Document Type

Honors Thesis

Publication Date

Spring 5-2017

Abstract

The yeast Saccharomyces cerevisiae uses a GPCR to direct the pheromone response pathway. Haploid yeast detect and respond to pheromone gradients produced by the opposite mating type to find a mating partner. At a high dose of pheromone, yeast will form a short, focused mating projection in order to mate with yeast that are close by. At lower doses of pheromone, the yeast form a broader projection which grows towards the source of pheromone. The pheromone is detected by a GPCR, Ste2, which activates the Gα, Gpa1, initiating the production of new gene products for mating, and polarizes the cytoskeleton in the direction of the source of the pheromone, facilitating gradient tracking. Cells expressing a mutant Gα are unable to track a gradient of pheromone. They also exhibit a broader projection than wild type cells, and reorient their polarity frequently, without regard for the gradient of pheromone. Evidence suggests that actin distribution may be affected. Actin polymerization is promoted by formins when bound by active Cdc42. Yeast have two formins, Bnr1 and Bni1 that are thought of as genetically redundant proteins, because the deletion of either protein does not lead to arrest of cell division. While they have functional overlap, other evidence suggests their functions are distinct. During mitosis, Bnr1 associates with the bud neck, while Bni1 associates with the polar cap in the emerging bud. We hypothesize that this hyperactive mutant Gα is able to direct more Bni1 to a larger area of the plasma membrane. If this were to happen, we predict the cell would then be able to polymerize actin cables to a broader area, resulting in a less focused polarized growth and the observed gradient tracking defects.

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