Microtubules form a multifunctional filamentous structure essential for the cell. In interphase, microtubules form networks in the cytoplasm and play pivotal roles in cell polarity and intracellular transport of various biomolecules. In mitosis, microtubules dramatically change their morphology to assemble the mitotic spindle, thereby pulling the chromosomes toward the spindle poles. One long-standing question is how microtubules are reorganized upon mitotic entry. Yeast cells undergo closed mitosis, in which the nuclear envelope persists, whereas higher eukaryotes undergo open mitosis, in which the nuclear envelope breaks down. Microtubule reorganization must be controlled by selective localization of microtubule-assembly factors. Recent findings in fission yeast indicate that several microtubule-associated proteins (MAPs) shuttle between the cytoplasm and the nucleus through regulation by Ran GTPase, the universal organizer of nucleocytoplasmic transport. Furthermore, the synergistic interplay of Ran and cyclin-dependent kinase (CDK) induces the critical spatiotemporal shift of modes in microtubule assembly from cytoplasmic arrays to nuclear spindles. A MAP complex Alp7/TACC-Alp14/TOG undergoes nucleocytoplasmic shuttling in interphase, whereas it is retained in the mitotic nucleus through a decrease of its nuclear export by CDK. Our understanding of how microtubules are reorganized during the cell cycle is beginning to emerge.

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细胞中的空间穿梭：细胞周期中的核质运输和微管组织

微管形成细胞必不可少的多功能丝状结构。在间期，微管在细胞质中形成网络，并在细胞极性和各种生物分子的细胞内转运中起关键作用。在有丝分裂中，微管显着改变其形态以组装有丝分裂纺锤体，从而将染色体拉向纺锤体两极。一个长期存在的问题是微管在有丝分裂进入时如何重组。酵母细胞进行封闭有丝分裂，其中核膜持续存在，而高等真核生物进行开放有丝分裂，其中核膜破裂。微管重组必须通过微管组装因子的选择性定位来控制。最近在裂殖酵母中的发现表明，几种微管相关蛋白 (MAP) 通过核质转运的通用组织者 Ran GTPase 的调节在细胞质和细胞核之间穿梭。此外，Ran 和细胞周期蛋白依赖性激酶 (CDK) 的协同相互作用诱导微管组装模式从细胞质阵列到核纺锤体的关键时空转变。MAP 复合物 Alp7/TACC-Alp14/TOG 在间期经历核质穿梭，而通过 CDK 减少其核输出而保留在有丝分裂核中。我们对微管在细胞周期中如何重组的理解开始浮出水面。Ran 和细胞周期蛋白依赖性激酶 (CDK) 的协同相互作用诱导微管组装模式从细胞质阵列到核纺锤体的关键时空转变。MAP 复合物 Alp7/TACC-Alp14/TOG 在间期经历核质穿梭，而通过 CDK 减少其核输出而保留在有丝分裂核中。我们对微管在细胞周期中如何重组的理解开始浮出水面。Ran 和细胞周期蛋白依赖性激酶 (CDK) 的协同相互作用诱导微管组装模式从细胞质阵列到核纺锤体的关键时空转变。MAP 复合物 Alp7/TACC-Alp14/TOG 在间期经历核质穿梭，而通过 CDK 减少其核输出而保留在有丝分裂核中。我们对微管在细胞周期中如何重组的理解开始浮出水面。