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SEC3 mutations are synthetically lethal with profilin mutations and cause defects in diploid-specific bud-site
B K Haarer1, A Corbett, Y Kweon
1Department of Anatomy and Cell Biology, University of Michigan, Ann Arbor 48109, USA. haarer@mail.utexas.edu
Genetics
|October 1, 1996
Summary
Mutating the yeast profilin gene (PFY1) revealed synthetic lethal mutations impacting cell growth. These mutations highlight the crucial role of the secretory pathway in maintaining cell polarity, especially in diploid yeast cells.
Area of Science:
- Cell Biology
- Molecular Genetics
- Yeast Genetics
Background:
- Yeast profilin (PFY1) plays a role in actin cytoskeleton organization.
- Mutations in PFY1 can cause cellular defects, but the full genetic interactions are not well understood.
- Understanding these interactions can shed light on fundamental cellular processes like polarity and secretion.
Purpose of the Study:
- To identify genes that are synthetically lethal with a specific mutation in the yeast profilin gene (pfy1-111).
- To investigate the cellular functions of these synthetic lethal genes, particularly their role in cell polarity and growth.
- To explore the relationship between the actin cytoskeleton and the secretory pathway in yeast.
Main Methods:
- Utilized a colony color-sectoring assay to screen for mutations synthetically lethal with pfy1-111.
- Phenotypic analysis of identified synthetic lethal mutations, including growth, morphology, and temperature sensitivity.
- Genetic characterization of the PSL1 gene, identified as SEC3, and its interaction with pfy1-111.
Main Results:
- Identified several 'profilin synthetic lethal' (psl) mutations that are lethal in combination with pfy1-111 but not with wild-type PFY1.
- The psl1 mutation, identified as the late secretory gene SEC3, caused a diploid-specific defect in bud-site selection.
- Mutations in other late secretory genes were also found to be synthetically lethal with pfy1-111, suggesting a broader interaction.
- Haploid cells with psl mutations budded normally, while homozygous diploid cells exhibited random budding.
Conclusions:
- There is an interdependence between the actin cytoskeleton and secretory processes in directing cell polarity and growth in yeast.
- The secretory pathway is particularly critical for maintaining budding polarity in diploid yeast cells.
- Profilin and the secretory pathway (specifically SEC3) interact genetically to ensure proper cell division and polarity.