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EMBO reports 7, 7, 716–721 (2006)
doi:10.1038/sj.embor.7400730
AOP Published online: 16 June 2006
ORC binding to TRF2 stimulates OriP replication
Constandache Atanasiu*, Zhong Deng*, Andreas Wiedmer, Julie Norseen & Paul M Lieberman
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The Wistar Institute, 3601 Spruce Street, Philadelphia, Pennsylvania 19104, USA
To whom correspondence should be addressed
Paul M Lieberman Tel: +1 215 898 9491; Fax: +1 215 898 0663; E-mail: lieberman@wistar.org
* These authors contributed equally to this work
Received 13 January 2006; Accepted 15 May 2006; Published online 16 June 2006.
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Abstract
In higher eukaryotes, the origin recognition complex (ORC) lacks sequence-specific DNA binding, and it remains unclear what other factors specify an origin of DNA replication. The Epstein–Barr virus origin of plasmid replication (OriP) recruits ORC, but the precise mechanism of ORC recruitment and origin activation is not clear. We now show that ORC is recruited selectively to the dyad symmetry (DS) region of OriP as a consequence of direct interactions with telomere repeat factor 2 (TRF2) and ORC1. TRF-binding sites within DS stimulate replication initiation and facilitate ORC recruitment in vitro and in vivo. TRF2, but not TRF1 or hRap1, recruits ORC from nuclear extracts. The amino-terminal domain of TRF2 associated with a specific region of ORC1 and was necessary for stimulation of DNA replication. These results support a model in which TRF2 stimulates OriP replication activity by direct binding with ORC subunits.
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