The checkpoint protein Rad24p of Saccharomyces cerevisiae is involved in processing Double-Strand Break ends, recombination partner choice and recovery after repair.
Yael Aylon, Martin Kupiec
Mol. Micro. and Biotech., Tel Aviv University, Ramat Aviv, Tel Aviv, 69978, Israel (ayalo@post.tau.ac.il)

Left unrepaired, broken chromosomes usually result in cell death. Checkpoint proteins sense this damage and trigger signal cascades that cause cell cycle arrest and contribute to repair and survival. We demonstrate that the checkpoint sensor protein, Rad24p, is key to survival of a single, repairable double-strand break (DSB). However, cell cycle delay is not the essential function of checkpoint activation. Surprisingly, despite low survival, rad24 mutants are proficient in DSB repair, albeit with protracted kinetics. Slow repair is due to inefficient processing of the broken ends, which also affects recombination partner choice. Unexpectedly, rad24 cells suffering from a single DSB eventually accumulate and die at the G₂/M phase of the cell cycle. This arrest depends on the spindle checkpoint protein, Mad2. We propose that unbalanced hyper-activation of the checkpoint response prevents recovery and results in death of rad24 cells.

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