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首页> 外文期刊>Cytoskeleton >Coupling between microtubule sliding, plus-end growth and spindle length revealed by kinesin-8 depletion.
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Coupling between microtubule sliding, plus-end growth and spindle length revealed by kinesin-8 depletion.

机译：微管滑动，正向增长和纺锤体8耗竭揭示的纺锤体长度之间的耦合。

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摘要

Mitotic spindle length control requires coordination between microtubule (MT) dynamics and motor-generated forces. To investigate how MT plus-end polymerization contributes to spindle length in Drosophila embryos, we studied the dynamics of the MT plus-end depolymerase, kinesin-8, and the effects of kinesin-8 inhibition using mutants and antibody microinjection. As expected, kinesin-8 was found to contribute to anaphase A. Furthermore, kinesin-8 depletion caused: (i) excessive polymerization of interpolar (ip) MT plus ends, which overgrow ipMT sliding rate that is coupled to MT plus-end polymerization; (iii) premature spindle elongation during metaphase/anaphase A; and (iv) an increase in the anaphase B spindle elongation rate which correlates linearly with the MT sliding rate. This is best explained by a revised "ipMT sliding/minus-end depolymerization" model for spindle length control which incorporates a coupling between ipMT plus end dynamics and the outward ipMT sliding that drives poleward flux and spindle elongation.
机译：有丝分裂纺锤体的长度控制需要微管（MT）动力学和电机产生的力之间的协调。为了研究MT末端聚合如何影响果蝇胚胎的纺锤长度，我们研究了MT末端解聚酶，kinesin-8的动力学以及使用突变体和抗体显微注射抑制kinesin-8的作用。如预期的那样，发现驱动蛋白8有助于后期A。此外，驱动蛋白8耗竭还导致：（i）极间（ip）MT末端的过度聚合，从而过度增加了与MT末端聚合反应相关的ipMT滑动速率。 ; （iii）在中期/后期A期间纺锤体过早伸长; （iv）B期后期主轴伸长率的增加与MT滑动率线性相关。修改后的用于主轴长度控制的“ ipMT滑动/负端解聚”模型可以最好地说明这一点，该模型在ipMT加上端动力学与驱动极向磁通和主轴伸长的向外ipMT滑动之间进行了耦合。

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