Myers Kenneth A, Baas Peter W
Department of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, PA 19104, USA.
J Cell Biol. 2007 Sep 10;178(6):1081-91. doi: 10.1083/jcb.200702074.
Kinesin-5 is a homotetrameric motor protein that interacts with adjacent microtubules in the mitotic spindle. Kinesin-5 is also highly expressed in developing postmitotic neurons. Axons of cultured neurons experimentally depleted of kinesin-5 grow up to five times longer than controls and display more branches. The faster growth rates are accompanied by a doubling of the frequency of transport of short microtubules, suggesting a major role for kinesin-5 in the balance of motor-driven forces on the axonal microtubule array. Live-cell imaging reveals that the effects on axonal length of kinesin-5 depletion are caused partly by a lower propensity of the axon and newly forming branches to undergo bouts of retraction. Overexpression of wild-type kinesin-5, but not a rigor mutant of kinesin-5, has the inverse effect on axonal length. These results indicate that kinesin-5 imposes restrictions on the growth of the axon and does so at least in part by generating forces on the axonal microtubule array.
驱动蛋白-5是一种同四聚体驱动蛋白，它与有丝分裂纺锤体中的相邻微管相互作用。驱动蛋白-5在发育中的有丝分裂后神经元中也高度表达。实验性去除驱动蛋白-5的培养神经元轴突生长长度比对照组多五倍，且分支更多。更快的生长速度伴随着短微管运输频率加倍，这表明驱动蛋白-5在轴突微管阵列上的动力平衡中起主要作用。活细胞成像显示，驱动蛋白-5缺失对轴突长度的影响部分是由于轴突和新形成的分支回缩的倾向较低。野生型驱动蛋白-5的过表达，而不是驱动蛋白-5的僵硬突变体，对轴突长度有相反的影响。这些结果表明，驱动蛋白-5对轴突生长施加限制，并且至少部分是通过在轴突微管阵列上产生力来实现的。
