Date Approved

2020

Date Posted

2-16-2021

Degree Type

Open Access Thesis

Degree Name

Master of Science (MS)

Department

Biology

Committee Member

Anne Casper, Ph.D., Chair

Committee Member

Aaron Liepman, Ph.D.

Committee Member

Daniel Clemans, Ph.D.

Abstract

Exo1p is one enzyme that plays a role in the repair of breaks in DNA caused by a variety of intrinsic and extrinsic factors. In this study, we hypothesized the following: (1) Lack of Exo1p will cause an increase in de novo telomere addition at DNA breaks, and (2) lack of the endonuclease Exo1p will lead to decreased fidelity of repair by homologous recombination at DNA breaks. A yeast model system was manipulated to induce replication stress, resulting in a break in DNA at fragile site FS2 on yeast chromosome III. The repair mechanism used was identified, and the resulting genome was analyzed. We did not observe increased de novo telomere formation at FS2 or decreased fidelity of repair by homologous recombination in cells lacking Exo1p. We conclude that the functional redundancy between Exo1p and other enzymes is sufficient to compensate for the loss of Exo1p function in the cell.

Included in

Biology Commons

Share

COinS