Antisense Transcription of Retrotransposons in XXXX : The Origin of Endogenous Small Interfering RNA Precursors.

@entity5427 @entity32289 @entity238
UNASSIGNED: Movement of transposons causes insertions, deletions and chromosomal rearrangements potentially leading to pre-mature lethality in @entity238 . To repress these elements and combat genomic instability, eukaryotes have evolved several small RNA mediated defense mechanisms. Specifically, in @entity238 somatic cells, endogenous small interfering (esi)RNAs suppress retrotransposon mobility. EsiRNAs are produced by @entity32289 processing of double-stranded RNA precursors, yet the origins of these precursors are unknown. We show that most transposon families are transcribed in both the sense and antisense direction in Dmel-2 cells. LTR retrotransposons Dm297, mdg1 and blood, and non-LTR retrotransposons juan and jockey transcripts are generated from intra element transcription start sites with canonical RNA polymerase II promoters. We also determined that retrotransposon antisense transcripts are less polyadenylated than sense transcripts, which may promote nuclear retention of antisense transcripts and the double-stranded RNAs they form. RNA-seq and small RNA-seq revealed that @entity32289 RNAi-depletion causes a decrease in the number of esiRNAs mapping to retrotransposons and an increase in expression of both S and @entity5427 retrotransposon transcripts. These data support a model in which double-stranded RNA precursors are derived from convergent transcription and processed by @entity32289 into esiRNAs that silence both sense and antisense retrotransposon transcripts. Reduction of sense retrotransposon transcripts potentially lowers element specific protein levels to prevent transposition. This mechanism preserves genomic integrity and is especially important for @entity238 fitness because mobile genetic elements are highly active.
