Lack of association between piRNA abundance and the deleterious capacity of transposable element families in Drosophila melanogaster. Erin S. Kelleher, Daniel A. Barbash. Molecular Biology and Genetics, Cornell University, Ithaca, NY.

   Transposable elements (TEs) are genomic parasites whose selfish propagation can disrupt functional sequences, and in extreme cases is associated with sterility and cancer. Homologous TE insertions further threaten genome integrity by acting as substrates for ectopic recombination. The piRNA pathway defends animal genomes against the harmful consequences of TE infection by imposing small-RNA mediated silencing, predominantly in the germline. Because silencing is targeted by TE-derived piRNAs, piRNA production is posited to be central to the evolution of genome defense.
   We harnessed genomic data sets from Drosophila melanogaster, including measures of piRNA, mRNA, and genome-wide abundance of TE families, along with estimates of TE-family age structure and risk of ectopic recombination, to address fundamental questions about the functional and evolutionary relationships between TE families and their regulatory piRNAs. We demonstrate that TE transcription, the degree of participation in the "ping-pong" cycle, and the number of insertions in piRNA clusters together explain the majority of variation in piRNA abundance between TE families. These results provide the first robust statistical support for the prevailing model of piRNA production. Intriguingly however, we discover that the most transpositionally active TE families, with the greatest capacity to induce harmful mutations or disrupt gametogenesis, are not necessarily the most abundant in the piRNA pool. Additionally, we find no evidence that piRNA abundance responds to selection against ectopic recombination. Our observations reveal that the deleterious capacity of a TE family is not associated with piRNA abundance, and point to more complex models of host adaptation to TE infection.