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Originally published as Genetics Published Articles Ahead of Print on July 5, 2005.
Genetics, Vol. 171, 489-501, October 2005, Copyright © 2005
doi:10.1534/genetics.105.045799
Genome-Wide Synthetic Lethal Screens Identify an Interaction Between the Nuclear Envelope Protein, Apq12p, and the Kinetochore in Saccharomyces cerevisiae
Ben Montpetit*,
Ken Thorne
,
Irene Barrett*,
Kim Andrews
,
Ravi Jadusingh,
Phil Hieter* and
Vivien Measday*,,1
* Michael Smith Laboratories, University of British Columbia, Vancouver, British Columbia V6T 1Z4, Canada, Wine Research Centre, University of British Columbia, Vancouver, British Columbia V6T 1Z4, Canada and Department of Medical Genetics and Microbiology, University of Toronto, Toronto, Ontario M5S 1A8, Canada
1 Corresponding author: Room 325, Wine Research Centre, 2205 East Mall, University of British Columbia, Vancouver, BC V6T 1Z4, Canada.
E-mail: vmeasday{at}interchange.ubc.ca
The maintenance of genome stability is a fundamental requirement for normal cell cycle progression. The budding yeast Saccharomyces cerevisiae is an excellent model to study chromosome maintenance due to its well-defined centromere and kinetochore, the region of the chromosome and associated protein complex, respectively, that link chromosomes to microtubules. To identify genes that are linked to chromosome stability, we performed genome-wide synthetic lethal screens using a series of novel temperature-sensitive mutations in genes encoding a central and outer kinetochore protein. By performing the screens using different mutant alleles of each gene, we aimed to identify genetic interactions that revealed diverse pathways affecting chromosome stability. Our study, which is the first example of genome-wide synthetic lethal screening with multiple alleles of a single gene, demonstrates that functionally distinct mutants uncover different cellular processes required for chromosome maintenance. Two of our screens identified APQ12, which encodes a nuclear envelope protein that is required for proper nucleocytoplasmic transport of mRNA. We find that apq12 mutants are delayed in anaphase, rereplicate their DNA, and rebud prior to completion of cytokinesis, suggesting a defect in controlling mitotic progression. Our analysis reveals a novel relationship between nucleocytoplasmic transport and chromosome stability.
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