DETECTIVE-I ELEMENTS INTRODUCED INTO DROSOPHILA AS TRANSGENES CAN REGULATE REACTIVITY AND PREVENT I-R-HYBRID DYSGENESIS

The I-R hybrid dysgenesis syndrome is characterized by a high level of sterility and I element transposition, occurring in the female offspr ing of crosses between males of inducer (I) strains, which contain ful l-length transposable I elements, and females of reactive (R) strains, devoid of functional I elements. The intensity of the syndrome in the dysgenic cross is essentially dependent on the reactivity level of th e R females, which is ultimately controlled by still unresolved polyge nic chromosomal determinants. In the work reported here, we have intro duced a transposition-defective I element with a 2.6 kb deletion withi n its second open reading frame into a highly reactive R strain, by P- mediated transgenesis. We demonstrate that this defective I element gr adually alters the level of reactivity in the three independent transg enic lines that were obtained, over several generations. After > 15 ge nerations, the transgenic Drosophila show strongly reduced reactivity, and finally become refractory to hybrid dysgenesis, without, however, acquiring the inducer phenotype. Induction of a low reactivity level is reversible - reactivity again increases upon transgene removal - an d is maternally inherited, as observed for the control of reactivity i n natural R strains. These results demonstrate that defective I elemen ts introduced as single-copy transgenes can act as regulators of react ivity, and suggest that some of the ancestral defective pericentromeri c I elements that can be found in all reactive strains could be the mo lecular determinants of reactivity.