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Transposable elements (TE) are selfish genetic elements that can cause harmful mutations. InDrosophila, it has been estimated that half of all spontaneous visible marker phenotypes are mutations caused by TE insertions. Because of the harm posed by TEs, eukaryotes have evolved systems of small RNA-based genome defense to limit transposition. However, as in all immune systems, there is a cost of autoimmunity and small RNA-based systems that silence TEs can inadvertently silence genes flanking TE insertions. In a screen for essential meiotic genes inDrosophila melanogaster, a truncatedDocretrotransposon within a neighboring gene was found to trigger the germline silencing ofald, theDrosophila Mps1homolog, a gene essential for meiosis. A subsequent screen for modifiers of this silencing identified a new insertion of aHoboDNA transposon in the same neighboring gene. Here we describe how the originalDocinsertion triggers flanking piRNA biogenesis and local gene silencing and how the additionalHoboinsertion leads to de-silencing by reducing flanking piRNA biogenesis triggered by the originalDocinsertion. These results support a model of TE-mediated silencing by piRNA biogenesis incisthat depends on local determinants of transcription. This may explain complex patterns of off-target gene silencing triggered by TEs within populations and in the laboratory. It also provides a mechanism of sign epistasis among TE insertions.Author SummaryTransposable elements (TEs) are selfish DNA elements that can move through genomes and cause mutation. In some species, the vast majority of DNA is composed of this form of selfish DNA. Because TEs can be harmful, systems of genome immunity based on small RNA have evolved to limit the movement of TEs. However, like all systems of immunity, it can be challenging for the host to distinguish self from non-self. Thus, TE insertions occasionally cause the small RNA silencing machinery to turn off the expression of critical genes. The rules by which this inadvertent form of autoimmunity causes gene silencing are not well understood. In this article, we describe a phenomenon whereby a TE insertion, rather than silencing a nearby gene, rescues the silencing of a gene caused by another TE insertion. This reveals a mode of TE interactionviasmall RNA silencing that may be important for understanding how TEs exert their effects on gene expression in populations and across species. |
