Human origin recognition complex binds to the region of the latent origin of DNA replication of Epstein-Barr virus
Epstein–Barr virus (EBV) replicates in its latent phase once per cell cycle in proliferating B cells. The latent origin of DNA replication, oriP, supports replication and stable maintenance of the EBV genome. OriP comprises two essential elements: the dyad symmetry (DS) and the family of repeats (FR...
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description | Epstein–Barr virus (EBV) replicates in its latent phase once per cell cycle in proliferating B cells. The latent origin of DNA replication, oriP, supports replication and stable maintenance of the EBV genome. OriP comprises two essential elements: the dyad symmetry (DS) and the family of repeats (FR), both containing clusters of binding sites for the transactivator EBNA1. The DS element appears to be the functional replicator. It is not yet understood how oriP‐dependent replication is integrated into the cell cycle and how EBNA1 acts at the molecular level. Using chromatin immunoprecipitation experiments, we show that the human origin recognition complex (hsORC) binds at or near the DS element. The association of hsORC with oriP depends on the DS element. Deletion of this element not only abolishes hsORC binding but also reduces replication initiation at oriP to background level. Co‐immunoprecipitation experiments indicate that EBNA1 is associated with hsORC in vivo. These results indicate that oriP might use the same cellular initiation factors that regulate chromosomal replication, and that EBNA1 may be involved in recruiting hsORC to oriP. |
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X. ; Hammerschmidt, Wolfgang</creator><creatorcontrib>Schepers, Aloys ; Ritzi, Marion ; Bousset, Kristine ; Kremmer, Elisabeth ; Yates, John L. ; Harwood, Janet ; Diffley, John F. X. ; Hammerschmidt, Wolfgang</creatorcontrib><description>Epstein–Barr virus (EBV) replicates in its latent phase once per cell cycle in proliferating B cells. The latent origin of DNA replication, oriP, supports replication and stable maintenance of the EBV genome. OriP comprises two essential elements: the dyad symmetry (DS) and the family of repeats (FR), both containing clusters of binding sites for the transactivator EBNA1. The DS element appears to be the functional replicator. It is not yet understood how oriP‐dependent replication is integrated into the cell cycle and how EBNA1 acts at the molecular level. Using chromatin immunoprecipitation experiments, we show that the human origin recognition complex (hsORC) binds at or near the DS element. The association of hsORC with oriP depends on the DS element. Deletion of this element not only abolishes hsORC binding but also reduces replication initiation at oriP to background level. Co‐immunoprecipitation experiments indicate that EBNA1 is associated with hsORC in vivo. These results indicate that oriP might use the same cellular initiation factors that regulate chromosomal replication, and that EBNA1 may be involved in recruiting hsORC to oriP.</description><identifier>ISSN: 0261-4189</identifier><identifier>ISSN: 1460-2075</identifier><identifier>EISSN: 1460-2075</identifier><identifier>DOI: 10.1093/emboj/20.16.4588</identifier><identifier>PMID: 11500385</identifier><identifier>CODEN: EMJODG</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>Animals ; B-Lymphocytes ; Binding Sites ; Deoxyribonucleic acid ; DNA ; DNA Replication ; DNA, Viral - biosynthesis ; DNA-Binding Proteins - metabolism ; EBNA1 ; EBNA1 gene ; Epstein-Barr virus ; Epstein-Barr Virus Nuclear Antigens - metabolism ; Herpesvirus 4, Human - genetics ; Herpesvirus 4, Human - physiology ; human origin recognition complex ; Humans ; ORC ; Origin Recognition Complex ; oriP ; OriP gene ; Rats ; Replication Origin ; Virus Latency ; Virus Replication</subject><ispartof>The EMBO journal, 2001-08, Vol.20 (16), p.4588-4602</ispartof><rights>Copyright © 2001 European Molecular Biology Organization</rights><rights>Copyright Oxford University Press(England) Aug 15, 2001</rights><rights>Copyright © 2001 European Molecular Biology Organization 2001</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6255-94089782cb40feb897fe1a45bf117e6bccb9a262fd23975fa0df3f7b5100e5373</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC125560/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC125560/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,728,781,785,886,1418,1434,27929,27930,45579,45580,46414,46838,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11500385$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schepers, Aloys</creatorcontrib><creatorcontrib>Ritzi, Marion</creatorcontrib><creatorcontrib>Bousset, Kristine</creatorcontrib><creatorcontrib>Kremmer, Elisabeth</creatorcontrib><creatorcontrib>Yates, John L.</creatorcontrib><creatorcontrib>Harwood, Janet</creatorcontrib><creatorcontrib>Diffley, John F. X.