MCAK activity at microtubule tips regulates spindle microtubule length to promote robust kinetochore attachment.
MCAK activity at microtubule tips regulates spindle microtubule length to promote robust kinetochore attachment.
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DOI：
10.1083/jcb.201108147
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发表时间：
2012-04-16
期刊：
影响因子：
--
通讯作者：
Wordeman L
中科院分区：
文献类型：
--
作者：
Domnitz SB;Wagenbach M;Decarreau J;Wordeman L
驱动蛋白 MCAK 与末端结合蛋白结合并拮抗中心体分离并促进着丝粒与纺锤体微管的牢固附着。有丝分裂着丝粒相关驱动蛋白 (MCAK) 是一种微管解聚驱动蛋白-13 成员，可以在间期和有丝分裂期间跟踪聚合微管尖端（以下简称尖端跟踪）。 MCAK 通过微管尖端定位信号 SKIP 与末端结合蛋白 (EB) 结合来跟踪微管尖端，SKIP 位于 MCAK 颈部和运动域的 N 末端。有丝分裂期间 MCAK 尖端跟踪行为的功能意义从未得到解释。在本文中，我们识别并定义了 MCAK 微管尖端相关群体特有的有丝分裂功能：组装双极纺锤体内微管长度的负调节。该功能取决于 MCAK 结合 EB 并追踪聚合非着丝粒微管尖端的能力。尽管这种活性在双极化过程中拮抗中心体分离，但它最终通过促进着丝粒与纺锤体微管的牢固附着而有利于分裂细胞。
The kinesin MCAK binds to end-binding proteins and antagonizes centrosome separation and promotes robust kinetochore attachments to spindle microtubules. Mitotic centromere-associated kinesin (MCAK) is a microtubule-depolymerizing kinesin-13 member that can track with polymerizing microtubule tips (hereafter referred to as tip tracking) during both interphase and mitosis. MCAK tracks with microtubule tips by binding to end-binding proteins (EBs) through the microtubule tip localization signal SKIP, which lies N terminal to MCAK’s neck and motor domain. The functional significance of MCAK’s tip-tracking behavior during mitosis has never been explained. In this paper, we identify and define a mitotic function specific to the microtubule tip–associated population of MCAK: negative regulation of microtubule length within the assembling bipolar spindle. This function depends on MCAK’s ability to bind EBs and track with polymerizing nonkinetochore microtubule tips. Although this activity antagonizes centrosome separation during bipolarization, it ultimately benefits the dividing cell by promoting robust kinetochore attachments to the spindle microtubules.
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