miRNA expression in E18.5 murine total lung tissue

Knockout of the ubiquitously expressed microRNA-17~92 cluster in mice produces a lethal developmental lung defect. We validated the equally widely expressed pro-apoptotic Bim gene as joint target of miR-17~92 cluster members. To study the contribution of miR-17~92:Bim interaction to miR-17~92 overall function, we set up a system of conditional mutagenesis of the Bim 3’UTR. Blocking miR-17~92:Bim interaction early in development phenocopied the lethal lung phenotype of miR-17~92 ablation. Thus, despite hundreds of overall predicted targets vital miRNA functions can be mediated by a single target gene. Total RNA was extracted from 5 wild type and 4 Bim3'UTRmut/mut E18.5 total lung tissues. 100 ng of total RNA per sample was used as input for nCounter gene expression analysis (NanoString Technologies).