在整个细胞周期过程中，有丝分裂起承上起下的作用。如果它出现异常，可导致染色体不稳定性并促进肿瘤的发生发展。SKAP是新近发现的一个定位于微管正末端的重要有丝分裂调控蛋白，我们前期的工作着眼于其参与调控微管与动点连接的研究，并证实SKAP桥联了动点的外层和微管的正末端，参与调控纺锤体的可塑性。但是我们对SKAP在有丝分裂期时空调节的分子机制及其动态可塑性等方面的了解还不是很全面。本项目将从激酶信号级联的角度进一步研究PLK1激酶对SKAP的调控，拟采用生物信息学、定点突变、活细胞观察、全内反射荧光显微镜等技术方法来系统评估磷酸化修饰对SKAP参与调控微管和动点连接、染色体排列及纺锤体可塑性的影响。此外，我们还将分析SKAP参与调控有丝分裂过程的分子信号通路及其具体的调控机制。本项目将是SKAP蛋白参与有丝分裂期功能研究的新切入点，并为阐明桥联动点外层和微管正末端蛋白的研究奠定工作基础。

Mitosis is the most dramatic, as well as critical event in the cell cycle. Errors in this process can lead to aneuploidy or genetic instability, fostering cell death or tumor development. SKAP is a newly defined microtubule plus end protein，our previous work focused on the regulation of kinetochore-microtubule interaction, we demonstrated that SKAP forms a link between kinetochore core complex KMN and dynamic spindle microtubules, and our studies indicated that SKAP represents an important function in regulating spindle plasticity. However, it still remains elusive as how is the mechanism underlying spatiotemporal regulation of SKAP. Using the combination of bioinformatics, site-directed mutagenesis, live-cell imaging, TIRF microscopy assay, we aim to systematically explore phosphorylation of SKAP by PLK1 kinase and analyze how these phosphorylation events modulate the function of SKAP in microtubule-kinetochore interaction, chromosome alignment and spindle plasticity. In addition, we will explore molecular mechanism of phosphorylation of SKAP during mitosis. Taken together, our work will give a new perspective of mitotic function of SKAP, it could also shed light on the analysis of specific proteins in linking outerkinetochore to microtubule plus ends.