Complex formation of Plk1 and INCENP required for metaphase-anaphase transition

被引:148
作者
Goto, H
Kiyono, T
Tomono, Y
Kawajiri, A
Urano, T
Furukawa, K
Nigg, EA
Inagaki, M [1 ]
机构
[1] Aichi Canc Ctr, Res Inst, Div Biochem, Nagoya, Aichi 4648681, Japan
[2] Natl Canc Ctr, Res Inst, Div Virol, Chuo Ku, Tokyo 1040045, Japan
[3] Shigei Med Res Inst, Div Mol & Cell Biol, Okayama 7010202, Japan
[4] Nagoya Univ, Grad Sch Med, Dept Biochem 2, Aichi 4668550, Japan
[5] Max Planck Inst Biochem, Dept Cell Biol, D-82152 Martinsried, Germany
关键词
D O I
10.1038/ncb1350
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Mitotic chromosomal dynamics is regulated by the coordinated activities of many mitotic kinases(1), such as cyclin-dependent kinase 1 (Cdk1)(2,3), Aurora-B-4 or Polo-like kinase 1 (Plk1)(5), but the mechanisms of their coordination remain unknown. Here, we report that Cdk1 phosphorylates Thr 59 and Thr 388 on inner centromere protein (INCENP), which regulates the localization(4) and kinase activity(6-8) of Aurora-B from prophase to metaphase. INCENP depletion disrupts Plk1 localization specifically at the kinetochore. This phenotype is rescued by the exogenous expression of INCENP wild type and INCENP mutated at Thr 59 to Ala (T59A), but not at Thr 388 to Ala (T388A). The replacement of endogenous INCENP with T388A resulted in the delay of progression from metaphase to anaphase. We propose that INCENP phosphorylation by Cdk1 is necessary for the recruitment of Plk1 to the kinetochore, and that the complex formation of Plk1 and Aurora-B on INCENP may play crucial roles in the regulation of chromosomal dynamics.
引用
收藏
页码:180 / U52
页数:12
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