Repression of Hybrid Dysgenesis in Drosophila melanogaster by Heat-Shock-Inducible Sense and Antisense P-Element Constructs

Abstract

Sets of sense and antisense P-element constructs controlled by a heat-shock-inducible promoter were tested for their ability to repress manifestations of P-element activity in vivo. As a group, the antisense constructs repressed pupal lethality, a somatic manifestation of P activity, and this repression was significantly enhanced by heat shock. Three of the 11 antisense constructs also repressed gonadal dysgenesis, a manifestation of P activity in the female germ line; however, none had any effect on P-element-mediated mutability in the male germ line. Among the 13 different heat-shock-inducible sense constructs that were tested, those containing the KP and DP elements were strong repressors of pupal lethality, gonadal dysgenesis and P-element-mediated mutability; however, individual lines carrying these constructs varied in their ability to repress each of these traits, presumably because of genomic position effects. With the exception of the sense construct that contained a complete P element, none of the sense or antisense constructs repressed a lacZ reporter gene driven by the P-element promoter. Overall, the experimental results suggest that in nature, P-element activity could be regulated by P-encoded polypeptides and by antisense P RNAs.

DNA binding by the KP repressor protein inhibits P-element transposase activity in vitro

“…Instead, it is hypothesized that the SP element is inserted into a genomic location such that an antisense RNA is produced which is responsible for the observed repression. The antisense RNA model was investigated more thoroughly in vivo using a series of transgenic Drosophila lines carrying transgenes that encoded P‐element antisense RNA (Simmons et al ., 1996). These lines are able to repress transposition in vivo , which provides evidence that is consistent with the antisense RNA model of transpositional repression.…”