</creatorcontrib><creatorcontrib>Hammerschmidt, Wolfgang</creatorcontrib><title>Human origin recognition complex binds to the region of the latent origin of DNA replication of Epstein-Barr virus</title><title>The EMBO journal</title><addtitle>EMBO J</addtitle><description>Epstein–Barr virus (EBV) replicates in its latent phase once per cell cycle in proliferating B cells. The latent origin of DNA replication, oriP, supports replication and stable maintenance of the EBV genome. OriP comprises two essential elements: the dyad symmetry (DS) and the family of repeats (FR), both containing clusters of binding sites for the transactivator EBNA1. The DS element appears to be the functional replicator. It is not yet understood how oriP‐dependent replication is integrated into the cell cycle and how EBNA1 acts at the molecular level. Using chromatin immunoprecipitation experiments, we show that the human origin recognition complex (hsORC) binds at or near the DS element. The association of hsORC with oriP depends on the DS element. Deletion of this element not only abolishes hsORC binding but also reduces replication initiation at oriP to background level. Co‐immunoprecipitation experiments indicate that EBNA1 is associated with hsORC in vivo. These results indicate that oriP might use the same cellular initiation factors that regulate chromosomal replication, and that EBNA1 may be involved in recruiting hsORC to oriP.</description><subject>Animals</subject><subject>B-Lymphocytes</subject><subject>Binding Sites</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA Replication</subject><subject>DNA, Viral - biosynthesis</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>EBNA1</subject><subject>EBNA1 gene</subject><subject>Epstein-Barr virus</subject><subject>Epstein-Barr Virus Nuclear Antigens - metabolism</subject><subject>Herpesvirus 4, Human - genetics</subject><subject>Herpesvirus 4, Human - physiology</subject><subject>human origin recognition complex</subject><subject>Humans</subject><subject>ORC</subject><subject>Origin Recognition Complex</subject><subject>oriP</subject><subject>OriP gene</subject><subject>Rats</subject><subject>Replication Origin</subject><subject>Virus Latency</subject><subject>Virus Replication</subject><issn>0261-4189</issn><issn>1460-2075</issn><issn>1460-2075</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkc1z1CAYxhlHx67VuxedjAdvaYGEEA4e2rp2ddb6MVpnvDCEhS1rAhFIbf97SbNu1UtP8PL8npcXHgCeIniAICsOVde4zSFOVXVQkrq-B2aorGCOISX3wQziCuUlqtkeeBTCBkJIaooegj2ECIRFTWbAL4ZO2Mx5szY280q6tTXROJtJ1_WtusoaY1chiy6LFyoB61Fz-qZqRVQ2_jGnw9dnRwnpWyNF3HLzPkRlbH4svM8ujR_CY_BAizaoJ9t1H3x9M_9yssiXH07fnhwtc1lhQnJWwprRGsumhFo1aa8VEiVpNEJUVY2UDRO4wnqFC0aJFnClC00bgiBUpKDFPng19e2HplMrmUb1ouW9N53w19wJw_9VrLnga3fJUbq-gsn_cuv37uegQuSdCVK1rbDKDYFThFCZ_vNOEFGGGKHjRC_-Azdu8DZ9Ak8AppjCEYITJL0LwSu9mxhBPqbOb1LnOFUVH1NPlud_v_TWsI05AWwCfplWXd_ZkM_fH7-jhBWMjN5nk9eKOHi1M9_q-aSbFPTVThb-B69oQQn_dnbKv386X378zM75ovgNkBHVzA</recordid><startdate>20010815</startdate><enddate>20010815</enddate><creator>Schepers, Aloys</creator><creator>Ritzi, Marion</creator><creator>Bousset, Kristine</creator><creator>Kremmer, Elisabeth</creator><creator>Yates, John L.</creator><creator>Harwood, Janet</creator><creator>Diffley, John F. 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X.</au><au>Hammerschmidt, Wolfgang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Human origin recognition complex binds to the region of the latent origin of DNA replication of Epstein-Barr virus</atitle><jtitle>The EMBO journal</jtitle><addtitle>EMBO J</addtitle><date>2001-08-15</date><risdate>2001</risdate><volume>20</volume><issue>16</issue><spage>4588</spage><epage>4602</epage><pages>4588-4602</pages><issn>0261-4189</issn><issn>1460-2075</issn><eissn>1460-2075</eissn><coden>EMJODG</coden><abstract>Epstein–Barr virus (EBV) replicates in its latent phase once per cell cycle in proliferating B cells. The latent origin of DNA replication, oriP, supports replication and stable maintenance of the EBV genome. OriP comprises two essential elements: the dyad symmetry (DS) and the family of repeats (FR), both containing clusters of binding sites for the transactivator EBNA1. The DS element appears to be the functional replicator. It is not yet understood how oriP‐dependent replication is integrated into the cell cycle and how EBNA1 acts at the molecular level. Using chromatin immunoprecipitation experiments, we show that the human origin recognition complex (hsORC) binds at or near the DS element. The association of hsORC with oriP depends on the DS element. Deletion of this element not only abolishes hsORC binding but also reduces replication initiation at oriP to background level. Co‐immunoprecipitation experiments indicate that EBNA1 is associated with hsORC in vivo. These results indicate that oriP might use the same cellular initiation factors that regulate chromosomal replication, and that EBNA1 may be involved in recruiting hsORC to oriP.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><pmid>11500385</pmid><doi>10.1093/emboj/20.16.4588</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals B-Lymphocytes Binding Sites Deoxyribonucleic acid DNA DNA Replication DNA, Viral - biosynthesis DNA-Binding Proteins - metabolism EBNA1 EBNA1 gene Epstein-Barr virus Epstein-Barr Virus Nuclear Antigens - metabolism Herpesvirus 4, Human - genetics Herpesvirus 4, Human - physiology human origin recognition complex Humans ORC Origin Recognition Complex oriP OriP gene Rats Replication Origin Virus Latency Virus Replication |
title | Human origin recognition complex binds to the region of the latent origin of DNA replication of Epstein-Barr virus |
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