Mek1 Suppression of Meiotic Double-Strand Break Repair Is Specific to Sister Chromatids, Chromosome Autonomous and Independent of Rec8 Cohesin Complexes

被引:35
作者
Callender, Tracy L. [1 ]
Hollingsworth, Nancy M. [1 ]
机构
[1] SUNY Stony Brook, Dept Biochem & Cell Biol, Stony Brook, NY 11794 USA
基金
美国国家卫生研究院;
关键词
HOP1; GENE; RECOMBINATION; DMC1; MEIOSIS; DNA; RAD51; HOMOLOGS; PROMOTES; PROTEIN; ROLES;
D O I
10.1534/genetics.110.117523
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
During meiosis, recombination is directed to occur between homologous chromosomes to create connections necessary for proper segregation at meiosis I. Partner choice is determined at the time of strand invasion and is mediated by two recombinases: Rad51 and the meiosis-specific Dmc1. In budding yeast, interhomolog bias is created in part by the activity of a meiosis-specific kinase, Mek1, which is localized to the protein cores of condensed sister chromatids. Analysis of meiotic double-strand break (DSB) repair in haploid and disomic haploid strains reveals that Mek1 suppresses meiotic intersister DSB repair by working directly on sister chromatids. Rec8 cohesin complexes are not required, however, either for suppression of intersister DSB repair or for the repair itself. Regulation of DSB repair in meiosis is chromosome autonomous such that unrepaired breaks on haploid chromosomes do not prevent interhomolog repair between disomic homologs. The pattern of DSB repair in haploids containing Dmc1 and/or Rad51 indicates that Mek1 acts on Rad51-specific recombination processes.
引用
收藏
页码:771 / 782
页数:12
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