The Effect of Hobo Transposon Excision on DNA repair in Drosophila melanogaster

Abstract

As the repository of genetic information, it is critical to organisms that DNA damage is repaired quickly and with high fidelity. When DNA damage is improperly repaired, it may cause diseases such as cancer and severe combined immunodeficiency. DNA can be mutated by numerous agents both external and internal. One internal source of DNA damage is from the transposition of transposable elements, including the P and hobo elements. Transposable elements “jump” out from one section of the DNA and reinsert into another, leaving double strand DNA breaks at the excision site. Hobo excisions are preferentially repaired by nonhomologous end‐joining, NHEJ. DNA repair and transposable elements themselves can be studied in Drosophila melanogaster. This study looked at the hobo on P, or HOP, element. The P element is located inside of the Hobo element; HOP8 is nonautonomous and needs hobo transposase to be supplied in trans. Curly winged, glazed eye female flies that have an inducible source of hobo transposase were crossed with HOP8 male flies and heat shocked to trigger transposition, leaving a double strand DNA break requiring repair behind. The resulting mosaic eyed male flies were then crossed with wild type female flies because mosaic eyes mark meiotic recombination in the P element. Female flies with white eyes indicating that hobo transposition occurred, were collected and stored in a freezer. Experiments are underway to determine the original location and new insertion sites of hobo using inverse PCR to further understand DNA repair.Support or Funding InformationAlbion College Foundation for Undergraduate Research, Scholarship, and Creative Activity (FURSCA)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.