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 expression of the actin severing enzyme Mical during dendrite pruning, and actin accumulation at presynapses, where cofilin is required for pruning. Our findings suggest specificity in mRNA export pathways and identify a role for actin disassembly during presynapse pruning.
Frommeyer et al. (Mon,) studied this question.