ORC binding to TRF2 stimulates OriP replication

67Citations
Citations of this article
45Readers
Mendeley users who have this article in their library.

This article is free to access.

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. © 2006 European Molecular Biology Organization.

Author supplied keywords

Cite

CITATION STYLE

APA

Atanasiu, C., Deng, Z., Wiedmer, A., Norseen, J., & Lieberman, P. M. (2006). ORC binding to TRF2 stimulates OriP replication. EMBO Reports, 7(7), 716–721. https://doi.org/10.1038/sj.embor.7400730

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free