Damage-induced phosphorylation of Sld3 is important to block late origin firing

Jaime Lopez-Mosqueda, Nancy L. Maas, Zophonias O. Jonsson, Lisa G. DeFazio-Eli, James Wohlschlegel and David P. Toczyski ()
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Jaime Lopez-Mosqueda: University of California, San Francisco, San Francisco, California 94158-9001, USA
Nancy L. Maas: University of California, San Francisco, San Francisco, California 94158-9001, USA
Zophonias O. Jonsson: University of California, Los Angeles, 615 Charles E. Young Dr. South BSRB 377A, Los Angeles, California 90095, USA
Lisa G. DeFazio-Eli: University of California, San Francisco, San Francisco, California 94158-9001, USA
James Wohlschlegel: University of California, Los Angeles, 615 Charles E. Young Dr. South BSRB 377A, Los Angeles, California 90095, USA
David P. Toczyski: University of California, San Francisco, San Francisco, California 94158-9001, USA

Nature, 2010, vol. 467, issue 7314, 479-483

Abstract: Stop at the intra-S checkpoint Two classes of kinases, CDK and DDK, facilitate the initiation of DNA replication in S phase. In two studies, the Diffley and Toczyski labs show that when damage is sensed, another kinase — the checkpoint kinase Rad53 — halts replication by inhibiting both the CDK and DDK pathways through the phosphorylation of Sld3 and Dbf4, respectively. These results reveal that regulation of the firing of origins is the means by which the intra-S checkpoint slows S phase.

Date: 2010
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DOI: 10.1038/nature09377

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