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Replication Factor C Complexes Play Unique Pro- and Anti-Establishment Roles in Sister Chromatid Cohesion

机译:复制因子C复合体在姐妹染色单体凝聚力中发挥独特的促和反建立作用

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摘要

Recent studies have lead to a rapid expansion of sister chromatid cohesion pathways. Of particular interest is the growth in classifications of anti-establishment factors—now including those that are cohesin-associated (Rad61/WAPL and Pds5) or DNA replication fork-associated (Elg1-RFC). In this study, we show that the two classes of anti-establishment complexes are indistinguishable when challenged both genetically and functionally. These findings suggest that both classes function in a singular pathway that is centered on Ctf7/Eco1 (herein termed Ctf7) regulation. The anti-establishment activity of Elg1-RFC complex is particular intriguing given that an alternate Ctf18-RFC complex exhibits robust pro-establishment activity. Here, we provide several lines of evidence, including the use of Ctf7 bypass suppressors, indicating that these activities are not simply antagonistic. Moreover, the results suggest that Ctf18-RFC is capable of promoting sister chromatid pairing reactions independent of Ctf7. The combination of these studies suggest a new model of sister chromatid pairing regulation.
机译:最近的研究导致姐妹染色单体内聚途径的快速扩展。特别引起关注的是抗建立因子分类的增长-现在包括与粘蛋白相关的那些(Rad61 / WAPL和Pds5)或与DNA复制叉子相关的那些(Elg1-RFC)。在这项研究中,我们表明当受到基因和功能挑战时,这两类反建立复合体是无法区分的。这些发现表明,这两个类别均以以Ctf7 / Eco1(以下称为Ctf7)调节为中心的单一途径起作用。鉴于替代的Ctf18-RFC复合物具有强大的促建立活性,因此Elg1-RFC复合物的抗建立活性特别有趣。在这里,我们提供了多方面的证据,包括使用Ctf7旁路抑制剂,表明这些活性并非简单的拮抗作用。此外,结果表明Ctf18-RFC能够促进独立于Ctf7的姐妹染色单体配对反应。这些研究的结合提出了姐妹染色单体配对调控的新模型。

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