Abstract
Women with mutations in the human BRCA2 gene ( hBRCA2 ) have an increased risk of developing breast and ovarian cancer throughout their lifetime. hBRCA2 transcribes proteins necessary for gene repair through homologous recombination (HR). In order to better understand the role of hBRCA2 in response to specific types of DNA damage, the present study evaluated HR in the budding yeast, Saccharomyces cerevisiae , using wildtype (WT) and rad52Δ mutant cells subject to spontaneous and UV damage in the presence or absence of hBRCA2. As expected, rad52Δ genotypes yielded lower recombination frequencies compared to WT in both spontaneous and UV exposure experiments. However, there was no significant difference between rad52Δ mutants with or without hBRCA2. Interestingly, higher UV exposure resulted in a relative increase in HR for only the rad52Δ mutant genotypes. The results demonstrate that hBRCA2 complementation may not be as substantial in spontaneous or UV DNA damage compared to double-strand break DNA damage, as previous work has shown.