Document Type

Honors Capstone Project

Date of Submission

Spring 5-1-2005

Capstone Advisor

Dr. Scott Erdman

Honors Reader

Dr. Melissa Pepling

Capstone Major

Biology

Capstone College

Arts and Science

Audio/Visual Component

no

Capstone Prize Winner

no

Won Capstone Funding

no

Honors Categories

Sciences and Engineering

Subject Categories

Biology

Abstract

In order for two haploid yeast cells to undergo normal fusion during mating, adhesive contacts are formed by a general class of fungal proteins termed “adhesins”. Within this family there is a subgroup of cell wall proteins termed “agglutinins” which are known to mediate aggregation, thereby increasing mating efficiency in liquid medium (Aga1p, Aga2p, Aga1p). In the absence of sufficient mating adhesive contacts we observed that cells undergo defective morphogenesis, apparently continuing to grow at their tips after fusing at the expense of laterally expanding their conjugation bridge. Based on these qualitative observations, I utilized differential interference microscopy to capture micrographs of mating cells of different mutants that lacked one or more of the yeast adhesin/agglutinin proteins Aga1p, Aga2p, Fig2p, and Agα1. From the micrographs collected, I determined the relative dimensions of the mating cells and analyzed them using various statistical methods. The study elucidated the necessity of these proteins for proper morphogenesis. In a related project I sought to identify cell wall genes whose inactivation led to deficiencies in mating when the mating partner lacked specific adhesins. Cell wall residency of the adhesins and the remodeling that the cell wall undergoes during cell-cell fusion are important and incompletely understood processes whose components might affect such crosses. I performed a large scale genomic screen of strains known to be defective in some aspect of cell wall organization. A collection of 170 cell wall mutant strains, each containing a replacement of a single yeast gene with a dominant drug resistance marker, was tested for mating deficiency in crosses to wild type and adhesion deficient partner strains. From this screen seven candidate gene mutations were identified that reproducibly satisfied the screen and hold promise for further study.

Creative Commons License

Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.

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