The DNA transposition system of hybrid dysgenesis in Drosophila melanogaster can function despite defects in host DNA repair

Genetic traits associated with the hybrid dysgenesis syndrome were quantified in strains deficient in two major host-coded DNA repair pathways, post-replication and excision repair. A defect in either (or both) pathway(s) fails to influence the frequency of male recombination or sex-linked recessive lethal mutations associated with hybrid dysgenesis, suggesting that the DNA transposable elements associated with this syndrome act independently of these cellular functions. However, when the post-replication repair pathway is blocked, the recovery of second chromosomes containing factors associated with hybrid dysgenesis activity is reduced. The decrease in recovery is associated with zygotic lethality.