微管动力蛋白 Kinesin-14 沿微管负端向驱动，将平行的微管排列整齐，从而控制中期纺锤体的长度。
Minus-end-directed Kinesin-14 motors align antiparallel microtubules to control metaphase spindle length.
机构信息
Department of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, MN 55455, USA.
MCD Biology, University of Colorado, Boulder, CO 80309, USA.
出版信息
Dev Cell. 2014 Oct 13;31(1):61-72. doi: 10.1016/j.devcel.2014.07.023.
During cell division, a microtubule-based mitotic spindle mediates the faithful segregation of duplicated chromosomes into daughter cells. Proper length control of the metaphase mitotic spindle is critical to this process and is thought to be achieved through a mechanism in which spindle pole separation forces from plus-end-directed motors are balanced by forces from minus-end-directed motors that pull spindle poles together. However, in contrast to this model, metaphase mitotic spindles with inactive kinesin-14 minus-end-directed motors often have shorter spindle lengths, along with poorly aligned spindle microtubules. A mechanistic explanation for this paradox is unknown. Using computational modeling, in vitro reconstitution, live-cell fluorescence microscopy, and electron microscopy, we now find that the budding yeast kinesin-14 molecular motor Kar3-Cik1 can efficiently align spindle microtubules along the spindle axis. This then allows plus-end-directed kinesin-5 motors to efficiently exert the outward microtubule sliding forces needed for proper spindle bipolarity.
在细胞分裂过程中，基于微管的有丝分裂纺锤体将复制的染色体准确地分配到子细胞中。中期有丝分裂纺锤体的适当长度控制对这个过程至关重要，据认为这是通过一种机制实现的，其中来自正向驱动蛋白的纺锤极分离力与来自负向驱动蛋白的拉力相平衡，后者将纺锤极拉到一起。然而，与这个模型相反，具有失活的驱动蛋白-14 负向驱动蛋白的中期有丝分裂纺锤体通常具有较短的纺锤体长度，以及排列不良的纺锤体微管。对于这个悖论，其机制解释尚不清楚。使用计算建模、体外重组、活细胞荧光显微镜和电子显微镜，我们现在发现，芽殖酵母驱动蛋白-14 分子马达 Kar3-Cik1 可以有效地将纺锤体微管沿着纺锤体轴对齐。这使得正向驱动蛋白-5 马达能够有效地发挥出适当的纺锤体双极性所需要的向外微管滑动力。
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