Although Piwi proteins and Piwi-interacting RNAs (piRNAs) genetically repress 
transposable elements (TEs), it is unclear how the highly diverse piRNA 
populations direct Piwi proteins to silence TE targets without silencing the 
entire transcriptome. To determine the capacity of piRNA-mediated silencing, we 
introduced reporter genes into Drosophila OSS cells, which express microRNAs 
(miRNAs) and piRNAs, and compared the Piwi pathway to the Argonaute pathway in 
gene regulation. Reporter constructs containing several target sites that were 
robustly silenced by miRNAs were not silenced to the same degrees by piRNAs. 
However, another set of reporters we designed to enable a large number of both 
TE-directed and genic piRNAs to bind were robustly silenced by the PIWI/piRNA 
complex in OSS cells. These reporters show that a bulk of piRNAs are required to 
pair to the reporter's transcripts and not the reporter's DNA sequence to engage 
PIWI-mediated silencing. Following our genome-wide study of PIWI-regulated 
targets in OSS cells, we assessed candidate gene elements with our reporter 
platform. These results suggest TE sequences are the most direct of PIWI 
regulatory targets while coding genes are less directly affected by PIWI 
targeting. Finally, our study suggests that the PIWI transcriptional silencing 
mechanism triggers robust chromatin changes on targets with sufficient piRNA 
binding, and preferentially regulates TE transcripts because protein-coding 
transcripts lack a threshold of targeting by piRNA populations. This reporter 
platform will facilitate future dissections of the PIWI-targeting mechanism.