Fin1-PP1 Helps Clear Spindle Assembly Checkpoint Protein Bub1 from Kinetochores in Anaphase

被引:18
作者
Bokros, Michael [1 ]
Gravenmier, Curtis [2 ,3 ]
Jin, Fengzhi [1 ]
Richmond, Daniel [1 ]
Wang, Yanchang [1 ]
机构
[1] Florida State Univ, Dept Biomed Sci, Coll Med, 1115 W Call St, Tallahassee, FL 32306 USA
[2] Florida State Univ, Dept Chem & Biochem, Tallahassee, FL 32306 USA
[3] Univ S Florida, Tampa, FL 33620 USA
来源
CELL REPORTS | 2016年 / 14卷 / 05期
关键词
YEAST SACCHAROMYCES-CEREVISIAE; BUDDING YEAST; MITOTIC EXIT; DNA-DAMAGE; PHOSPHATASE; 2A; KINASE; CDC14; PHOSPHORYLATION; ATTACHMENT; SEPARASE;
D O I
10.1016/j.celrep.2016.01.007
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The spindle assembly checkpoint (SAC) monitors chromosome attachment defects, and the assembly of SAC proteins at kinetochores is essential for its activation, but the SAC disassembly process remains unknown. We found that deletion of a 14-3-3 protein, Bmh1, or hyperactivation of Cdc14 early anaphase release (FEAR) allows premature SAC silencing in budding yeast, which depends on a kinetochore protein Fin1 that forms a complex with protein phosphatase PP1. Previous works suggest that FEAR-dependent Fin1 dephosphorylation promotes Bmh1-Fin1 dissociation, which enables kinetochore recruitment of Fin1-PP1. We found persistent kinetochore association of SAC protein Bub1 in fin1 Delta mutants after anaphase entry. Therefore, we revealed a mechanism that clears SAC proteins from kinetochores. After anaphase entry, FEAR activation promotes kinetochore enrichment of Fin1-PP1, resulting in SAC disassembly at kinetochores. This mechanism is required for efficient SAC silencing after SAC is challenged, and untimely Fin1-kinetochore association causes premature SAC silencing and chromosome missegregation.
引用
收藏
页码:1074 / 1085
页数:12
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