in human iPSC-derived neuronal progenitors affected ANK3 and CACNB3 mRNA and protein expression and resulted in defects in neuronal differentiation as measured morphologically and biochemically through analysis of pre- and post-synaptic markers. Conversely, suppression of miR-34a expression enhanced dendritogenesis. Expanded profiling of the consequence of miR-34a overexpression revealed effects on a number of additional genes critical to neurodevelopment and implicated in the etiology of BD by recent human genetic studies16, 30. Taken together, our data highlight miR-34a as an important miRNA for BD and expand the knowledge on its effects on neuronal development.
