Meeting Abstract
Transposable elements (TE) are obligate genetic parasites that guarantee transmission to offspring by replicating in the nuclei of germline cells. TE replication harms hosts by causing DNA damage and deleterious mutations that prevent the production of viable gametes. In response, hosts can employ two different strategies to minimize these effects: resistance and tolerance. Resistance mechanisms prevent TE replication, while tolerance mechanisms allow host cells to withstand the damaging effects of TE activity. However, cellular mechanisms of tolerance remain largely unknown. P-elements are a type TE whose transposition causes damage to the Drosophila germline. We recently identified the bruno gene as a possible source of natural variation in tolerance of D. melanogaster females to P-element transposition. bruno loss of function alleles are strong suppressors of P-element-induced germline loss, but bruno has no known function in TE regulation. To conclusively evaluate the extent to which bruno regulates P-element transposition, and attempt to confirm its role as a tolerance factor, we are comparing P-element expression and excision rates between bruno mutants and wild-type flies. If P-element transposition is independent of bruno, then expression and excision should not differ between bruno genotypes. Alternatively, if expression and excision are reduced in mutants when compared to wild-type, it will suggest that bruno influences germline loss by positively-regulating P-element activity.
