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姐妹染色单体黏连重塑与减数分裂重组。

Sister chromatid cohesion remodeling and meiotic recombination.

作者信息

Kateneva Anna V, Dresser Michael E

机构信息

Program in Molecular, Cell and Developmental Biology, Oklahoma Medical Research Foundation, Department of Cell Biology, Oklahoma University Health Sciences Center, Oklahoma City, Oklahoma 73104, USA.

出版信息

Cell Cycle. 2006 Mar;5(5):467-71. doi: 10.4161/cc.5.5.2498. Epub 2006 Mar 1.

Abstract

Proper control of cohesion along the chromosome arms is essential for segregation of homologous chromosomes in meiosis. In a recent study we reported that Tid1p, a protein previously implicated in recombination, is required for resolution of Mcd1p-dependent cohesion in meiosis. Here we demonstrate that Pds5p and Dmc1p promote this cohesion. Pds5p is known to be required for maintenance of cohesion while Dmc1p is recognized as essential for meiotic recombination. Finding that the same defect in separation of sister chromatids could be suppressed by disrupting the functions of these proteins supports the emerging recognition that cohesion is remodeled during recombination and further indicates that cohesion is modified specifically to regulate meiotic recombination. We also find that overexpression of the regulatory subunit of Cdc7p kinase, Dbf4p, suppresses the tid1delta sporulation defect, suggesting a role for Cdc7p/Dbf4p in regulating cohesion.

摘要

在减数分裂中,对染色体臂上黏连的适当控制对于同源染色体的分离至关重要。在最近的一项研究中,我们报道了Tid1p(一种先前与重组有关的蛋白质)是减数分裂中解决依赖于Mcd1p的黏连所必需的。在这里,我们证明Pds5p和Dmc1p促进这种黏连。已知Pds5p是维持黏连所必需的,而Dmc1p被认为是减数分裂重组所必需的。发现通过破坏这些蛋白质的功能可以抑制姐妹染色单体分离中的相同缺陷,这支持了一种新的认识,即黏连在重组过程中会被重塑,并且进一步表明黏连被特异性修饰以调节减数分裂重组。我们还发现Cdc7p激酶的调节亚基Dbf4p的过表达抑制了tid1delta孢子形成缺陷,这表明Cdc7p/Dbf4p在调节黏连中起作用。

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