GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE80nnn/GSE80439/primaryOK2000000GenomicsMultiomicsMus musculus Rattus norvegicusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE80439GEOGSE0falsemiR-219 Cooperates with miR-338 in Myelination and Promotes Myelin Repair in the CNSmicroRNAs (miRNAs) have been implicated in oligodendrogenesis and demyelinating diseases; however, identification of individual miRNAs responsible has remained elusive. Through targeted mutagenesis, we find that miR-219 is required for proper oligodendrocyte differentiation and myelination in vivo. Deletion of miR-338 together with miR-219 further exacerbates hypomyelination phenotypes. Temporally specific ablation reveals a critical role for miR-219 in oligodendrocyte remyelination after demyelination, while overexpression of miR-219 promotes precocious oligodendrocyte maturation and myelin regeneration. Accordingly, administration of miR-219 mimics to lysolecithin-induced demyelinating lesions in the murine spinal cord and brain enhances myelin restoration. Through integrating analyses of transcriptome profiling and biotin-affinity miRNA pull-down, we identify a set of stage-specific targets of miR-219, including Etv5 and Lingo1, as oligodendrocyte differentiation inhibitors. Inhibiting Etv5 and Lingo1 leads to a partial rescue of differentiation defects observed in miR-219-mutant OLs in vitro. Together, our findings identify context-specific miRNA-regulated checkpoints that control CNS myelinogenesis and myelin repair.2017/04/21GSE80439GSM2127368GSM2127379GSM2127369GSM2127371GSM2127372GSM2127373GSM2127374GSM2127375GSM2127376GSM2127377GSM2127378GSM2127380GSM2127370GSM21273811311214844SRP07349980439Mus musculus Rattus norvegicus[28350989]