Bovine herpesvirus 1 immediate-early protein (bICP0) interacts with the histone acetyltransferase p300, which stimulates productive infection and gC promoter activity
| Autor: | Joe Zhou, Yange Zhang, Vicki Geiser, Yunquan Jiang, Clinton Jones |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Gene Expression Regulation
Viral Genes Viral Ubiquitin-Protein Ligases Molecular Sequence Data Cell Cycle Proteins In Vitro Techniques Transfection Immediate early protein Cell Line Viral Proteins Transcription (biology) Virology Ring finger medicine Animals Humans p300-CBP Transcription Factors Amino Acid Sequence Promoter Regions Genetic Gene Herpesvirus 1 Bovine Histone Acetyltransferases Cell Nucleus Histone Acetyltransferase p300 biology Promoter Zinc Fingers Histone acetyltransferase Herpesviridae Infections Molecular biology HDAC1 medicine.anatomical_structure Mutation biology.protein Trans-Activators Cattle Rabbits Transcription Factors |
| Zdroj: | The Journal of general virology. 87(Pt 7) |
| ISSN: | 0022-1317 |
| Popis: | The immediate-early protein, bICP0, ofBovine herpesvirus 1(BHV-1) transactivates viral promoters and stimulates productive infection. bICP0 is expressed constitutively during productive infection, as its gene contains an immediate-early and an early promoter. Like other ICP0 homologues encoded by members of the subfamilyAlphaherpesvirinae, bICP0 contains a zinc RING finger located near its N terminus. Mutations that disrupt the bICP0 zinc RING finger impair its ability to activate transcription, stimulate productive infection, inhibit interferon-dependent transcription in certain cell types and regulate subnuclear localization. bICP0 also interacts with a cellular chromatin-remodelling enzyme, histone deacetylase 1 (HDAC1), and can relieve HDAC1-mediated transcriptional repression, suggesting that bICP0 inhibits silencing of the viral genome. In this study, it was shown that bICP0 interacted with the histone acetyltransferase p300 during productive infection and in transiently transfected cells. In addition, p300 enhanced BHV-1 productive infection and transactivated a late viral promoter (gC). In contrast, a CH3-domain deletion mutant of p300, which is a dominant-negative mutant, did not activate the gC promoter. bICP0 and p300 cooperated to activate the gC promoter, suggesting that there is a synergistic effect on promoter activation. As p300 can activate certain antiviral signalling pathways (for example, interferon), it was hypothesized that interactions between p300 and bICP0 may dampen the antiviral response following infection. |
| Databáze: | OpenAIRE |
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