Aurora B kinase is essential for faithful chromosome segregation during mitosis. During (pro)metaphase, Aurora B is concentrated at the inner centromere by the kinases Haspin and Bub1. However, how Haspin and Bub1 collaborate to control Aurora B activity at centromeres remains unclear. Here, we show that either Haspin or Bub1 activity is sufficient to recruit Aurora B to a distinct chromosomal locus. Moreover, we identified a small, Bub1 kinase–dependent Aurora B pool that supported faithful chromosome segregation in otherwise unchallenged cells. Joined inhibition of Haspin and Bub1 activities fully abolished Aurora B accumulation at centromeres. While this impaired the correction of erroneous KT–MT attachments, it did not compromise the mitotic checkpoint, nor the phosphorylation of the Aurora B kinetochore substrates Hec1, Dsn1, and Knl1. This suggests that Aurora B substrates at the kinetochore are not phosphorylated by centromere-localized pools of Aurora B, and calls for a reevaluation of the current spatial models for how tension affects Aurora B–dependent kinetochore phosphorylation.

中文翻译：

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阐明 Haspin 和 Bub1 在有丝分裂过程中对 Aurora B 功能的贡献

Aurora B 激酶对于有丝分裂过程中染色体的忠实分离至关重要。在（前）中期，Aurora B 通过激酶 Haspin 和 Bub1 集中于内部着丝粒。然而，Haspin 和 Bub1 如何合作控制着丝粒上的 Aurora B 活性仍不清楚。在这里，我们表明 Haspin 或 Bub1 活性足以将 Aurora B 招募到不同的染色体位点。此外，我们还发现了一个小型的 Bub1 激酶依赖性 Aurora B 池，它支持在其他未受到挑战的细胞中实现忠实的染色体分离。联合抑制 Haspin 和 Bub1 活性可完全消除 Aurora B 在着丝粒处的积累。虽然这损害了错误 KT-MT 连接的纠正，但它并没有损害有丝分裂检查点，也没有损害 Aurora B 着丝粒底物 Hec1、Dsn1 和 Knl1 的磷酸化。这表明着丝粒处的 Aurora B 底物不会被着丝粒定位的 Aurora B 池磷酸化，并需要重新评估当前的空间模型，以了解张力如何影响 Aurora B 依赖的着丝粒磷酸化。