DNA was stained with DAPI (blue). defense mechanism against viruses that can generate double-stranded RNA (dsRNA). Long dsRNA is processed by a ribonuclease Ecscr enzyme, Dicer, into small interfering RNAs (siRNAs), guiding degradation of homologous mRNA (1). This mechanism was adapted to control the expression and transposition of endogenous transposable elements in different organisms (212). A distinct class of short RNAs, repeat associated short interfering RNAs (rasiRNAs), 2427 nt long, is Bosentan involved in the silencing of retrotransposons in theDrosophilagerm line (13). Importantly, rasiRNA production does not require processing of a dsRNA precursor by Dicer, a key enzyme for microRNA and siRNA production (13). Sense and antisense rasiRNAs specific to different classes of retrotransposons, long terminal repeat (LTR) and non-LTR elements are revealed in libraries of short RNAs (12,14) and by northern analysis (15,16). Although the mechanism of rasiRNA processing still remains unclear, it is obvious that antisense transcripts are important participants in this process. First of all, antisense transcripts of transposable elements serve as a source for rasiRNA generation. A certain amount of rasiRNA is produced from heterochromatic loci enriched in damaged inactive copies of transposable elements (11,12). These small RNAs are believed to originate from a putative long, single-stranded precursor. Theflamenco/COMlocus has been shown to regulate the activity of the retroviralgypsyelement (17) and two other retroelements,IdefixandZAM(18). rasiRNAs originating from theflamencolocus are proposed to control the activities ofIdefix, ZAMandgypsyretrotransposons in theDrosophilagermline (12). Similar orientation of the copies of these elements in theflamencolocus results in the production of mainly antisense rasiRNAs. Some other describedDrosophilaand mouse loci generate small RNAs from both strands as a result of mixed orientations of transposable elements within the loci (11,12). Primary short RNAs guide the generation of additional short RNAs of both polarities. According to the ping-pong amplification model, sense rasiRNAs result from the processing of long sense transcripts with the assistance of PIWI- or Aubergine (Aub)-associated antisense rasiRNAs and sense rasiRNAs in the complex with Bosentan Ago3 guide the cleavage of antisense transcripts to produce additional antisense rasiRNAs (12,19). Being either the primary source of rasiRNA production or the template for subsequent amplification, antisense transcripts are apparently necessary for the RNA silencing process. Antisense transcripts of transposable elements can be generated in different ways. They may be derived from read-through transcription from an adjacent external promoter, which has been documented, Bosentan for example, in theCaenorhabditis eleganstransposon Tc1 (4). Several examples of retrotransposon antisense internal promoters were described, although their functional significance is unclear. A testis-specific antisense promoter of the LTR retrotransposonmicropiainDrosophila hydeidrives expression of the transcript complementary to the reverse transcriptase open reading frame (ORF) (20). Antisense promoters located in the 5 untranslated region (UTR) downstream of the sense transcription start site are found in the human non-LTR elements L1 (2123) and theDrosophilaF-element (24). Antisense L1-specific short RNAs complementary to the region of overlapping transcripts were shown to contribute significantly to the RNAi-mediated silencing of L1 (25). Additionally, theChlamydomonas reinhardiielement TOC1 (26), theTripanosoma bruceiretroelement TRS (27) and theDictyostelium discoideumretroelement DRE (28) are transcribed in both directions. These data suggest multiple sources for transposon-specific antisense RNA origination. TheHeT-A,TARTandTAHREfamilies ofDrosophilanon-LTR retrotransposons play important roles in the cell, providing telomere repair (2932). Telomeres inDrosophilaare maintained by transpositions.