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Recombination protein Tid1p controls resolution of cohesin-dependent linkages in meiosis in Saccharomyces cerevisiae

机译:重组蛋白Tid1p控制酿酒酵母减数分裂中黏着蛋白依赖性键的解析

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摘要

Sister chromatid cohesion and interhomologue recombination are coordinated to promote the segregation of homologous chromosomes instead of sister chromatids at the first meiotic division. During meiotic prophase in Saccharomyces cerevisiae, the meiosis-specific cohesin Rec8p localizes along chromosome axes and mediates most of the cohesion. The mitotic cohesin Mcd1p/Scc1p localizes to discrete spots along chromosome arms, and its function is not clear. In cells lacking Tid1p, which is a member of the SWI2/SNF2 family of helicase-like proteins that are involved in chromatin remodeling, Mcd1p and Rec8p persist abnormally through both meiotic divisions, and chromosome segregation fails in the majority of cells. Genetic results indicate that the primary defect in these cells is a failure to resolve Mcd1p-mediated connections. Tid1p interacts with recombination enzymes Dmc1p and Rad51p and has an established role in recombination repair. We propose that Tid1p remodels Mcd1p-mediated cohesion early in meiotic prophase to facilitate interhomologue recombination and the subsequent segregation of homologous chromosomes.
机译:姊妹染色单体的内聚和同源重组是协调的,以促进同源染色体的分离,而不是在第一次减数分裂分裂时的姊妹染色单体。在酿酒酵母的减数分裂前期,减数分裂特有的黏着蛋白Rec8p沿着染色体轴定位并介导大多数黏着力。有丝分裂粘附蛋白Mcd1p / Scc1p定位于沿染色体臂的离散点,其功能尚不清楚。在缺乏Tid1p的细胞中,Tid1p是参与染色质重塑的解旋酶样蛋白的SWI2 / SNF2家族的成员,Mcd1p和Rec8p通过两种减数分裂分裂异常持续存在,并且大多数细胞的染色体分离失败。遗传结果表明,这些细胞的主要缺陷是无法解决Mcd1p介导的连接。 Tid1p与重组酶Dmc1p和Rad51p相互作用,并且在重组修复中具有确定的作用。我们提出,Tid1p在减数分裂前期重塑Mcd1p介导的内聚力,以促进同源重组和随后的同源染色体分离。

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