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首页> 外文期刊>Molecular and Cellular Biology >MCAK-Independent Functions of ch-Tog/XMAP215 in Microtubule Plus-End Dynamics
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MCAK-Independent Functions of ch-Tog/XMAP215 in Microtubule Plus-End Dynamics

机译：ch-Tog / XMAP215在微管正态动力学中与MCAK无关的功能

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The formation of a functional bipolar mitotic spindle is essential for genetic integrity. In human cells, the microtubule polymerase XMAP215/ch-Tog ensures spindle bipolarity by counteracting the activity of the microtubule-depolymerizing kinesin XKCM1/MCAK. Their antagonistic effects on microtubule polymerization confer dynamic instability on microtubules assembled in cell-free systems. It is, however, unclear if a similar interplay governs microtubule behavior in mammalian cells in vivo. Using real-time analysis of spindle assembly, we found that ch-Tog is required to produce or maintain long centrosomal microtubules after nuclear-envelope breakdown. In the absence of ch-Tog, microtubule assembly at centrosomes was impaired and microtubules were nondynamic. Interkinetochore distances and the lengths of kinetochore fibers were also reduced in these cells. Codepleting MCAK with ch-Tog improved kinetochore fiber length and interkinetochore separation but, surprisingly, did not rescue centrosomal microtubule assembly and microtubule dynamics. Our data therefore suggest that ch-Tog has at least two distinct roles in spindle formation. First, it protects kinetochore microtubules from depolymerization by MCAK. Second, ch-Tog plays an essential role in centrosomal microtubule assembly, a function independent of MCAK activity. Thus, the notion that the antagonistic activities of MCAK and ch-Tog determine overall microtubule stability is too simplistic to apply to human cells.
机译：功能性双极有丝分裂纺锤体的形成对于遗传完整性至关重要。在人类细胞中，微管聚合酶XMAP215 / ch-Tog通过抵消微管解聚的驱动蛋白XKCM1 / MCAK的活性来确保纺锤体双极性。它们对微管聚合的拮抗作用使无细胞系统中组装的微管具有动态不稳定性。然而，尚不清楚类似的相互作用是否在体内控制哺乳动物细胞中的微管行为。使用主轴组件的实时分析，我们发现在核被膜破裂后，ch-Tog才能产生或维持长的中心体微管。在没有ch-Tog的情况下，中心体的微管组装受到损害，并且微管没有动力。在这些细胞中，线粒间的距离和线粒体纤维的长度也减少了。用ch-Tog置换MCAK可以改善线粒体纤维长度和线粒体间的分离，但令人惊讶的是，它不能挽救中心体微管的组装和微管动力学。因此，我们的数据表明ch-Tog在纺锤体形成中至少具有两个不同的作用。首先，它可以保护线粒体微管不被MCAK解聚。其次，ch-Tog在中心体微管组装中起着至关重要的作用，该功能独立于MCAK活性。因此，MCAK和ch-Tog的拮抗活性决定总体微管稳定性的观点过于简单，无法应用于人类细胞。

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