Identification of double-stranded RNAs modulated by ADAR1

Endogenous double-stranded RNA (dsRNA) triggers pro-inflammatory signaling and has been shown to accumulate in Alzheimer's disease (AD), but the origins of this dsRNA are incompletely understood. Transposable elements (TEs), which are non-coding DNA sequences capable of forming dsRNA, are a potential endogenous source of dsRNA in AD. We generated dsRNA immunoprecipitation (J2 dsRNA antibody) data on astrocytes treated with or without a siRNA to knock down the dsRNA editing enzyme ADAR1. We analyzed TE transcripts enriched in dsRNA pools when ADAR1 was knocked down, and we identified putative dsRNA-prone TEs, which were also present in secondary analyses of datasets profiling RNAs bound to PKR, MDA5, and the p110 isoform of ADAR1. Overall design: RNA-seq of J2 immunoprecipitated RNAs (RIP), and control RNAs (input), in ADAR1 and scramble siRNA treated primary human astrocytes