tailieunhanh - Báo cáo khoa học: "Epstein-Barr Nuclear Antigen 1 modulates replication of oriP-plasmids by impeding replication and transcription fork migration through the family of repeat"

Epstein-Barr Nuclear Antigen 1 modulates replication of oriP-plasmids by impeding replication and transcription fork migration through the family of repeat | Virology Journal BioMed Central Research Epstein-Barr Nuclear Antigen I modulates replication of oriP-plasmids by impeding replication and transcription fork migration through the family of repeats Ashok Aiyar 1 2 Siddhesh Aras2 Amber Washington 2 Gyanendra Singh 1 and Ronald B Luftig2 Open Access Address 1Stanley S. Scott Cancer Center LSU Health Sciences Center 533 Bolivar Street New Orleans LA 70112 USA and 2Department of Microbiology LSU Health Sciences Center 1901 Perdido Street New Orleans LA 70112 USA Email Ashok Aiyar - aaiyar@ Siddhesh Aras - saras@ Amber Washington - awash8@ Gyanendra Singh - gsingh@ Ronald B Luftig - rlufti@ Corresponding author fEqual contributors Published 5 March 2009 Received 7 February 2009 Accepted 5 March 2009 Virology Journal 2009 6 29 doi l 743-422X-6-29 This article is available from http content 6 1 29 2009 Aiyar et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Epstein-Barr virus is replicated once per cell-cycle and partitioned equally in latently infected cells. Both these processes require a single viral cis-element termed oriP and a single viral protein EBNAl. EBNAl binds two clusters of binding sites in oriP termed the dyad symmetry element DS and the family of repeats FR which function as a replication element and partitioning element respectively. Wild-type FR contains 20 binding sites for EBNAl. Results We and others have determined previously that decreasing the number of EBNAl-binding sites in FR increases the efficiency with which or P-plasmids are replicated. Here we demonstrate that the wild-type number of binding sites in FR impedes the migration of replication and .