I am utilizing flies with mutations in various DNA repair genes to increase the probability of isolating mutations in various genes following transposon excision and repair. Specifically, I am characterizing the DNA double-strand break repair defect in Drosophila mutants lacking the mus309 DNA helicase.  It appears that there is aberrant repair of an induced DSB in the absence of this helicase. The repair allows for either an increase in resection of the broken ends or an inability to repair resected DNA, thus leaving a much larger deletion at the break site.  My goal is to refine this technique as a useful way of generating mutations in genes of interest using the thousands of P, Minos, and Piggybac transposon lines that have been created.

I am also using zinc finger nuclease technology to generate targeted mutations in genes thought to be important in alternative double-strand break repair pathways.