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Molecular and Cellular Biology, June 2001, p. 3820-3829, Vol. 21, No. 11
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.11.3820-3829.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Loss of HCF-1-Chromatin Association Precedes Temperature-Induced Growth Arrest of tsBN67 Cells

Joanna Wysocka,1 Patrick T. Reilly,1,2 and Winship Herr1,*

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 3 January 2001/Returned for modification 5 February 2001/Accepted 5 March 2001

Human HCF-1 is a large, highly conserved, and abundant nuclear protein that plays an important but unknown role in cell proliferation. It also plays a role in activation of herpes simplex virus immediate-early gene transcription by the viral regulatory protein VP16. A single proline-to-serine substitution in the HCF-1 VP16 interaction domain causes a temperature-induced arrest of cell proliferation in hamster tsBN67 cells and prevents transcriptional activation by VP16. We show here that HCF-1 is naturally bound to chromatin in uninfected cells through its VP16 interaction domain. HCF-1 is chromatin bound in tsBN67 cells at permissive temperature but dissociates from chromatin before tsBN67 cells stop proliferating at the nonpermissive temperature, suggesting that loss of HCF-1 chromatin association is the primary cause of the temperature-induced tsBN67 cell proliferation arrest. We propose that the role of HCF-1 in cell proliferation is to regulate gene transcription by associating with a multiplicity of DNA-bound transcription factors through its VP16 interaction domain.

* Corresponding author. Mailing address: Cold Spring Harbor Laboratory, P.O. Box 100, 1 Bungtown Rd., Cold Spring Harbor, NY 11724. Phone:(516) 367-8401. Fax: (516) 367-8454. E-mail: herr{at}cshl.org.

Molecular and Cellular Biology, June 2001, p. 3820-3829, Vol. 21, No. 11
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.11.3820-3829.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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