Date Approved

7-25-2014

Date Posted

11-4-2014

Degree Type

Open Access Thesis

Degree Name

Master of Science (MS)

Department

Biology

Committee Member

Dr. Anne Casper, Ph.D, Chair

Committee Member

Dr. Aaron Liepman, Ph.D

Committee Member

Dr. Jim VandenBosch, Ph.D

Abstract

Common fragile sites (CFS) are areas of the genome that tend to break when DNA replication is stressed or partially inhibited. Breaks at CFS can lead to gene deletions and amplifications that can result in the genesis of cancer cells. There is controversy about the mechanism of CFS instability. This study examines whether an AT-rich sequence called a flexibility peak from FRA16D can induce mitotic recombination events that lead to loss of heterozygosity (LOH) on chromosome III in Saccharomyces cerevisiae. Two experimental yeast strains containing flexibility peak Flex1-(AT)15 from FRA16D were compared to a control strain lacking the Flex1 sequence in their ability to induce mitotic recombination events, such as reciprocal crossovers (RCOs), break-induced replication (BIR), and chromosome loss. Overall, Flex1 does not appear to act as a hotspot for mitotic recombination. Contextual features may be more important factors in the instability of FRA16D.

Included in

Biology Commons

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