Timely and precise control of Aurora B kinase, the chromosomal passenger complex (CPC) catalytic subunit, is essential for accurate chromosome segregation and cytokinesis. Post-translational modifications of CPC subunits are directly involved in controlling Aurora B activity. Here, we identified a highly conserved acidic STD-rich motif of INCENP that is phosphorylated during mitosis in vivo and by Plk1 in vitro and is involved in controlling Aurora B activity. By using an INCENP conditional-knockout cell line, we show that impairing the phosphorylation status of this region disrupts chromosome congression and induces cytokinesis failure. In contrast, mimicking constitutive phosphorylation not only rescues cytokinesis but also induces ectopic furrows and contractile ring formation in a Plk1- and ROCK1-dependent manner independent of cell cycle and microtubule status. Our experiments identify the phospho-regulation of the INCENP STD motif as a novel mechanism that is key for chromosome alignment and cytokinesis.This article has an associated First Person interview with the first author of the paper.

中文翻译：

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由 INCENP STD 基序的拟磷突变触发的细胞周期独立皱纹需要 Plk1。

及时准确地控制 Aurora B 激酶，即染色体乘客复合物 (CPC) 催化亚基，对于准确的染色体分离和胞质分裂至关重要。CPC 亚基的翻译后修饰直接参与控制 Aurora B 的活性。在这里，我们确定了一个高度保守的酸性富含 STD 的 INCENP 基序，它在体内有丝分裂期间和体外被 Plk1 磷酸化，并参与控制 Aurora B 活性。通过使用 INCENP 条件敲除细胞系，我们表明损害该区域的磷酸化状态会破坏染色体大会并诱导胞质分裂失败。相比之下，模拟组成型磷酸化不仅可以挽救胞质分裂，而且还以 Plk1 和 ROCK1 依赖性方式诱导异位沟和收缩环形成，而与细胞周期和微管状态无关。我们的实验确定了 INCENP STD 基序的磷酸化调节是染色体排列和胞质分裂的关键新机制。本文与论文第一作者进行了相关的第一人称采访。