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Epigenetic Repression of Herpes Simplex Virus Infection by the Nucleosome Remodeler CHD3
Upon infection, the genome of herpes simplex virus is rapidly incorporated into nucleosomes displaying histone modifications characteristic of heterochromatic structures. The initiation of infection requires complex viral-cellular interactions that ultimately circumvent this repression by utilizing...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Society of Microbiology
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3903285/ https://www.ncbi.nlm.nih.gov/pubmed/24425734 http://dx.doi.org/10.1128/mBio.01027-13 |
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author | Arbuckle, Jesse H. Kristie, Thomas M. |
author_facet | Arbuckle, Jesse H. Kristie, Thomas M. |
author_sort | Arbuckle, Jesse H. |
collection | PubMed |
description | Upon infection, the genome of herpes simplex virus is rapidly incorporated into nucleosomes displaying histone modifications characteristic of heterochromatic structures. The initiation of infection requires complex viral-cellular interactions that ultimately circumvent this repression by utilizing host cell enzymes to remove repressive histone marks and install those that promote viral gene expression. The reversion of repression and activation of viral gene expression is mediated by the cellular coactivator HCF-1 in association with histone demethylases and methyltransferases. However, the mechanisms and the components that are involved in the initial repression remain unclear. In this study, the chromatin remodeler chromodomain helicase DNA binding (CHD3) protein is identified as an important component of the initial repression of the herpesvirus genome. CHD3 localizes to early viral foci and suppresses viral gene expression. Depletion of CHD3 results in enhanced viral immediate early gene expression and an increase in the number of transcriptionally active viral genomes in the cell. Importantly, CHD3 can recognize the repressive histone marks that have been detected in the chromatin associated with the viral genome and this remodeler is important for ultimately reducing the levels of accessible viral genomes. A model is presented in which CHD3 represses viral infection in opposition to the actions of the HCF-1 coactivator complex. This dynamic, at least in part, determines the initiation of viral infection. |
format | Online Article Text |
id | pubmed-3903285 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | American Society of Microbiology |
record_format | MEDLINE/PubMed |
spelling | pubmed-39032852014-01-30 Epigenetic Repression of Herpes Simplex Virus Infection by the Nucleosome Remodeler CHD3 Arbuckle, Jesse H. Kristie, Thomas M. mBio Research Article Upon infection, the genome of herpes simplex virus is rapidly incorporated into nucleosomes displaying histone modifications characteristic of heterochromatic structures. The initiation of infection requires complex viral-cellular interactions that ultimately circumvent this repression by utilizing host cell enzymes to remove repressive histone marks and install those that promote viral gene expression. The reversion of repression and activation of viral gene expression is mediated by the cellular coactivator HCF-1 in association with histone demethylases and methyltransferases. However, the mechanisms and the components that are involved in the initial repression remain unclear. In this study, the chromatin remodeler chromodomain helicase DNA binding (CHD3) protein is identified as an important component of the initial repression of the herpesvirus genome. CHD3 localizes to early viral foci and suppresses viral gene expression. Depletion of CHD3 results in enhanced viral immediate early gene expression and an increase in the number of transcriptionally active viral genomes in the cell. Importantly, CHD3 can recognize the repressive histone marks that have been detected in the chromatin associated with the viral genome and this remodeler is important for ultimately reducing the levels of accessible viral genomes. A model is presented in which CHD3 represses viral infection in opposition to the actions of the HCF-1 coactivator complex. This dynamic, at least in part, determines the initiation of viral infection. American Society of Microbiology 2014-01-14 /pmc/articles/PMC3903285/ /pubmed/24425734 http://dx.doi.org/10.1128/mBio.01027-13 Text en Copyright © 2014 Arbuckle and Kristie. http://creativecommons.org/licenses/by-nc-sa/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-ShareAlike 3.0 Unported license (http://creativecommons.org/licenses/by-nc-sa/3.0/) , which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Arbuckle, Jesse H. Kristie, Thomas M. Epigenetic Repression of Herpes Simplex Virus Infection by the Nucleosome Remodeler CHD3 |
title | Epigenetic Repression of Herpes Simplex Virus Infection by the Nucleosome Remodeler CHD3 |
title_full | Epigenetic Repression of Herpes Simplex Virus Infection by the Nucleosome Remodeler CHD3 |
title_fullStr | Epigenetic Repression of Herpes Simplex Virus Infection by the Nucleosome Remodeler CHD3 |
title_full_unstemmed | Epigenetic Repression of Herpes Simplex Virus Infection by the Nucleosome Remodeler CHD3 |
title_short | Epigenetic Repression of Herpes Simplex Virus Infection by the Nucleosome Remodeler CHD3 |
title_sort | epigenetic repression of herpes simplex virus infection by the nucleosome remodeler chd3 |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3903285/ https://www.ncbi.nlm.nih.gov/pubmed/24425734 http://dx.doi.org/10.1128/mBio.01027-13 |
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