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Journal of Virology, January 2002, p. 195-207, Vol. 76, No. 1
0022-538X/01/$04.00+0     DOI: 10.1128/JVI.76.1.195-207.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Identification of a Motif in the C Terminus of Herpes Simplex Virus Regulatory Protein ICP4 That Contributes to Activation of Transcription

James W. Bruce and Kent W. Wilcox*

Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin 53226

Received 23 April 2001/ Accepted 26 September 2001

Expression of most viral genes during productive infection by herpes simplex virus is regulated by the viral protein ICP4 (also called IE175 or Vmw175). The N-terminal portion of ICP4 contains well-defined transactivation, DNA binding, and dimerization domains that contribute to promoter regulation. The C-terminal half of ICP4 contributes to the activity of ICP4, but the functional motifs have not been well mapped. To localize functional motifs in the C-terminal half of ICP4, we have compared the relative specific activities of ICP4 variants in transient-transfection assays. Deletion of the C-terminal 56 residues reduces the specific activity more than 10-fold. Mutational analysis identified three consecutive residues (1252 to 1254) that are conserved in ICP4 orthologs and are essential for full activity, especially in the context of ICP4 variants with a deletion in the N-terminal transactivation domain. Recombinant viruses that encode variants of ICP4 with mutations in the N-terminal transactivation domain and/or the extreme C terminus were constructed. The phenotypes of these recombinant viruses support the hypothesis that efficient promoter activation by ICP4 requires motifs at both the N and C termini. The data suggest that the C terminus of ICP4 functions not as an independent transactivation domain but as an enhancer of the ICP4 N-terminal transactivation domain. The data provide further support for the hypothesis that some ICP4 motifs required for promoter activation are not required for promoter repression and suggest that ICP4 utilizes different cellular factors for activation or repression of viral promoters.

* Corresponding author. Mailing address: Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, 8701 Watertown Plank Rd., Milwaukee, WI 53226. Phone: (414) 456-8425. Fax: (414) 456-6535. E-mail: kwilcox{at}mcw.edu.

Journal of Virology, January 2002, p. 195-207, Vol. 76, No. 1
0022-538X/01/$04.00+0     DOI: 10.1128/JVI.76.1.195-207.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Kuddus, R. H., DeLuca, N. A. (2007). DNA-Dependent Oligomerization of Herpes Simplex Virus Type 1 Regulatory Protein ICP4. J. Virol. 81: 9230-9237 [Abstract] [Full Text]  
  • Delhon, G., Moraes, M. P., Lu, Z., Afonso, C. L., Flores, E. F., Weiblen, R., Kutish, G. F., Rock, D. L. (2003). Genome of Bovine Herpesvirus 5. J. Virol. 77: 10339-10347 [Abstract] [Full Text]  
  • Compel, P., DeLuca, N. A. (2003). Temperature-Dependent Conformational Changes in Herpes Simplex Virus ICP4 That Affect Transcription Activation. J. Virol. 77: 3257-3268 [Abstract] [Full Text]  


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