scholarly journals Dual Detection of Chromosomes and Microtubules by the Chromosomal Passenger Complex Drives Spindle Assembly

2010 ◽  
Vol 18 (6) ◽  
pp. 903-912 ◽  
Author(s):  
Boo Shan Tseng ◽  
Lei Tan ◽  
Tarun M. Kapoor ◽  
Hironori Funabiki
2012 ◽  
Vol 31 (6) ◽  
pp. 1467-1479 ◽  
Author(s):  
Teresa Rivera ◽  
Cristina Ghenoiu ◽  
Miriam Rodríguez-Corsino ◽  
Satoru Mochida ◽  
Hironori Funabiki ◽  
...  

2020 ◽  
Vol 31 (20) ◽  
pp. 2207-2218 ◽  
Author(s):  
Mary Kate Bonner ◽  
Julian Haase ◽  
Hayden Saunders ◽  
Hindol Gupta ◽  
Biyun Iris Li ◽  
...  

This study provides the molecular mechanism for the interaction of Sgo1 with the chromosomal passenger complex and explores the specific role of Sgo1 in regulating Aurora B functions that ensure the equal segregation of chromosomes.


Cell ◽  
2004 ◽  
Vol 118 (2) ◽  
pp. 187-202 ◽  
Author(s):  
Srinath C Sampath ◽  
Ryoma Ohi ◽  
Oliver Leismann ◽  
Adrian Salic ◽  
Andrei Pozniakovski ◽  
...  

2020 ◽  
Author(s):  
Lin-Ing Wang ◽  
Tyler DeFosse ◽  
Rachel A. Battaglia ◽  
Victoria F. Wagner ◽  
Kim S. McKim

AbstractThe chromosomes in the oocytes of many animals appear to promote bipolar spindle assembly. In Drosophila oocytes, spindle assembly requires the chromosomal passenger complex (CPC), which consists of INCENP, Borealin, Survivin and Aurora B. To determine what recruits the CPC to the chromosomes and its role in spindle assembly, we developed a strategy to manipulate the function and localization of INCENP, which is critical for recruiting the Aurora B kinase. We found that an interaction between Borealin and HP1 is crucial for the initial recruitment of the CPC to the chromosomes and is sufficient to build kinetochores and recruit spindle microtubules. We also found that HP1 moves from the chromosomes to the spindle microtubules along with the CPC, and based on this, propose a mechanism for how the CPC moves from the chromosomes to the microtubules. Within the central spindle, rather than at the centromeres, the CPC and HP1 are required for homologous chromosome bi-orientation.


Genetics ◽  
2012 ◽  
Vol 192 (2) ◽  
pp. 417-429 ◽  
Author(s):  
Sarah J. Radford ◽  
Janet K. Jang ◽  
Kim S. McKim

2007 ◽  
Vol 18 (11) ◽  
pp. 4553-4564 ◽  
Author(s):  
Gerben Vader ◽  
Carin W.A. Cruijsen ◽  
Tanja van Harn ◽  
Martijn J.M. Vromans ◽  
René H. Medema ◽  
...  

The chromosomal passenger complex (CPC) is a critical regulator of chromosome segregation during mitosis by correcting nonbipolar microtubule-kinetochore interactions. By severing these interactions, the CPC is thought to create unattached kinetochores that are subsequently sensed by the spindle assembly checkpoint (SAC) to prevent premature mitotic exit. We now show that spindle checkpoint function of the CPC and its role in eliminating nonbipolar attachments can be uncoupled. Replacing the chromosomal passenger protein INCENP with a mutant allele that lacks its coiled-coil domain results in an overt defect in a SAC-mediated mitotic arrest in response to taxol treatment, indicating that this domain is critical for CPC function in spindle checkpoint control. Surprisingly, this mutant could restore alignment and cytokinesis during unperturbed cell divisions and was capable of resolving syntelic attachments. Also, Aurora-B kinase was localized and activated normally on centromeres in these cells, ruling out a role for the coiled-coil domain in general Aurora-B activation. Thus, mere microtubule destabilization of nonbipolar attachments by the CPC is insufficient to install a checkpoint-dependent mitotic arrest, and additional, microtubule destabilization–independent CPC signaling toward the spindle assembly checkpoint is required for this arrest, potentially through amplification of the unattached kinetochore-derived checkpoint signal.


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