The DNA transposition system of hybrid dysgenesis inDrosophila melanogastercan function despite defects in host DNA repair

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Abstract
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.