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The Drosophila Kinesin-13 KLP59D Impacts Pacman- and Flux-based Chromosome Movement

机译:果蝇驱动蛋白13KLP59D影响基于Pacman和通量的染色体运动。

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摘要

Chromosome movements are linked to the active depolymerization of spindle microtubule (MT) ends. Here we identify the kinesin-13 family member, KLP59D, as a novel and uniquely important regulator of spindle MT dynamics and chromosome motility in Drosophila somatic cells. During prometaphase and metaphase, depletion of KLP59D, which targets to centrosomes and outer kinetochores, suppresses the depolymerization of spindle pole–associated MT minus ends, thereby inhibiting poleward tubulin Flux. Subsequently, during anaphase, loss of KLP59D strongly attenuates chromatid-to-pole motion by suppressing the depolymerization of both minus and plus ends of kinetochore-associated MTs. The mechanism of KLP59D's impact on spindle MT plus and minus ends appears to differ. Our data support a model in which KLP59D directly depolymerizes kinetochore-associated plus ends during anaphase, but influences minus ends indirectly by localizing the pole-associated MT depolymerase KLP10A. Finally, electron microscopy indicates that, unlike the other Drosophila kinesin-13s, KLP59D is largely incapable of oligomerizing into MT-associated rings in vitro, suggesting that such structures are not a requisite feature of kinetochore-based MT disassembly and chromosome movements.
机译:染色体运动与纺锤体微管(MT)末端的主动解聚有关。在这里,我们确定驱动蛋白13家族成员KLP59D是果蝇体细胞中纺锤体MT动态和染色体运动的新型且独特的重要调节剂。在前中期和中期,针对中心体和外部动植物的KLP59D耗竭抑制了纺锤极相关的MT负端的解聚,从而抑制了极向微管蛋白通量。随后,在后期,KLP59D的丢失会通过抑制与线粒体相关的MT的负端和正端的解聚,极大地减弱了染色单体到极点的运动。 KLP59D对主轴MT正负端的影响机制似乎有所不同。我们的数据支持一个模型,其中KLP59D在后期会直接解聚与线粒体相关的正端,但会通过定位与极相关的MT解聚酶KLP10A间接影响负端。最后,电子显微镜表明,与其他果蝇驱动蛋白-13s不同,KLP59D在体外无法寡聚成MT相关环,这表明此类结构不是基于动线粒体的MT分解和染色体运动的必要特征。

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