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首页> 外文期刊>Neuron >Branch-Specific Microtubule Destabilization Mediates Axon Branch Loss during Neuromuscular Synapse Elimination
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Branch-Specific Microtubule Destabilization Mediates Axon Branch Loss during Neuromuscular Synapse Elimination

机译：特定于分支的微管去稳定介导神经肌肉突触消除过程中轴突分支损失。

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摘要

Developmental axon remodeling is characterized by the selective removal of branches from axon arbors. The mechanisms that underlie such branch loss are largely unknown. Additionally, how neuronal resources are specifically assigned to the branches of remodeling arbors is not understood. Here we show that axon branch loss at the developing mouse neuromuscular junction is mediated by branch-specific microtubule severing, which results in local disassembly of the microtubule cytoskeleton and loss of axonal transport in branches that will subsequently dismantle. Accordingly, pharmacological microtubule stabilization delays neuromuscular synapse elimination. This branch-specific disassembly of the cytoskeleton appears to be mediated by the microtubule-severing enzyme spastin, which is dysfunctional in some forms of upper motor neuron disease. Our results demonstrate a physiological role for a neurodegeneration-associated modulator of the cytoskeleton, reveal unexpected cell biology of branch-specific axon plasticity and underscore the mechanistic similarities of axon loss in development and disease.
机译：发育中的轴突重塑的特征在于从轴突柄上选择性除去分支。造成这种分支丢失的机制在很大程度上尚不清楚。此外，还不清楚如何将神经元资源专门分配给重塑乔木的分支。在这里，我们显示在发展中的小鼠神经肌肉接头处的轴突分支丢失是由分支特异性微管切断介导的，这导致微管细胞骨架的局部拆卸和分支中轴突运输的丢失，随后将其拆除。因此，药理学微管稳定化延迟了神经肌肉突触的消除。细胞骨架的这种分支特异性拆卸似乎是由微管切割酶spastin介导的，spastin在某些形式的上运动神经元疾病中是功能失调的。我们的结果证明了神经退行性相关的细胞骨架调节剂的生理作用，揭示了分支特异性轴突可塑性的出乎意料的细胞生物学，并强调了轴突丧失在发育和疾病中的机制相似性。

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