The role of the kinesin-13 neck in microtubule depolymerization
The role of the kinesin-13 neck in microtubule depolymerization
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DOI：
10.4161/cc.5.16.3134
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发表时间：
2006-08-15
期刊：
影响因子：
4.3
通讯作者：
Milligan, Ronald A.
中科院分区：
文献类型：
--
作者：
Moores, Carolyn A.;Cooper, Jeremy;Milligan, Ronald A.
为了确保遗传完整性，复制的染色体必须准确地分配给子细胞——这一过程是在微管纺锤体上完成的。 Kinesin-13 马达通过执行受调控的微管解聚作用在此过程中发挥着重要作用。我们着手剖析这些驱动蛋白的解聚机制，特别是它们保守的颈部序列的作用。我们使用单体驱动蛋白-13 MCAK，由颈部和运动核心组成，具有很强的解聚活性。在存在不可水解的 ATP 类似物的情况下，该构建体诱导微管周围形成环。这些环由微管蛋白原丝构成，这些原丝被驱动蛋白 13 马达弯曲，该马达参与其 ATP 酶循环的 ATP 结合步骤。我们的数据表明，环-微管相互作用是由颈部介导的，并支持驱动蛋白-13颈部在解聚效率中发挥作用的观点，通过优化微管末端微管蛋白的释放来发挥作用。
To ensure genetic integrity, replicated chromosomes must be accurately distributed to daughter cells-a process that is accomplished on the microtubule spindle. Kinesin-13 motors play an essential role in this process by performing regulated microtubule depolymerization. We set out to dissect the depolymerization mechanism of these kinesins, and in particular, the role of their conserved neck sequence. We used a monomeric kinesin-13 MCAK, consisting of the neck and motor core, which has strong depolymerizing activity. In the presence of a non-hydrolysable ATP analogue, this construct induced formation of rings around microtubules. The rings are built from tubulin protofilaments that are bent by the kinesin-13 motor engaged at the ATP-binding step of its ATPase cycle. Our data suggest that the ring-microtubule interaction is mediated by the neck and support the idea of a role for the kinesin-13 neck in depolymerization efficiency, acting by optimizing release of tubulin from microtubule ends.