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MiRNA expression in Abelson virus transformed fetal liver B cell progenitors

ABSTRACT: Knockout of the ubiquitously expressed microRNA-17~92 cluster in mice produces a lethal developmental defect and blocked B lymphopoiesis. We validated the equally widely expressed Bcl2l11 gene as joint target of miR-17~92 cluster members. Bcl2l11 encodes the pro-apoptotic protein BIM, central to life-death decisions in most mammalian cells. 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 in the mouse. Blocking miR-17~92:Bim interaction early in development phenocopied the lethal developmental defect of miR-17~92 ablation. In contrast, hematopoietic and B lineage specific mutagenesis, while selectively compromising B lineage cell fitness, left hematopoietic cell compartments untouched as long as the cells expressed Bim biallelically. Thus, despite hundreds of overall predicted targets vital miRNA functions can be mediated by a single target gene, depending on cellular context and level of target gene expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE123672 | GEO | 2019/11/13

REPOSITORIES: GEO

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