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Genes Dev. 2002 Sep 15;16(18):2327-32.

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

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  • 1Department of Molecular Pharmacology, Stanford University, Stanford, California 94305-5174, USA.

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 Polalpha 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.

PMID:
12231621
PMCID:
PMC187437
DOI:
10.1101/gad.1013502
[PubMed - indexed for MEDLINE]
Free PMC Article
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