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The meiotic recombination checkpoint is regulated by checkpoint rad + genes in fission yeast
Author(s) -
Shimada Midori,
Nabeshima Kentaro,
Tougan Takahiro,
Nojima Hiroshi
Publication year - 2002
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/21.11.2807
Subject(s) - biology , g2 m dna damage checkpoint , homologous recombination , meiosis , recombination , fission , genetics , yeast , schizosaccharomyces , genetic recombination , flp frt recombination , schizosaccharomyces pombe , cell cycle checkpoint , chek1 , microbiology and biotechnology , gene , saccharomyces cerevisiae , cell cycle , physics , quantum mechanics , neutron
During the course of meiotic prophase, intrinsic double‐strand breaks (DSBs) must be repaired before the cell can engage in meiotic nuclear division. Here we investigate the mechanism that controls the meiotic progression in Schizosaccharomyces pombe that have accumulated excess meiotic DSBs. A meiotic recombination‐defective mutant, meu13Δ , shows a delay in meiotic progression. This delay is dependent on rec12 + , namely on DSB formation. Pulsed‐field gel electrophoresis analysis revealed that meiotic DSB repair in meu13Δ was retarded. We also found that the delay in entering nuclear division was dependent on the checkpoint rad + , cds1 + and mek1 + (the meiotic paralog of Cds1/Chk2). This implies that these genes are involved in a checkpoint that provides time to repair DSBs. Consistently, the induction of an excess of extrinsic DSBs by ionizing radiation delayed meiotic progression in a rad17 + ‐dependent manner. dmc1Δ also shows meiotic delay, however, this delay is independent of rec12 + and checkpoint rad + . We propose that checkpoint monitoring of the status of meiotic DSB repair exists in fission yeast and that defects other than DSB accumulation can cause delays in meiotic progression.