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J Cell Biol. 2017 Apr 3;216(4):911-923. doi: 10.1083/jcb.201609123. Epub 2017 Mar 17.

An engineered minimal chromosomal passenger complex reveals a role for INCENP/Sli15 spindle association in chromosome biorientation.

Author information

1
Department of Chromosome Biology, Max F. Perutz Laboratories, University of Vienna, 1030 Vienna, Austria.
2
Ludwig Institute for Cancer Research, University of California, San Diego, La Jolla, CA 92093.
3
Department of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, CA 92093.
4
Ludwig Institute for Cancer Research, University of California, San Diego, La Jolla, CA 92093 christopher.campbell@univie.ac.at abdesai@ucsd.edu.
5
Department of Chromosome Biology, Max F. Perutz Laboratories, University of Vienna, 1030 Vienna, Austria christopher.campbell@univie.ac.at abdesai@ucsd.edu.

Abstract

The four-subunit chromosomal passenger complex (CPC), whose enzymatic subunit is Aurora B kinase, promotes chromosome biorientation by detaching incorrect kinetochore-microtubule attachments. In this study, we use a combination of truncations and artificial dimerization in budding yeast to define the minimal CPC elements essential for its biorientation function. We engineered a minimal CPC comprised of the dimerized last third of the kinase-activating Sli15/INCENP scaffold and the catalytic subunit Ipl1/Aurora B. Although native Sli15 is not oligomeric, artificial dimerization suppressed the biorientation defect and lethality associated with deletion of a majority of its microtubule-binding domain. Dimerization did not act through a physical clustering-based kinase activation mechanism but instead promoted spindle association, likely via a putative helical domain in Sli15 that is essential even when dimerized and is required to target kinetochore substrates. Based on the engineering and characterization of a minimal CPC, we suggest that spindle association is important for active Ipl1/Aurora B complexes to preferentially destabilize misattached kinetochores.

PMID:
28314741
PMCID:
PMC5379952
DOI:
10.1083/jcb.201609123
[Indexed for MEDLINE]
Free PMC Article

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