Date Approved

2015

Date Posted

7-22-2015

Degree Type

Campus Only Senior Honors Thesis

Department

Biology

First Advisor

Anne Casper

Second Advisor

Aaron Liepman

Abstract

Common fragile sites (CFSs) are specific loci on chromosomes that display instability when exposed to conditions of replication stress. CFSs are associated with the deletion of tumor suppressor genes and the amplification of oncogenes. There are multiple hypotheses to explain CFS instability. One such hypothesis could be supported by flexibility peaks. Flexibility peaks are AT-rich sequence motifs that are hypothesized to instigate breaks in human CFSs. It has been shown that breaks at a yeast fragile site stimulate repair through homologous recombination events that lead to loss of heterozygosity. Here, we have examined whether a flexibility peak found in human CFS FRA3B stimulates homologous recombination events that lead to loss of heterozygosity when inserted onto a chromosome of the yeast Saccharomyces cerevisiae. Overall, it does not appear that the inserted human CFS flexibility peak induces homologous recombination events in yeast. These results may indicate that sequence related factors are not as important to chromosome breakage as contextual factors such as a lack of origins of replication.

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