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Sister chromatid cohesion remodeling and meiotic recombination.

机译:姐妹染色单体内聚重塑和减数分裂重组。

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摘要

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.
机译:沿染色体臂正确控制内聚力对于减数分裂中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是一种先前与重组有关的蛋白,它是减数分裂中Mcd1p依赖性内聚力的解析所必需的。在这里,我们证明Pds5p和Dmc1p促进了这种凝聚力。已知需要Pds5p来维持内聚力,而Dmc1p被认为是减数分裂重组必不可少的。发现可以通过破坏这些蛋白的功能来抑制姐妹染色单体分离中的相同缺陷,这支持了人们逐渐认识到内聚在重组过程中会发生重塑,并进一步表明内聚被特异性修饰以调节减数分裂重组。我们还发现,Cdc7p激酶Dbf4p的调节亚基的过表达抑制了tid1delta孢子形成缺陷,表明Cdc7p / Dbf4p在调节内聚力中发挥了作用。

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