Plasma Cell-Specific Transcription Factor XBP-1s Binds to and Transactivates the Epstein-Barr Virus BZLF1 Promoter
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| Published in | Journal of Virology Vol. 81; no. 24; pp. 13566 - 13577 |
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| Format | Journal Article |
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01.12.2007
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| AbstractList | Epstein-Barr virus (EBV) in vivo is known to establish persistent infection in resting, circulating memory B cells and to productively replicate in plasma cells. Until now, the molecular mechanism of how EBV switches from latency to lytic replication in vivo was not known. Here, we report that the plasma cell differentiation factor, XBP-1s, activates the expression of the master regulator of EBV lytic activation, BZLF1. Using reporter assays, we observed that XBP-1s was able to transactivate the BZLF1 promoter, Zp, in a plasma cell line and other lymphoid cell lines but, interestingly, not in epithelial cell lines. We have identified an XBP-1s binding site on the ZID/ZII region of Zp, which when abolished by site-directed mutagenesis led to abrogation of XBP-1s binding and promoter activation. Using the chromatin immunoprecipitation assay, we observed direct binding of XBP-1s to endogenous Zp in an EBV-infected plasma cell line. Finally, in the same cell line, we observed that overexpression of XBP-1s resulted in increased expression of BZLF1, while knockdown of XBP-1s with short hairpin RNA drastically reduces BZLF1 expression. We suggest that EBV harnesses the B-cell terminal differentiation pathway via XBP-1s as a physiological signal to reactivate and begin viral replication. We are currently investigating other signals, such as the endoplasmic reticulum stress response proteins, which act upstream of XBP-1s, to identify other interacting factors that initiate and/or amplify the lytic switch. Article Usage Stats Services JVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue JVI About JVI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy JVI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0022-538X Online ISSN: 1098-5514 Copyright © 2014 by the American Society for Microbiology. For an alternate route to JVI .asm.org, visit: JVI ABSTRACT Epstein-Barr virus (EBV) in vivo is known to establish persistent infection in resting, circulating memory B cells and to productively replicate in plasma cells. Until now, the molecular mechanism of how EBV switches from latency to lytic replication in vivo was not known. Here, we report that the plasma cell differentiation factor, XBP-1s, activates the expression of the master regulator of EBV lytic activation, BZLF1. Using reporter assays, we observed that XBP-1s was able to transactivate the BZLF1 promoter, Zp, in a plasma cell line and other lymphoid cell lines but, interestingly, not in epithelial cell lines. We have identified an XBP-1s binding site on the ZID/ZII region of Zp, which when abolished by site-directed mutagenesis led to abrogation of XBP-1s binding and promoter activation. Using the chromatin immunoprecipitation assay, we observed direct binding of XBP-1s to endogenous Zp in an EBV-infected plasma cell line. Finally, in the same cell line, we observed that overexpression of XBP-1s resulted in increased expression of BZLF1, while knockdown of XBP-1s with short hairpin RNA drastically reduces BZLF1 expression. We suggest that EBV harnesses the B-cell terminal differentiation pathway via XBP-1s as a physiological signal to reactivate and begin viral replication. We are currently investigating other signals, such as the endoplasmic reticulum stress response proteins, which act upstream of XBP-1s, to identify other interacting factors that initiate and/or amplify the lytic switch. |
| Author | David A. Thorley-Lawson Chia Chi Sun |
| AuthorAffiliation | Department of Pathology, Tufts University School of Medicine, Jaharis Building, Boston, Massachusetts 02111 |
| AuthorAffiliation_xml | – name: Department of Pathology, Tufts University School of Medicine, Jaharis Building, Boston, Massachusetts 02111 |
| Author_xml | – sequence: 1 givenname: Chia Chi surname: Sun fullname: Sun, Chia Chi organization: Department of Pathology, Jaharis Building, Tufts University School of Medicine, 150 Harrison Ave., Boston, MA 02111, USA – sequence: 2 givenname: David A surname: Thorley-Lawson fullname: Thorley-Lawson, David A |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/17898050$$D View this record in MEDLINE/PubMed |
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Mendeley... Epstein-Barr virus (EBV) in vivo is known to establish persistent infection in resting, circulating memory B cells and to productively replicate in plasma... ABSTRACT Epstein-Barr virus (EBV) in vivo is known to establish persistent infection in resting, circulating memory B cells and to productively replicate in... |
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| StartPage | 13566 |
| SubjectTerms | Animals Cell Differentiation Cell Line Cercopithecus aethiops COS Cells DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Epstein-Barr virus Gene Expression Regulation, Viral Genome and Regulation of Viral Gene Expression HeLa Cells Herpesvirus 4, Human - genetics Herpesvirus 4, Human - metabolism Herpesvirus 4, Human - physiology Humans Jurkat Cells Nuclear Proteins - genetics Nuclear Proteins - metabolism Plasma Cells - virology Promoter Regions, Genetic - genetics Regulatory Factor X Transcription Factors Trans-Activators - genetics Trans-Activators - metabolism Transcription Factors - genetics Transcription Factors - metabolism Transcriptional Activation Viral Proteins - genetics Viral Proteins - metabolism Virus Activation Virus Replication X-Box Binding Protein 1 |
| Title | Plasma Cell-Specific Transcription Factor XBP-1s Binds to and Transactivates the Epstein-Barr Virus BZLF1 Promoter |
| URI | http://jvi.asm.org/content/81/24/13566.abstract https://www.ncbi.nlm.nih.gov/pubmed/17898050 https://search.proquest.com/docview/20374684 https://pubmed.ncbi.nlm.nih.gov/PMC2168822 |
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