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A requirement for replication in activation of the ATR-dependent DNA damage checkpoint

By Patrick J. Lupardus, Tony Byun, Muh-ching Yee, Mohammad Hekmat-Nejad and Karlene A. Cimprich

Abstract

Using the Xenopus egg extract system, we investigated the involvement of DNA replication in activation of the DNA damage checkpoint. We show here that DNA damage slows replication in a checkpoint-independent manner and is accompanied by replication-dependent recruitment of ATR and Rad1 to chromatin. We also find that the replication proteins RPA and Polα accumulate on chromatin following DNA damage. Finally, damage-induced Chk1 phosphorylation and checkpoint arrest are abrogated when replication is inhibited. These data indicate that replication is required for activation of the DNA damage checkpoint and suggest a unifying model for ATR activation by diverse lesions during S phase

Topics: Research Communication
Publisher: Cold Spring Harbor Laboratory Press
Year: 2002
DOI identifier: 10.1101/gad.1013502
OAI identifier: oai:pubmedcentral.nih.gov:187437
Provided by: PubMed Central
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