Date Approved

2016

Date Posted

4-27-2016

Degree Type

Open Access Senior Honors Thesis

Department

Biology

First Advisor

Dr. Anne Casper

Second Advisor

Aaron Liepman

Abstract

Common fragile sites are regions of the genome prone to gaps and breakage under replication stress. Repair of breaks at CFS can occur through homologous recombination. yet may lead to loss of heterozygosity (LOH) events that manifest themselves as gene conversions. Gene conversions associated with LOH have the potential to deactivate tumor suppressor genes, driving tumor progression. Using the yeast model, Saccharomyces cerevisiae, evidence of two types of gene conversions has emerged: short-tract and long-tract gene conversions. Gene conversion maps show a high frequency of short-tract gene conversions ending near or at the SUP4-o tRNA, in yeast strain Y657 that contains SUP4-o. We hypothesized that termination of these tracts is due to replication fork pause sites created by SUP4-o. We find the 2% difference in frequency of terminations between Y657, and our experimental yeast strain that contains SUP4-o, AMC355, does not provide statistical support for our hypothesis of SUP4-o causing termination of gene conversion tracts. We see that gene conversions near SUP4-o vary in their tract length. These gene conversions have implications for possible LOH after repair at fragile sites and may contribute to cancer progression.

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