Tripin/hSgo2 recruits MCAK to the inner centromere to correct defective kinetochore attachments

被引:112
作者
Huang, Haomin
Feng, Jie
Famulski, Jakub
Rattner, Jerome B.
Liu, Song Tao
Kao, Gary D.
Muschel, Ruth
Chan, Gordon K. T.
Yen, Tim J.
机构
[1] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA
[2] Univ Alberta, Dept Oncol, Fac Med & Dent, Edmonton, AB T6G 1Z2, Canada
[3] Univ Calgary, Fac Med, Dept Cell Biol & Anat, Calgary, AB T2N 4N1, Canada
[4] Univ Penn, Sch Med, Dept Radiat Oncol, Philadelphia, PA 19104 USA
[5] Univ Oxford, Oxford OX3 7LJ, England
关键词
D O I
10.1083/jcb.200701122
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
hSgo2 (previously annotated as Tripin) was recently reported to be a new inner centromere protein that is essential for centromere cohesion (Kitajima et al., 2006). In this study, we show that hSgo2 exhibits a dynamic distribution pattern, and that its localization depends on the l and Aurora B kinases. hSgo2 is concentrated at the inner centromere of unattached kinetochores, but extends toward the kinetochores that are under tension. This localization pattern is reminiscent of MCAK, which is a microtubule depolymerase that is believed to be a key component of the error correction mechanism at kinetochores. Indeed, we found that hSgo2 is essential for MCAK to localize to the centromere. Delocalization of MCAK accounts for why cells depleted of hSgo2 exhibit kinetochore attachment defects that go uncorrected, despite a transient delay in the onset of anal Consequently, these cells exhibit a high frequency of lagging chromosomes when they enter anaphase. We confirmed that hSgo2 is associated with PP2A, and we propose that it contributes to the spatial regulation of MCAK activity within inner centromere and kinetochore.
引用
收藏
页码:413 / 424
页数:12
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