Accurate chromosome segregation requires kinetochores on duplicated chromatids to biorient by attaching to dynamic microtubules from opposite spindle poles, which exerts forces to bring kinetochores under tension. However, kinetochores initially bind to MTs indiscriminately, resulting in errors that must be corrected. While the Aurora B protein kinase destabilizes low-tension attachments by phosphorylating kinetochores, low-tension attachments are intrinsically less stable than those under higher tension in vitro independent of Aurora activity. Intrinsic tension-sensitive behavior requires the microtubule regulator Stu2 (budding yeast Dis1/XMAP215 ortholog), which we demonstrate here is likely a conserved function for the TOG protein family. The human TOG protein, chTOG, localizes to kinetochores independent of microtubules by interacting with Hec1. We identify a chTOG mutant that regulates microtubule dynamics but accumulates erroneous kinetochore-microtubule attachments that Aurora B fails to destabilize. Thus, TOG proteins confer a unique, intrinsic error correction activity to kinetochores that ensures accurate chromosome segregation.

中文翻译：

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chTOG是保守的有丝分裂错误校正因子

准确的染色体分离需要复制的染色质上的动植物通过附着在来自相反纺锤极的动态微管上来进行生物取向，这会施加力使动植物处于张力下。但是，动植物最初会不加区别地绑定到MT，从而导致必须纠正的错误。尽管Aurora B蛋白激酶通过使动植物磷酸化来破坏低张力附件的稳定性，但低张力附件本质上不如在体外处于较高张力下的附件稳定，而与Aurora活性无关。内在的张力敏感行为需要微管调节剂Stu2（发芽酵母Dis1 / XMAP215正向同源物），我们在这里证明这可能是TOG蛋白家族的保守功能。人类TOG蛋白chTOG 通过与Hec1相互作用定位到独立于微管的动植物。我们确定了一个chTOG突变体，该突变体调节微管动力学，但积累了极光B无法稳定的错误的动粒-微管附件。因此，TOG蛋白赋予动植物独特的，固有的纠错活性，可确保准确的染色体分离。