Previous Article | Next Article ![]()
Journal of Virology, December 2001, p. 12402-12411, Vol. 75, No. 24
Cold Spring Harbor Laboratory, Cold Spring
Harbor, New York 11724,1 and Program in
Molecular and Cellular Biology, State University of New York, Stony
Brook, New York 117942
Received 1 June 2001/Accepted 12 September 2001
The human herpes simplex virus (HSV) protein VP16 induces formation
of a transcriptional regulatory complex with two cellular factors
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.24.12402-12411.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Stabilization but Not the Transcriptional Activity
of Herpes Simplex Virus VP16-Induced Complexes Is Evolutionarily
Conserved among HCF Family Members
the
POU homeodomain transcription factor Oct-1 and the cell
proliferation factor HCF-1
to activate viral immediate-early-gene transcription. Although the cellular role of Oct-1 in transcription is
relatively well understood, the cellular role of HCF-1 in cell proliferation is enigmatic. HCF-1 and the related protein HCF-2 form an
HCF protein family in humans that is related to a Caenorhabditis elegans homolog called CeHCF. In this study, we show that all three proteins can promote VP16-induced-complex formation, indicating that VP16 targets a highly conserved function of HCF proteins. The
resulting VP16-induced complexes, however, display different transcriptional activities. In contrast to HCF-1 and CeHCF, HCF-2 fails
to support VP16 activation of transcription effectively. These results
suggest that, along with HCF-1, HCF-2 could have a role, albeit
probably a different role, in HSV infection. CeHCF can mimic HCF-1 for
both association with viral and cellular proteins and transcriptional
activation, suggesting that the function(s) of HCF-1 targeted by VP16
has been highly conserved throughout metazoan evolution.
*
Corresponding author. Mailing address: Cold Spring
Harbor Laboratory, P.O. Box 100, Cold Spring Harbor, NY 11724. Phone: (516) 367-8401. Fax: (516) 367-8454. E-mail:
herr{at}cshl.org.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»