Abstract
Saccharomyces cerevisiae cells lacking the SEP1 (also known as XRN1, KEM1, DST2, RAR5) gene function exhibit a number of phenotypes in cellular processes related to microtubule function. Mutant cells show increased sensitivity to the microtubule-destabilizing drug benomyl, increased chromosome loss, a karyogamy defect, impaired spindle pole body separation, and defective nuclear migration towards the bud neck. Analysis of the arrest morphology and of the survival during arrest strongly suggests a structural defect accounting for the benomyl hypersensitivity, rather than a regulatory defect in a checkpoint. Biochemical analysis of the purified Sep1 protein demonstrates its ability to promote the polymerization of porcine brain and authentic S. cerevisiae tubulin into flexible microtubules in vitro. Furthermore, Sep1 co-sediments with these microtubules in sucrose cushion centrifugation. Genetic analysis of double mutant strains containing a mutation in SEP1 and in one of the genes coding for α- or β-tubulin further suggests interaction between Sep1 and microtubules. Taken together these three lines of evidence constitute compelling evidence for a role of Sep1 as an accessory protein in microtubule function in the yeast S. cerevisiae.
Original language | English (US) |
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Pages (from-to) | 1057-1066 |
Number of pages | 10 |
Journal | EMBO Journal |
Volume | 14 |
Issue number | 6 |
State | Published - 1995 |
Externally published | Yes |
Keywords
- Benomyl
- MAP
- Spindle pole body
- Tubulin
- Yeast
ASJC Scopus subject areas
- Cell Biology
- Genetics