To remodel functional neuronal connectivity, neurons often alter dendrite arbors through elimination and subsequent regeneration of dendritic branches. However, the intrinsic mechanisms underlying this developmentally programmed dendrite regeneration and whether it shares common machinery with injury-induced regeneration remain largely unknown. Drosophila class IV dendrite arborization (C4da) sensory neurons regenerate adult-specific dendrites after eliminating larval dendrites during metamorphosis. Here we show that the microRNA miR-87 is a critical regulator of dendrite regeneration in Drosophila. miR-87 knockout impairs dendrite regeneration after developmentally-programmed pruning, whereas miR-87 overexpression in C4da neurons leads to precocious initiation of dendrite regeneration. Genetic analyses indicate that the transcriptional repressor Tramtrack69 (Ttk69) is a functional target for miR-87-mediated repression as ttk69 expression is increased in miR-87 knockout neurons and reducing ttk69 expression restores dendrite regeneration to mutants lacking miR-87 function. We further show that miR-87 is required for dendrite regeneration after acute injury in the larval stage, providing a mechanistic link between developmentally programmed and injury-induced dendrite regeneration. These findings thus indicate that miR-87 promotes dendrite regrowth during regeneration at least in part through suppressing Ttk69 in Drosophila sensory neurons and suggest that developmental and injury-induced dendrite regeneration share a common intrinsic mechanism to reactivate dendrite growth.

为了重塑功能性神经元连通性，神经元通常通过消除和随后再生树突分支来改变树突状乔木。然而，这种发育程序化的枝晶再生的基本内在机制以及它是否与损伤诱导的再生共享共同的机制仍然未知。果蝇类IV树突乔木（C4da）感觉神经元消除变态期间的幼虫树突后，重新生成成人特定的树突。在这里，我们显示microRNA miR-87是果蝇中树突再生的关键调节剂。miR-87基因敲除削弱了发育程序修剪后的枝晶再生，而miR-87C4da神经元的过度表达导致早熟的树突再生。遗传分析表明，转录阻遏物Tramtrack69（Ttk69）是miR-87介导的阻遏的功能靶标，因为ttk69在miR-87敲除神经元中的表达增加，而ttk69表达的降低将树突再生恢复为缺乏miR-87功能的突变体。我们进一步表明，在幼虫期急性损伤后，树突再生需要miR-87，这在发育程序化和损伤诱导的树突再生之间提供了机械联系。这些发现因此表明miR-87通过抑制果蝇感觉神经元中的Ttk69至少在一定程度上促进了树突再生，并表明发育和损伤诱导的树突再生具有共同的内在机制来重新激活树突生长。