A FRET-based study reveals site-specific regulation of spindle position checkpoint proteins at yeast centrosomes

被引:21
作者
Gryaznova, Yuliya [1 ]
Caydasi, Ayse Koca [1 ,2 ]
Malengo, Gabriele [3 ]
Sourjik, Victor [3 ,4 ,5 ]
Pereira, Gislene [1 ,2 ]
机构
[1] German Canc Res Ctr, DKFZ ZMBH Alliance, Heidelberg, Germany
[2] Heidelberg Univ, Ctr Organismal Studies, Heidelberg, Germany
[3] Heidelberg Univ, Ctr Mol Biol, DKFZ ZMBH Alliance, Heidelberg, Germany
[4] Max Planck Inst Terr Microbiol, D-35043 Marburg, Germany
[5] LOEWE Res Ctr Synthet Microbiol, Marburg, Germany
来源
ELIFE | 2016年 / 5卷
关键词
CELL-CYCLE CHECKPOINTS; PROMOTES MITOTIC EXIT; GAMMA-TUBULIN COMPLEX; IN-VITRO REGULATION; BUDDING YEAST; POLE BODY; SACCHAROMYCES-CEREVISIAE; KINASE KIN4; BINDING-PROTEIN; LIVE CELLS;
D O I
10.7554/eLife.14029
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
The spindle position checkpoint (SPOC) is a spindle pole body (SPB, equivalent of mammalian centrosome) associated surveillance mechanism that halts mitotic exit upon spindle misorientation. Here, we monitored the interaction between SPB proteins and the SPOC component Bfa1 by FRET microscopy. We show that Bfa1 binds to the scaffold-protein Nud1 and the gamma-tubulin receptor Spc72. Spindle misalignment specifically disrupts Bfa1-Spc72 interaction by a mechanism that requires the 14-3-3-family protein Bmh1 and the MARK/PAR-kinase Kin4. Dissociation of Bfa1 from Spc72 prevents the inhibitory phosphorylation of Bfa1 by the polo-like kinase Cdc5. We propose Spc72 as a regulatory hub that coordinates the activity of Kin4 and Cdc5 towards Bfa1. In addition, analysis of spc72 Delta cells shows that a mitotic-exit-promoting dominant signal, which is triggered upon elongation of the spindle into the bud, overrides the SPOC. Our data reinforce the importance of daughter-cell-associated factors and centrosome-based regulations in mitotic exit and SPOC control.
引用
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页数:27
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