Genetics, Vol. 164, 855-865, July 2003, Copyright © 2003

The Mitotic DNA Damage Checkpoint Proteins Rad17 and Rad24 Are Required for Repair of Double-Strand Breaks During Meiosis in Yeast

Miki Shinoharaa,b, Kazuko Sakaia, Tomoko Ogawac, and Akira Shinoharaa,d
a Department of Biology, Graduate School of Science, Osaka University, Osaka, 560-0043 Japan,
b Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, 734-8553 Japan,
c Iwate College for Nursing, Iwate, 020-0151 Japan
d Precursory Research for Embryonic Science and Technology, JST, Toyonaka, Osaka, 560-0043 Japan

Corresponding author: Akira Shinohara, Graduate School of Science, Osaka University, 1-1 Machikaneyama, Toyonaka, Osaka, 560-0043 Japan., ashino{at}bio.sci.osaka-u.ac.jp (E-mail)

Communicating editor: M. E. ZOLAN

We show here that deletion of the DNA damage checkpoint genes RAD17 and RAD24 in Saccharomyces cerevisiae delays repair of meiotic double-strand breaks (DSBs) and results in an altered ratio of crossover-to-noncrossover products. These mutations also decrease the colocalization of immunostaining foci of the RecA homologs Rad51 and Dmc1 and cause a delay in the disappearance of Rad51 foci, but not of Dmc1. These observations imply that RAD17 and RAD24 promote efficient repair of meiotic DSBs by facilitating proper assembly of the meiotic recombination complex containing Rad51. Consistent with this proposal, extra copies of RAD51 and RAD54 substantially suppress not only the spore inviability of the rad24 mutant, but also the {gamma}-ray sensitivity of the mutant. Unexpectedly, the entry into meiosis I (metaphase I) is delayed in the checkpoint single mutants compared to wild type. The control of the cell cycle in response to meiotic DSBs is also discussed.




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