首页> 外文期刊>Genetics: A Periodical Record of Investigations Bearing on Heredity and Variation >Mek1 Suppression of Meiotic Double-Strand Break Repair Is Specific to Sister Chromatids, Chromosome Autonomous and Independent of Rec8 Cohesin Complexes
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Mek1 Suppression of Meiotic Double-Strand Break Repair Is Specific to Sister Chromatids, Chromosome Autonomous and Independent of Rec8 Cohesin Complexes

机译:Mek1减数分裂双链断裂修复的抑制特定于姊妹染色单体,染色体自主和独立于rec8黏着蛋白复合物。

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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.
机译:在减数分裂过程中,定向重组发生在同源染色体之间,以建立减数分裂I正确分离所必需的连接。伙伴选择在链入侵时确定,并由两种重组酶介导:Rad51和减数分裂特异性Dmc1。在发芽的酵母中,同源性偏倚部分是由减数分裂特异性激酶Mek1的活性造成的,Mek1定位于浓缩姐妹染色单体的蛋白核心。单倍体和二体单倍体菌株的减数分裂双链断裂(DSB)修复分析表明,Mek1通过直接作用于姐妹染色单体来抑制减数分裂姐妹DSB修复。但是,对于抑制伴侣间DSB修复或修复本身,都不需要Rec8黏着蛋白复合物。减数分裂中DSB修复的调控是染色体自主的,因此单倍体染色体上未修复的断裂不会阻止二体同源物之间的同源间修复。包含Dmc1和/或Rad51的单倍体中DSB修复的模式表明Mek1在Rad51特异性重组过程中起作用。

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