Kateneva Anna V, Konovchenko Anton A, Guacci Vincent, Dresser Michael E
Program in Molecular, Cell, and Developmental Biology, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104.
J Cell Biol. 2005 Oct 24;171(2):241-53. doi: 10.1083/jcb.200505020. Epub 2005 Oct 17.
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.
姐妹染色单体黏连与同源重组相互协调,以促进同源染色体而非姐妹染色单体在第一次减数分裂时的分离。在酿酒酵母的减数分裂前期,减数分裂特异性黏连蛋白Rec8p沿染色体轴定位,并介导大部分黏连作用。有丝分裂黏连蛋白Mcd1p/Scc1p定位于染色体臂上的离散位点,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SWI2/SNF2家族的成员,Mcd1p和Rec8p在两次减数分裂中均异常持续存在,并且大多数细胞中的染色体分离失败。遗传学结果表明,这些细胞中的主要缺陷是未能解决Mcd1p介导的连接。Tid1p与重组酶Dmc1p和Rad51p相互作用,并在重组修复中发挥既定作用。我们提出,Tid1p在减数分裂前期早期重塑Mcd1p介导的黏连,以促进同源重组及随后同源染色体的分离。