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 nonsense-mediated decay (NMD) 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 bi-orientation. 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 iml3∆ or chl4∆ 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.
Original language | English |
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Pages (from-to) | 3203-3215 |
Number of pages | 13 |
Journal | G3: Genes | Genomes | Genetics |
Volume | 7 |
Issue number | 9 |
Early online date | 28 Jul 2017 |
DOIs | |
Publication status | Published - 7 Sept 2017 |
Keywords
- Bir1
- Chromosome bi - orientation
- Kinetochore
- Iml3 - Chl4 complex
- Yeast