octamer binding protein Oct-1, are transcriptional factors regulated in a cell cycle-dependent manner. {alpha}TIF is a protein made late in infection but packaged with the virion to transactivate viral genes in newly infected cells. In light of the accumulation of large amounts of {alpha}TIF, the absence of {alpha} gene expression late in infection suggested the possibility that one or more transcriptional factors required for {alpha} gene expression is modified late in infection. Here we report that Oct-1 is posttranscriptionally modified late in infection, that the modification is mediated by the virus but does not involve viral protein kinases or cdc2 kinase activated by the virus late in infection, and that the modified Oct-1 has a reduced affinity for its cognate DNA site. These results are consistent with the hypothesis that modification of Oct-1 transcriptional factor could account at least in part for the shutoff of {alpha} gene expression late in infection.

* Corresponding author. Mailing address: The Marjorie B. Kovler Viral Oncology Laboratories, 910 E. 58th St., Chicago, IL 60637. Phone: (773) 702-1898. Fax: (773) 702-1631. E-mail: Bernard.Roizman{at}bsd.uchicago.edu.

Journal of Virology, November 2003, p. 11927-11932, Vol. 77, No. 22
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.22.11927-11932.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Mesplede, T., Island, M.-L., Christeff, N., Petek, F., Doly, J., Navarro, S. (2005). The POU Transcription Factor Oct-1 Represses Virus-Induced Interferon A Gene Expression. Mol. Cell. Biol. 25: 8717-8731 [Abstract] [Full Text]  
  • Nogueira, M. L., Wang, V. E. H., Tantin, D., Sharp, P. A., Kristie, T. M. (2004). Herpes simplex virus infections are arrested in Oct-1-deficient cells. Proc. Natl. Acad. Sci. USA 101: 1473-1478 [Abstract] [Full Text]  


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