Neurite and synapse pruning are conserved mechanisms that adapt neuronal circuitry to different developmental stages. Drosophila sensory c4da neurons prune their larval dendrites and their presynaptic terminals during metamorphosis using a gene expression programme that is induced by the steroid hormone ecdysone and involves posttranscriptional regulation pathways. Here we show that loss of the helicase UAP56, an important mediator of nuclear mRNA export, causes strong dendrite and presynapse pruning defects. Loss of UAP56 is linked to actin regulation, as it causes defects in the ecdysone-induced expression of the actin severing enzyme Mical during metamorphosis and actin accumulation at pruning presynapses. In support of an important role of actin regulation during presynaptic pruning, we find that cofilin is required for this process. Our findings highlight the role of posttranscriptional regulation in neuronal remodeling and identify an actin disassembly factor required for presynapse pruning.
Frommeyer et al. (Fri,) studied this question.