Kinetochores connect centromeric chromatin to spindle microtubules during mitosis. Neurons are post-mitotic, so it was surprising to identify transcripts of structural kinetochore (KT) proteins and regulatory chromosome passenger complex (CPC) and spindle assembly checkpoint (SAC) proteins in Drosophila neurons after dendrite injury. To test whether these proteins function during dendrite regeneration, post-mitotic RNAi was performed and dendrites or axons were removed using laser microsurgery. Reduction of KT, CPC and SAC proteins decreased dendrite regeneration without affecting axon regeneration. To understand whether neuronal functions of these proteins rely on microtubules, we analyzed microtubule behavior in uninjured neurons. The number of growing plus, but not minus, ends increased in dendrites with reduced KT, CPC and SAC proteins, while axonal microtubules were unaffected. Increased dendritic microtubule dynamics was independent of DLK-mediated stress, but was rescued by concurrent reduction of γTubulin, the core microtubule nucleation protein. Reduction of γTubulin also rescued dendrite regeneration in backgrounds containing kinetochore RNAi transgenes. We conclude that kinetochore proteins function post-mitotically in neurons to suppress dendritic microtubule dynamics by inhibiting nucleation.

在有丝分裂过程中，动粒将着丝粒染色质连接到纺锤体微管。神经元是有丝分裂后的，因此在果蝇中鉴定结构动粒 (KT) 蛋白和调节染色体乘客复合体 (CPC) 和纺锤体组装检查点 (SAC) 蛋白的转录本令人惊讶树突损伤后的神经元。为了测试这些蛋白质在树突再生过程中是否起作用，进行了有丝分裂后的 RNAi，并使用激光显微手术去除了树突或轴突。KT、CPC 和 SAC 蛋白的减少减少了树突再生而不影响轴突再生。为了了解这些蛋白质的神经元功能是否依赖于微管，我们分析了未受伤神经元中的微管行为。在 KT、CPC 和 SAC 蛋白减少的树突中，增长的正端（但不是负端）数量增加，而轴突微管不受影响。增加的树突微管动力学与 DLK 介导的压力无关，但可以通过同时减少 γ微管蛋白（核心微管成核蛋白）来挽救。在含有动粒 RNAi 转基因的背景中，γ微管蛋白的减少也挽救了树突再生。我们得出结论，动粒蛋白在神经元中有丝分裂后起作用，通过抑制成核来抑制树突微管动力学。