Articles

< Previous                        
Aurora B kinase activation requires survivin priming phosphorylation by PLK1 Free
Youjun Chu1, Phil Y. Yao2, Wenwen Wang1, Dongmei Wang1, Zhikai Wang1,2, Liangyu Zhang1,2, Yuejia Huang1,2, Yuwen Ke1, Xia Ding1,3, and Xuebiao Yao1,*
1Anhui Key Laboratory of Cellular Dynamics and Chemical Biology, University of Science and Technology of China, Hefei 230027, China
2Department of Physiology, Morehouse School of Medicine, Atlanta, GA 30310, USA
3Department of Medicine, Beijing University of Chinese Medicine, Beijing 100086, China *Correspondence to:Xuebiao Yao, E-mail: yaoxb@ustc.edu.cn
J Mol Cell Biol, Volume 3, Issue 4, August 2011, 260-267,  https://doi.org/10.1093/jmcb/mjq037
Keyword: Aurora B, kinase sensor, phospho-CENP-A, PLK1, survivin
During cell division, chromosome segregation is orchestrated by the interaction of spindle microtubules with the centromere. Accurate attachment of spindle microtubules to kinetochore requires the chromosomal passenger of Aurora B kinase complex with borealin, INCENP and survivin (SUR). The current working model argues that SUR is responsible for docking Aurora B to the centromere whereas its precise role in Aurora B activation has been unclear. Here, we show that Aurora B kinase activation requires SUR priming phosphorylation at Ser20 which is catalyzed by polo-like kinase 1 (PLK1). Inhibition of PLK1 kinase activity or expression of non-phosphorylatable SUR mutant prevents Aurora B activation and correct spindle microtubule attachment. The PLK1-mediated regulation of Aurora B kinase activity was examined in real-time mitosis using fluorescence resonance energy transfer-based reporter and quantitative analysis of native Aurora B substrate phosphorylation. We reason that the PLK1-mediated priming phosphorylation is critical for orchestrating Aurora B activity in centromere which is essential for accurate chromosome segregation and faithful completion of cytokinesis.