The effect of BRCA2 mutation on female fertility in Drosophila
Jennifer Merrill*, Brenda Manzano Winkler, Mohamed Noor
*Corresponding author: Jennifer Merrill
The Ohio State University College of Medicine, Columbus, OH, USA
Department of Biology, Duke University, Durham, NC, USA
F1000Posters 2012, 3: 815 (poster) [English]
Poster [20.46 MB]
American Genetic Association Annual Symposium 2012, 14 - 16 Jul 2012, P000
BRCA1 and BRCA2 function in homologous meiotic recombination, and mutations in these genes cause human breast and ovarian cancer. Nonetheless, disruptive mutations in these genes are present at an unexpectedly high frequency in human populations. A recent study by Smith et al., suggested that BRCA1/2 mutations are maintained because they increase the early-life fertility of their carriers (1), however further study of this unexpected fitness advantage in humans is impeded by family planning strategies. Drosophila BRCA2 (dmbrca2) also functions in DNA repair by homologous recombination and interacts with Rad51, just like its human counterpart, and thus may experience similar selective pressures. We produced flies heterozygous for a BRCA2 knockout and compared fecundity to flies not bearing a mutation to test for a fitness advantage similar to that observed in humans.
In contrast to humans, Drosophila that are heterozygous for a P-element disruption of BRCA2 do not show increased numbers of eggs as compared to their wild-type counterparts, indicating that disruption of this gene does not confer a similar reproductive advantage across species.
No relevant competing interests disclosed.
National Institutes of Health (NIH), GM086445
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