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A Bir1-Sli15 complex connects centromeres to microtubules and is required to sense kinetochore tension.


ABSTRACT: Proper connections between centromeres and spindle microtubules are of critical importance in ensuring accurate segregation of the genome during cell division. Using an in vitro approach based on the sequence-specific budding yeast centromere, we identified a complex of the chromosomal passenger proteins Bir1 and Sli15 (Survivin and INCENP) that links centromeres to microtubules. This linkage does not require Ipl1/Aurora B kinase, whose targeting and activation are controlled by Bir1 and Sli15. Ipl1 is the tension-dependent regulator of centromere-microtubule interactions that ensures chromosome biorientation on the spindle. Elimination of the linkage between centromeres and microtubules mediated by Bir1-Sli15 phenocopies mutations that selectively cripple Ipl1 kinase activation. These findings lead us to propose that the Bir1-Sli15-mediated linkage, which bridges centromeres and microtubules and includes the Aurora kinase-activating domain of INCENP family proteins, is the tension sensor that relays the mechanical state of centromere-microtubule attachments into local control of Ipl1 kinase activity.

SUBMITTER: Sandall S 

PROVIDER: S-EPMC2265205 | biostudies-literature | 2006 Dec

REPOSITORIES: biostudies-literature

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A Bir1-Sli15 complex connects centromeres to microtubules and is required to sense kinetochore tension.

Sandall Sharsti S   Severin Fedor F   McLeod Ian X IX   Yates John R JR   Oegema Karen K   Hyman Anthony A   Desai Arshad A  

Cell 20061201 6


Proper connections between centromeres and spindle microtubules are of critical importance in ensuring accurate segregation of the genome during cell division. Using an in vitro approach based on the sequence-specific budding yeast centromere, we identified a complex of the chromosomal passenger proteins Bir1 and Sli15 (Survivin and INCENP) that links centromeres to microtubules. This linkage does not require Ipl1/Aurora B kinase, whose targeting and activation are controlled by Bir1 and Sli15.  ...[more]

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