In meiosis, crossover formation between homologous chromosomes is essential for faithful segregation. However, misplaced meiotic recombination can have catastrophic consequences on genome stability. Within pericentromeres, crossovers are associated with meiotic chromosome missegregation. In organisms ranging from yeast to humans, pericentromeric crossovers are repressed. We previously identified a role for the kinetochore-associated Ctf19 complex (Ctf19c) in pericentromeric crossover suppression. Here, we develop a dCas9/CRISPR-based system that allows ectopic targeting of Ctf19c-subunits. Using this approach, we query sufficiency in meiotic crossover suppression, and identify Ctf19 as a mediator of kinetochore-associated crossover control. The effect of Ctf19 is encoded in its NH2-terminal tail, and depends on residues important for the recruitment of the Scc2-Scc4 cohesin regulator. This work provides insight into kinetochore-derived control of meiotic recombination. We establish an experimental platform to investigate and manipulate meiotic crossover control. This platform can easily be adapted in order to investigate other aspects of chromosome biology.

中文翻译：

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基于 dCas9 的系统确定了 Ctf19 在动粒衍生的减数分裂重组抑制中的核心作用。

在减数分裂中，同源染色体之间的交叉形成对于忠实分离至关重要。然而，错误的减数分裂重组可能对基因组稳定性产生灾难性后果。在着丝粒周围，交叉与减数分裂染色体错误分离有关。在从酵母到人类的生物体中，着丝粒周围的交叉受到抑制。我们之前确定了着丝粒相关的 Ctf19 复合物 (Ctf19c) 在着丝粒周围交叉抑制中的作用。在这里，我们开发了一种基于 dCas9/CRISPR 的系统，可以异位靶向 Ctf19c 亚基。使用这种方法，我们询问减数分裂交叉抑制的充分性，并将 Ctf19 确定为着丝粒相关交叉控制的介体。Ctf19 的作用是在其 NH2 末端尾部编码的，并且取决于对 Scc2-Scc4 粘连蛋白调节因子的募集很重要的残基。这项工作提供了对减数分裂重组的着丝粒衍生控制的见解。我们建立了一个实验平台来研究和操纵减数分裂交叉控制。该平台可以很容易地进行调整，以研究染色体生物学的其他方面。