This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Placek, B. J.
Right arrow Articles by Berger, S. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Placek, B. J.
Right arrow Articles by Berger, S. L.

 Previous Article  |  Next Article 

Journal of Virology, February 2009, p. 1416-1421, Vol. 83, No. 3
0022-538X/09/$08.00+0     doi:10.1128/JVI.01276-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

The Histone Variant H3.3 Regulates Gene Expression during Lytic Infection with Herpes Simplex Virus Type 1 {triangledown}

Brandon J. Placek,1 Jing Huang,1 Jennifer R. Kent,2 Jean Dorsey,1 Lyndi Rice,1 Nigel W. Fraser,2 and Shelley L. Berger1*

Gene Expression and Regulation Program, The Wistar Institute,1 Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia, Pennysylvania2

Received 19 June 2008/ Accepted 5 November 2008

It has been proposed that incorporation of the histone variant H3.3 within actively transcribed regions of a genome helps to facilitate transcription. In this report we use lytic infection by herpes simplex virus type 1 (HSV-1) as a model to examine the temporal profile of histone H3 incorporation and to determine whether the variant histone H3.3 has a direct effect on transcription. We find that canonical H3.1 and variant H3.3 exhibit distinct temporal associations with the genome in cell lines expressing equal amounts of epitope-tagged H3 variants. At the earliest times examined after infection, the HSV-1 genome is incorporated into chromatin that predominantly contains the variant H3.3, whereas incorporation of canonical H3.1 occurs later in infection and is dependent on replication of the HSV-1 genome. Further, inhibition of H3.3 association, via reduced expression of the H3.3 chaperone HIRA, significantly reduces the levels of HSV-1 mRNA. These findings show that incorporation of H3.3 facilitates transcription, and they provide new evidence for a regulatory role of chromatin composition during HSV-1 acute infection.


* Corresponding author. Mailing address: The Wistar Institute, 3601 Spruce St., Room 201, Philadelphia, PA 19104. Phone: (215) 898-3922. Fax: (215) 898-0663. E-mail: berger{at}wistar.org

{triangledown} Published ahead of print on 12 November 2008.


Journal of Virology, February 2009, p. 1416-1421, Vol. 83, No. 3
0022-538X/09/$08.00+0     doi:10.1128/JVI.01276-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Kutluay, S. B., Triezenberg, S. J. (2009). Regulation of Histone Deposition on the Herpes Simplex Virus Type 1 Genome during Lytic Infection. J. Virol. 83: 5835-5845 [Abstract] [Full Text]