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Molecular and Cellular Biology, September 2003, p. 6585-6596, Vol. 23, No. 18
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.18.6585-6596.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

The Checkpoint Protein Rad24 of Saccharomyces cerevisiae Is Involved in Processing Double-Strand Break Ends and in Recombination Partner Choice

Yael Aylon and Martin Kupiec*

Department of Molecular Microbiology and Biotechnology, Tel Aviv University, Ramat Aviv 69978, Israel

Received 4 April 2003/ Returned for modification 8 May 2003/ Accepted 24 June 2003

Upon chromosomal damage, cells activate a checkpoint response that includes cell cycle arrest and a stimulation of DNA repair. The checkpoint protein Rad24 is key to the survival of a single, repairable double-strand break (DSB). However, the low survival of rad24 cells is not due to their inability to arrest cell cycle progression. In rad24 mutants, processing of the broken ends is delayed and protracted, resulting in extended kinetics of DSB repair and in cell death. The limited resection of rad24 mutants also affects recombination partner choice by a mechanism dependent on the length of the interacting homologous donor sequences. Unexpectedly, rad24 cells with a DSB eventually accumulate and die at the G2/M phase of the cell cycle. This arrest depends on the spindle checkpoint protein Mad2.

* Corresponding author. Mailing address: Department of Molecular Microbiology and Biotechnology, Tel Aviv University, Ramat Aviv 69978, Israel. Phone: 972 3 640 9031. Fax: 972 3 640 9407. E-mail: martin{at}post.tau.ac.il.

Molecular and Cellular Biology, September 2003, p. 6585-6596, Vol. 23, No. 18
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.18.6585-6596.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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