Replication from oriP of Epstein-Barr virus requires human ORC and is inhibited by geminin

被引：231
作者：
Dhar, SK
Yoshida, K
Machida, Y
Khaira, P
Chaudhuri, B
Wohlschlegel, JA
Leffak, M
Yates, J
Dutta, A
机构：
[1] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Boston, MA 02115 USA
[3] Wright State Univ, Dept Biochem & Mol Biol, Dayton, OH 45435 USA
[4] Roswell Pk Canc Inst, Dept Canc Genet, Buffalo, NY 14263 USA
来源：
CELL | 2001年 / 106卷 / 03期
关键词：
D O I：
10.1016/S0092-8674(01)00458-5
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
A hypomorphic mutation made in the ORC2 gene of a human cancer cell line through homologous recombination decreased Orc2 protein levels by 90%. The G1 phase of the cell cycle was prolonged, but there was no effect on the utilization of either the c-Myc or beta -globin cellular origins of replication. Cells carrying this mutation failed to support the replication of a plasmid bearing the oriP replicator of Epstein Barr virus (EBV), and this defect was rescued by reintroduction of Orc2. Orc2 specifically associates with oriP in cells, most likely through its interaction with EBNA1. Geminin, an inhibitor of the mammalian replication initiation complex, inhibits replication from oriP. Therefore, ORC and the human replication initiation apparatus is required for replication from a viral origin of replication.
引用
收藏
页码：287 / 296
页数：10
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