Abstract
In Drosophila gonads, transposable elements (TEs) are repressed by the Piwi-interacting RNA (piRNA) pathway operating both co-transcriptionally and post-transcriptionally. In the non-gonadal tissues, TEs are mainly repressed by the short interfering RNA (siRNA) pathway with Argonaute 2 (Ago2) functioning as an effector protein. It is generally assumed that this pathway acts at the post-transcriptional level. However, recent data point to its possible involvement in co-transcriptional silencing as well. Here, using DamID, we found a drastic decrease in HP1a on TEs (especially on the LTR-containing retrotransposons) and other heterochromatin regions in Ago2-mutant Drosophila brain. HP1a reduction is accompanied by the increased chromatin accessibility of TEs, indicating their derepression. Accordingly, several LTR-containing retrotransposons were up-regulated in the larval brain of Ago2 mutants. Moreover, upon the knock-down of lamin Dm0 in neurons, HP1a was increased predominantly on the same set of TEs that had reduced HP1a binding in Ago2 mutants. We hypothesize that, since Ago2 was localized to the common complex with lamin Dm0, the depletion of the latter may release Ago2 in the nucleoplasm, thus enhancing the recruitment of HP1a on TEs. Our findings support the hypothesis that TEs in the Drosophila brain are silenced, in part, through Ago2-mediated recruitment of HP1a.
