DNA end resection, homologous recombination and DNA damage checkpoint activation require CDK1

Grzegorz Ira, Achille Pellicioli, Alitukiriza Balijja, Xuan Wang, Simona Fiorani, Walter Carotenuto, Giordano Liberi, Debra Bressan, Lihong Wan, Nancy M. Hollingsworth, James E. Haber () and Marco Foiani ()
Additional contact information
Grzegorz Ira: Brandeis University
Achille Pellicioli: F.I.R.C. Institute of Molecular Oncology Foundation
Alitukiriza Balijja: F.I.R.C. Institute of Molecular Oncology Foundation
Xuan Wang: Brandeis University
Simona Fiorani: F.I.R.C. Institute of Molecular Oncology Foundation
Walter Carotenuto: F.I.R.C. Institute of Molecular Oncology Foundation
Giordano Liberi: F.I.R.C. Institute of Molecular Oncology Foundation
Debra Bressan: Brandeis University
Lihong Wan: SUNY Stony Brook
Nancy M. Hollingsworth: SUNY Stony Brook
James E. Haber: Brandeis University
Marco Foiani: F.I.R.C. Institute of Molecular Oncology Foundation

Nature, 2004, vol. 431, issue 7011, 1011-1017

Abstract: Abstract A single double-strand break (DSB) induced by HO endonuclease triggers both repair by homologous recombination and activation of the Mec1-dependent DNA damage checkpoint in budding yeast1,2,3,4,5,6. Here we report that DNA damage checkpoint activation by a DSB requires the cyclin-dependent kinase CDK1 (Cdc28) in budding yeast. CDK1 is also required for DSB-induced homologous recombination at any cell cycle stage. Inhibition of homologous recombination by using an analogue-sensitive CDK1 protein7,8 results in a compensatory increase in non-homologous end joining. CDK1 is required for efficient 5′ to 3′ resection of DSB ends and for the recruitment of both the single-stranded DNA-binding complex, RPA, and the Rad51 recombination protein. In contrast, Mre11 protein, part of the MRX complex, accumulates at unresected DSB ends. CDK1 is not required when the DNA damage checkpoint is initiated by lesions that are processed by nucleotide excision repair. Maintenance of the DSB-induced checkpoint requires continuing CDK1 activity that ensures continuing end resection. CDK1 is also important for a later step in homologous recombination, after strand invasion and before the initiation of new DNA synthesis.

Date: 2004
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DOI: 10.1038/nature02964

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