Germline silencing of transposable elements is essential for the maintenance of 
genome integrity. Recent results indicate that this repression is largely 
achieved through a RNA silencing pathway that involves Piwi-interacting RNAs 
(piRNAs). However the repressive mechanisms are not well understood. To address 
this question, we used the possibility to disrupt the repression of the 
Drosophila I element retrotransposon by hybrid dysgenesis. We show here that the 
repression of the functional I elements that are located in euchromatin requires 
proteins of the piRNA pathway, and that the amount of ovarian I element piRNAs 
correlates with the strength of the repression in the female germline. Antisense 
RNAs, which are likely used to produce antisense piRNAs, are transcribed by 
heterochromatic defective I elements, but efficient production of these 
antisense small RNAs requires the presence in the genome of euchromatic 
functional I elements. Finally, we demonstrate that the piRNA-induced silencing 
of the functional I elements is at least partially posttranscriptional. In a 
repressive background, these elements are still transcribed, but some of their 
sense transcripts are kept in nurse cell nuclear foci together with those of the 
Doc retrotransposon. In the absence of I element piRNAs, either in dysgenic 
females or in mutants of the piRNA silencing pathway, sense I element 
transcripts are transported toward the oocyte where retrotransposition occurs. 
Our results indicate that piRNAs are involved in a posttranscriptional 
gene-silencing mechanism resulting in RNA nuclear accumulation.