Journal
EMBO REPORTS
Volume 7, Issue 7, Pages 716-721Publisher
WILEY
DOI: 10.1038/sj.embor.7400730
Keywords
ORC; TRF2; origin; replication; EBV
Categories
Funding
- NCI NIH HHS [R01 CA093606, CA93606] Funding Source: Medline
- NIGMS NIH HHS [T32 GM008216, 5-T32-GM08216-18] Funding Source: Medline
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available