姐妹染色单体向子代细胞的高保真性分配是基因组遗传稳定的关键因素。染色体在有丝分裂过程中依赖于纺锤体均等地分配到两个子代细胞。任何微小的纺锤体组装和动力学问题均将导致染色体向子代细胞的不均匀分配和细胞分裂的失败。驱动蛋白不仅通过结合纺锤体内的微管来参与纺锤体的组装以及维护纺锤体形态的时空特异性，而且通过与染色体上的大蛋白质复合体-动点的相互作用来参与染色体的捕获以及分配。虽然驱动蛋白的有丝分裂期功能已经获得的一定程度的了解，但是它们调控纺锤体动力学过程的详尽分子机理仍然有待于进一步的研究，特别是不同类型的驱动蛋白如何协同地调控纺锤体的动力学过程仍然未知。因此，我们拟充分利用多种生物学技术手段如:生物化学、荧光标记活细胞显微观察、酵母遗传学，以裂殖酵母为模式体系来详尽剖析驱动蛋白调控纺锤体的动力学机理。该研究为加深对基因组遗传稳定性异常相关疾病，特别是肿瘤的发生和发展的认识提供坚实的理论基础。

The faithful segregation of sister chromatids into two new daughter cells during mitosis ensures genomic stability, and this process depends on the spindle. Malfunctions of the spindle can cause chromosome missegregation, leading to cell division failure. Many types of proteins are involved in spindle assembly and dynamics. Among these proteins, kinesins are emerging as key players in organizing spindle microtubules and regulating dynamics of these spindle microtubules. Although kinesins have been the focus of intense study, how multiple mitotic kinesins synergize to regulate spindle dynamics in different stages of mitosis remains elusive. In this proposal, we aim to combine biochemistry, yeast genetics and live-cell microscopy techniques to dissect the roles of kinesins in regulating spindle dynamics in metaphase and anaphase, and to reveal the mechanisms underlying spindle stability in metaphase and spindle elongation in anaphase. As chromosome missegregation can cause aneuploidy, a hallmark of cancer, our proposed study will not only reveal the molecular basis of mitotic spindle dynamics but also provide insights into developing new strategies for cancer prevention and intervention.