Borealin dimerization mediates optimal CPC checkpoint function by enhancing localization to centromeres and kinetochores.
Borealin dimerization mediates optimal CPC checkpoint function by enhancing localization to centromeres and kinetochores.
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DOI：
10.1038/ncomms7775
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发表时间：
2015-04-09
影响因子：
16.6
通讯作者：
Taylor, William R.
中科院分区：
文献类型：
--
作者：
Bekier, Michael E.;Mazur, Travis;Rashid, Maisha S.;Taylor, William R.
染色体乘客复合体（CPC）定位于着丝粒，在那里它响应于不适当的动粒间张力而激活有丝分裂检查点。这种误差校正功能对于正确的染色体分离是必不可少的。在这里，我们定义了CPC定位和功能的几个关键特征。首先，Borealin二聚化结构域抑制着丝粒处的动态交换以允许最佳CPC功能。其次，当有丝分裂纺锤体被破坏时，Borealin二聚化对于靶向接近动粒的CPC亚群是必不可少的。该亚群也是完整CPC检查点功能所需的。在动粒处CPC池的存在表明误差校正比从Aurora B磷酸化梯度模型预测的更复杂。最后，Haspin激酶在维持缓慢交换的着丝粒Borealin池中起关键作用，而Aurora B和Mps1在维持CPC定位中起最小作用，一旦细胞处于有丝分裂中。
The Chromosomal Passenger Complex (CPC) localizes to centromeres where it activates the mitotic checkpoint in response to inappropriate inter-kinetochore tension. This error correction function is essential for proper chromosome segregation. Here we define several critical features of CPC localization and function. First, the Borealin dimerization domain suppresses dynamic exchange at the centromere to allow optimal CPC function. Second, Borealin dimerization is essential to target a subpopulation of CPC proximal to the kinetochore when the mitotic spindle is disrupted. This subpopulation is also needed for full CPC checkpoint function. The existence of a pool of CPC at the kinetochore suggests that error correction is more complicated than predicted from the Aurora B phosphorylation gradient model. Finally, Haspin kinase plays a key role in maintaining the slowly exchanging centromere Borealin pool, while Aurora B and Mps1 play minimal roles in maintaining CPC localization once cells are in mitosis.
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