Kinesin 5-independent poleward flux of kinetochore microtubules in PtK1 cells
Kinesin 5-independent poleward flux of kinetochore microtubules in PtK1 cells
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DOI：
10.1083/jcb.200601075
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发表时间：
2006-04-24
影响因子：
7.8
通讯作者：
Salmon, ED
中科院分区：
文献类型：
--
作者：
Cameron, LA;Yang, G;Salmon, ED
在高等真核生物中，纺锤体中排列和分离染色体的力产生稳定的动粒微管(MTS[kMTs])。在一些非哺乳动物系统中，通量是由四聚体动蛋白EG5(动蛋白5)驱动的，它向负端滑动反平行的MT。然而，我们发现，在哺乳动物培养细胞(PtK1)中抑制Kinesin 5只会导致KMT流量从类似于0.7到类似于0.5微米/分钟的轻微降低，这与缺乏反平行MTS的单极纺锤体的速率相同。这些数据表明，这些细胞中的大部分kMT的极向通量不是由EG5驱动的。相反，我们倾向于一种极性的“拉入”机制，在这种机制中，位于动粒纤维减去末端的去聚合酶对向极地的通量做出了主要贡献。在流动着丝粒纤维的负端检测到一个候选基因Kif2a(Kinesin 13)。Kif2a被dynein/dynactin抑制使纺锤体断裂时，Kif2a仍然与K纤维的末端相关，而这些K纤维流动。
Forces in the spindle that align and segregate chromosomes produce a steady poleward flux of kinetochore microtubules (MTs [kMTs]) in higher eukaryotes. In several nonmammalian systems, flux is driven by the tetrameric kinesin Eg5 ( kinesin 5), which slides antiparallel MTs toward their minus ends. However, we find that the inhibition of kinesin 5 in mammalian cultured cells (PtK1) results in only minor reduction in the rate of kMT flux from similar to 0.7 to similar to 0.5 mu m/ min, the same rate measured in monopolar spindles that lack antiparallel MTs. These data reveal that the majority of poleward flux of kMTs in these cells is not driven by Eg5. Instead, we favor a polar "pulling-in" mechanism in which a depolymerase localized at kinetochore fiber minus ends makes a major contribution to poleward flux. One candidate, Kif2a ( kinesin 13), was detected at minus ends of fluxing kinetochore fibers. Kif2a remains associated with the ends of K fibers upon disruption of the spindle by dynein/dynactin inhibition, and these K fibers flux.