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首页> 外文期刊>Current Biology: CB >Loss of Kif18A Results in Spindle Assembly Checkpoint Activation at Microtubule-Attached Kinetochores
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Loss of Kif18A Results in Spindle Assembly Checkpoint Activation at Microtubule-Attached Kinetochores

机译：KIF18A的丧失导致MICROTUBUER附着的运动学中的主轴组件检查点激活

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摘要

The spindle assembly checkpoint (SAC) halts anaphase progression until all kinetochores have obtained bipolar, stable attachments to the mitotic spindle. Upon initial attachment, chromosomes undergo oscillatory movements to reach metaphase. Once a chromosome is correctly attached and positioned, these oscillatory movements are reduced by the motor protein Kif18A, and loss of Kif18A results in chromosome hyper-oscillations. By using a haploid genetic approach, we found that loss of Kif18A is lethal in wild-type human HAP1 cells, but not in SAC-deficient HAP1 cells. Unexpectedly, we found that the hyper-oscillations after Kif18A loss are not associated with chromosome missegregations. Rather, we found that loss of Kif18A results in a loss of tension across a subset of kinetochores accompanying SAC activation. Strikingly, the SAC-active kinetochores appear to have established fully functional kinetochore-microtubule (k-Mt) attachments, allowing proper chromosome segregation. These findings shed new light on the role of Kif18A in chromosome segregation and demonstrate that the SAC can be activated at kinetochores that are occupied by fully functional k-Mts that lack tension.
机译：主轴组件检查点（SAC）停止后期进展，直到所有Kinetochores都获得了双极，稳定的有丝分裂轴的附着物。在初始附着时，染色体经历振荡运动以达到中期。一旦染色体正确连接并定位，就通过电动机蛋白质KIF18A减少了这些振荡运动，并且损失的kif18a导致染色体超振荡。通过使用单倍体遗传方法，我们发现在野生型人HAP1细胞中致死KIF18A的丧失，但不在囊缺陷的HAP1细胞中。出乎意料的是，我们发现KIF18A损失后的超振荡与染色体错误造成无关。相反，我们发现kif18a的损失导致伴随囊激活的kinetochores子集中的张力丧失。尖锐的是，囊活性的动力学似乎已经建立了完全功能性的Kinetochore-Microotumule（K-MT）附件，允许适当的染色体隔离。这些发现揭示了KIF18a在染色体偏析中的作用，并证明囊可以在缺乏张力的全功能K-MTS占据的kinetochores上激活。

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