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A functional link between bir1 and the Saccharomyces cerevisiae Ctf19 kinetochore complex revealed through quantitative fitness analysis

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    Rights statement: Copyright © 2017 Makrantoni et al. doi: https://doi.org/10.1534/g3.117.300089 Manuscript received May 14, 2017; accepted for publication July 25, 2017; published Early Online July 28, 2017. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Original languageEnglish
Pages (from-to)3203-3215
Number of pages13
JournalG3
Volume7
Issue number9
DOIs
Publication statusPublished - 1 Sep 2017

Abstract

The chromosomal passenger complex (CPC) is a key regulator of eukaryotic cell division, consisting of the protein kinase Aurora B/Ipl1 in association with its activator (INCENP/Sli15) and two additional proteins (Survivin/Bir1 and Borealin/Nbl1). Here, we report a genome-wide genetic interaction screen in Saccharomyces cerevisiae using the bir1-17 mutant, identifying through quantitative fitness analysis deletion mutations that act as enhancers and suppressors. Gene knockouts affecting the Ctf19 kinetochore complex were identified as the strongest enhancers of bir1-17, while mutations affecting the large ribosomal subunit or the mRNA nonsensemediated decay pathway caused strong phenotypic suppression. Thus, cells lacking a functional Ctf19 complex become highly dependent on Bir1 function and vice versa. The negative genetic interaction profiles of bir1-17 and the cohesin mutant mcd1-1 showed considerable overlap, underlining the strong functional connection between sister chromatid cohesion and chromosome biorientation. Loss of some Ctf19 components, such as Iml3 or Chl4, impacted differentially on bir1-17 compared with mutations affecting other CPC components: despite the synthetic lethality shown by either iml3Δ or chl4Δ in combination with bir1-17, neither gene knockout showed any genetic interaction with either ipl1-321 or sli15-3. Our data therefore imply a specific functional connection between the Ctf19 complex and Bir1 that is not shared with Ipl1.

    Research areas

  • Bir1, Chromosome biorientation, Iml3-Chl4 complex, Kinetochore, Yeast

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