The mitotic DNA damage checkpoint proteins Rad17 and Rad24 are required for repair of double-strand breaks during meiosis in yeast.
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.
Mesh Terms:
Blotting, Southern, Cell Cycle Proteins, Crossing Over, Genetic, DNA Damage, DNA Repair, DNA-Binding Proteins, Electrophoresis, Agar Gel, Gamma Rays, Gene Deletion, Intracellular Signaling Peptides and Proteins, Meiosis, Microscopy, Fluorescence, Nuclear Proteins, Plasmids, Rad51 Recombinase, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins
Blotting, Southern, Cell Cycle Proteins, Crossing Over, Genetic, DNA Damage, DNA Repair, DNA-Binding Proteins, Electrophoresis, Agar Gel, Gamma Rays, Gene Deletion, Intracellular Signaling Peptides and Proteins, Meiosis, Microscopy, Fluorescence, Nuclear Proteins, Plasmids, Rad51 Recombinase, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins
Genetics
Date: Jul. 01, 2003
PubMed ID: 12871899
View in: Pubmed Google Scholar
Download Curated Data For This Publication
16800
Switch View:
- Interactions 2