Abstract
Transposable elements (TEs) are genomic parasites that propagate by exploiting its host reproductive machinery. However, some hosts have evolved the ability to silence TE activity, whereas others have not. We are investigating the population dynamics of TE host-silencing pathways, particularly copia long terminal repeat retrotransposon in Drosophila melanogaster. Here, we identify large effect genes involved in copia suppression by using a semi-quantitative analysis to assay levels of copia plasmids (believed to be an intermediate of transposition) in 98 recombinant inbred lines constructed from a line exhibiting high copia transpositions and a line exhibiting no transpositions. The results revealed that the influence of copia copy number and transcription level on copia plasmid concentrations are weak and that genomic factors, presumably encoded by the host, have stronger effects on transposition rates. We mapped a QTL affecting copia plasmid concentration within the 33A-43E cytological region of the second chromosome and applied a quantitative deficiency complementation analysis on this chromosomal region. One out of the two large effect deficiencies on copia plasmid concentrations corresponded to the vasa gene, an important component of the nuage-piwi RNA TE-silencing machinery. We hypothesize that copia suppression occurs by the joint action of several post-transcriptional mechanisms with at least one of the blocks taking place in the nuage.
