Gene manipulation combined with behavior analysis reveals a role of miR-9 in modulating basal-ganglia-dependent developmental vocal learning and adult vocal performance via regulating the FOXP1/FOXP2 gene network and dopamine signaling in songbirds.

During neurogenesis, Neurogenin 1 activates the microRNA miR-9, which directly targets the Jak-Stat pathway to inhibit astrogliogenesis.

Conditional transgenic miR-9 sponge mice exhibit developmental defects in dendrite growth due to up-regulation of the transcriptional repressor REST.

Stochasticity introduced computationally into a gene expression oscillator creates heterogeneity in the time of differentiation of identical cells and offers robustness to the progenitor state and the outcome of cell division.

The identification of SMA-miR supports the pathogenic role of skeletal muscle in spinal muscular atrophy and, integrated in the SMA-score, may help to improve the phenotypic prediction for patients.

Mir155 showed a catabolic effect on osteogenesis and bone mass phenotype via interaction with the S1pr1 gene, suggesting inhibition of Mir155 as a potential approach to bone regeneration and bone defect healing.

Primate-specific miR-934 mediates neurogenesis and downstream neuronal differentiation processes, modulating the expression of genes associated with the subplate, a region most prominent in primates, emerging during early cortical development.

microRNA-1 plays an essential role in the development and functioning of the heart by ensuring that genes for striated, rather than smooth, muscle are expressed there.

Coordinate control of lysosomal v-ATPase subunits and biogenesis factor TFEB by miR-1 identifies a key regulatory axis with strong links to age-related proteotoxic disease.

c-Maf is a novel key regulator of the type 3-to-1 conversion of CCR6^– ILC3s that controls the functional plasticity of ILC3s by acting as a cell-intrinsic gatekeeper of T-bet expression.