Accepted: A placental mammal-specific microRNA cluster acts as a natural brake for sociability in mice

Did you ever wonder how ncRNAs could influence behavior ?

Then, you would probably like to read on it in our new EMBO reports manuscript by

Lackinger, M., Sungur, A.Ö., Daswani, R., Soutschek, M., Bicker, S., Stemmler, L., Wüst, T., Fiore, R., Dieterich, C., Schwarting, R.K.W., Wöhr, M. and Schratt, G.

Aberrant synaptic function is thought to underlie social deficits in neurodevelopmental disorders such as autism and schizophrenia. microRNAs have been shown to regulate synapse development and plasticity, their potential involvement in the control of social behaviour in mammals however remains unexplored. Here we show that deletion of the large placental mammal-specific miR379-410 cluster in mice unexpectedly leads to hypersocial behaviour, which is accompanied by increased excitatory synaptic transmission and exaggerated expression of ionotropic glutamate receptor complexes in the hippocampus. Bioinformatics further allowed us to identify five “hub” microRNAs whose deletion accounts for a large part of the upregulation of excitatory synaptic genes, including Cnih2, Dlgap3, Prr7 and Src. Thus, miR379-410 is a natural brake for sociability and interfering with specific members of this cluster could represent a therapeutic strategy for social deficits in neurodevelopmental disorders.