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
Google Scholar
Right arrow Articles by Kwiatkowski, D. L.
Right arrow Articles by Bloom, D. C.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kwiatkowski, D. L.
Right arrow Articles by Bloom, D. C.

 Previous Article  |  Next Article 

Journal of Virology, August 2009, p. 8173-8181, Vol. 83, No. 16
0022-538X/09/$08.00+0     doi:10.1128/JVI.00686-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

The Polycomb Group Protein Bmi1 Binds to the Herpes Simplex Virus 1 Latent Genome and Maintains Repressive Histone Marks during Latency{triangledown}

Dacia L. Kwiatkowski,1 Hilary W. Thompson,2 and David C. Bloom1*

Department of Molecular Genetics & Microbiology, University of Florida College of Medicine, Gainesville, Florida,1 Section of Biostatistics, School of Public Health, Louisiana State University Health Sciences Center, New Orleans, Louisiana2

Received 2 April 2009/ Accepted 26 May 2009

The mechanism by which herpes simplex virus 1 (HSV-1) establishes latency in sensory neurons is largely unknown. Recent studies indicate that epigenetic modifications of the chromatin associated with the latent genome may play a key role in the transcriptional control of lytic genes during latency. In this study, we found both constitutive and facultative types of heterochromatin to be present on the latent HSV-1 genome. Deposition of the facultative marks trimethyl H3K27 and histone variant macroH2A varied at different sites on the genome, whereas the constitutive marker trimethyl H3K9 did not. In addition, we show that in the absence of the latency-associated transcript (LAT), the latent genome shows a dramatic increase in trimethyl H3K27, suggesting that expression of the LAT during latency may act to promote an appropriate heterochromatic state that represses lytic genes but is still poised for reactivation. Due to the presence of the mark trimethyl H3K27, we examined whether Polycomb group proteins, which methylate H3K27, were present on the HSV-1 genome during latency. Our data indicate that Bmi1, a member of the Polycomb repressive complex 1 (PRC1) maintenance complex, associates with specific sites in the genome, with the highest level of enrichment at the LAT enhancer. To our knowledge, these are the first data demonstrating that a virus can repress its gene transcription to enter latency by exploiting the mechanism of Polycomb-mediated repression.

* Corresponding author. Mailing address: Department of Molecular Genetics & Microbiology, Box 100266, University of Florida College of Medicine, Gainesville, FL 32610-0266. Phone: (352) 392-8520. Fax: (352) 392-3133. E-mail: dbloom{at}ufl.edu

{triangledown} Published ahead of print on 10 June 2009.

Journal of Virology, August 2009, p. 8173-8181, Vol. 83, No. 16
0022-538X/09/$08.00+0     doi:10.1128/JVI.00686-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»