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1: J Virol. 2008 Nov 12. [Epub ahead of print]
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The histone variant H3.3 regulates gene expression during lytic infection by Herpes Simplex Virus, HSV-1.

Placek BJ, Huang J, Kent JR, Dorsey J, Rice L, Fraser NW, Berger SL.

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

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-1 (HSV-1) as a model to examine the temporal profile of histone H3 incorporation and whether the variant histone H3.3 has a direct effect on transcription. We find that canonical H3.1 and variant H3.3 exhibit distinct timing in their genome association 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 provide new evidence for a regulatory role of chromatin composition during HSV-1 acute infection.

PMID: 19004946 [PubMed - as supplied by publisher]