{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,24]],"date-time":"2025-09-24T10:27:48Z","timestamp":1758709668152},"reference-count":67,"publisher":"American Society for Microbiology","issue":"23","license":[{"start":{"date-parts":[[2011,12,1]],"date-time":"2011-12-01T00:00:00Z","timestamp":1322697600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2011,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>The architecture of the varicella-zoster virus (VZV) origin of DNA replication (OriS) differs significantly from that of the herpes simplex virus (HSV) DNA replication origin. Novel aspects of the VZV OriS include a GA-rich region, three binding sites for the VZV origin-binding protein (OBP) all on the same strand and oriented in the same direction, and a partial OBP binding site of unknown function. We have designated this partial binding site Box D and have investigated the role it plays in DNA replication and flanking gene expression. This has been done with a model system using a replication-competent plasmid containing OriS and a replication- and transcription-competent dual-luciferase reporter plasmid containing both the OriS and the intergenic region between VZV open reading frames (ORFs) 62 and 63. We have found that (i) Box D is a negative regulator of DNA replication independent of flanking gene expression, (ii) the mutation of Box D results in a decrease in flanking gene expression, thus a sequence within the VZV OriS affects transcription, which is in contrast to results reported for HSV-1, (iii) there is a specific Box D complex formed with infected cell extracts in electrophoretic mobility shift assay experiments, (iv) supershift assays show that this complex contains the VZV ORF29 single-strand DNA-binding protein, and (v) the formation of this complex is dependent on the presence of CGC motifs in Box D and its downstream flanking region. These findings show that the VZV ORF29 protein, while required for DNA replication, also plays a novel role in the suppression of that process.<\/jats:p>","DOI":"10.1128\/jvi.05501-11","type":"journal-article","created":{"date-parts":[[2011,9,22]],"date-time":"2011-09-22T04:40:52Z","timestamp":1316666452000},"page":"12188-12200","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":7,"title":["A Sequence within the Varicella-Zoster Virus (VZV) OriS Is a Negative Regulator of DNA Replication and Is Bound by a Protein Complex Containing the VZV ORF29 Protein"],"prefix":"10.1128","volume":"85","author":[{"given":"Mohamed I.","family":"Khalil","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology and the Witebsky Center for Microbial Pathogenesis and Immunology, University at Buffalo, Buffalo, New York 14214"},{"name":"Department of Molecular Biology, National Research Center, Dokki, Cairo, Egypt"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ann","family":"Arvin","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics and Microbiology and Immunology, Stanford University School of Medicine, G311, Stanford, California 94305"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jeremy","family":"Jones","sequence":"additional","affiliation":[{"name":"Department of Molecular Pharmacology, Beckman Research Institute, City of Hope, 1500 East Duarte Road, Duarte, California 91010"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"William T.","family":"Ruyechan","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology and the Witebsky Center for Microbial Pathogenesis and Immunology, University at Buffalo, Buffalo, New York 14214"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.74.17.7842-7850.2000"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.virol.2010.01.007"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.80.1.440-450.2006"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1086\/514276"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.80.9.4491-4500.2006"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.01204-07"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.68.6.3841-3849.1994"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.78.21.11833-11840.2004"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.67.7.4246-4251.1993"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.79.8.5069-5077.2005"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.01220-06"},{"key":"e_1_3_2_13_2","first-page":"2773","volume-title":"Fields virology","author":"Cohen J. 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