GSE126041
Next generation sequencing of MA-10 mouse Leydig tumor cells facilitates quantitative analysis of SINE B2-antisense transcripts with the RNAi system: wild type and Dicer1-knockdown transcriptomes
We report the comparison between SINE B2-AS transcriptome profiling and Dicer1-deficient-cell transcriptome profiling using RNA-seq analysis. We report that thousands of SINE B2 copies encode long B2-AS transcripts, which are constantly degraded by Dicer1. This new class of B2-AS transcripts regulates the expression of SINE B2 sense (B2-S) transcripts. Long B2-S is the main cause of cellular toxicity likely mediated by the multifunctional protein TSPO. Some B2-AS transcripts are putative miRNAs interconnected with the RNAi system. We propose that B2-AS transcripts have evolved as a self-defense mechanism to subvert the host RNAi system. Overall design: Sequencing of SINE B2-AS specific transcripts and its comparison to the transcriptomes between Dicer1-deficienct cells vs. wild-type cells