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Molecular and Cellular Biology, August 2003, p. 5939-5946, Vol. 23, No. 16
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.16.5939-5946.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Replication Checkpoint Kinase Cds1 Regulates Recombinational Repair Protein Rad60

Michael N. Boddy,1* Paul Shanahan,1 W. Hayes McDonald,2 Antonia Lopez-Girona,1 Eishi Noguchi,1 John R. Yates III,2 and Paul Russell1,2

Department of Molecular Biology,1 Department of Cell Biology, The Scripps Research Institute, La Jolla, California 920372

Received 28 March 2003/ Returned for modification 16 April 2003/ Accepted 15 May 2003

Genome integrity is protected by Cds1 (Chk2), a checkpoint kinase that stabilizes arrested replication forks. How Cds1 accomplishes this task is unknown. We report that Cds1 interacts with Rad60, a protein required for recombinational repair in fission yeast. Cds1 activation triggers Rad60 phosphorylation and nuclear delocalization. A Rad60 mutant that inhibits regulation by Cds1 renders cells specifically sensitive to replication fork arrest. Genetic and biochemical studies indicate that Rad60 functions codependently with Smc5 and Smc6, subunits of an SMC (structural maintenance of chromosomes) complex required for recombinational repair. These studies indicate that regulation of Rad60 is an important part of the replication checkpoint response controlled by Cds1. We propose that control of Rad60 regulates recombination events at stalled forks.

* Corresponding author. Mailing address: Department of Molecular Biology, The Scripps Research Institute, 10550 North Torrey Pines Rd., La Jolla, CA 92037. Phone: (858) 784-7042. Fax: (858) 784-2265. E-mail: nboddy{at}scripps.edu.

Molecular and Cellular Biology, August 2003, p. 5939-5946, Vol. 23, No. 16
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.16.5939-5946.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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