Neuronal polarization is facilitated by the formation of axons with parallel arrays of plus-end-out and dendrites with the nonuniform orientation of microtubules. In C. elegans, the posterior lateral microtubule (PLM) neuron is bipolar with its two processes growing along the anterior–posterior axis under the guidance of Wnt signaling. Here we found that loss of the Kinesin-13 family microtubule-depolymerizing enzyme KLP-7 led to the ectopic extension of axon-like processes from the PLM cell body. Live imaging of the microtubules and axonal transport revealed mixed polarity of the microtubules in the short posterior process, which is dependent on both KLP-7 and the minus-end binding protein PTRN-1. KLP-7 is positively regulated in the posterior process by planar cell polarity components of Wnt involving rho-1/rock to induce mixed polarity of microtubules, whereas it is negatively regulated in the anterior process by the unc-73/ced-10 cascade to establish a uniform microtubule polarity. Our work elucidates how evolutionarily conserved Wnt signaling establishes the microtubule polarity in neurons through Kinesin-13.

中文翻译：

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Wnt 信号传导通过调节 Kinesin-13 建立神经元中的微管极性

具有正端输出平行阵列的轴突和具有不均匀方向微管的树突的形成促进了神经元极化。在线虫中，后外侧微管（PLM）神经元是双极的，其两个突起在 Wnt 信号传导的引导下沿前后轴生长。在这里，我们发现，Kinesin-13 家族微管解聚酶 KLP-7 的缺失导致 PLM 细胞体中轴突样突起的异位延伸。微管和轴突运输的实时成像揭示了短后突中微管的混合极性，这取决于 KLP-7 和负端结合蛋白 PTRN-1。KLP-7 在后部过程中受到涉及 rho-1/rock 的 Wnt 平面细胞极性成分的正向调节，以诱导微管的混合极性，而在前部过程中则受到 unc-73/ced-10 级联的负向调节，从而诱导微管的混合极性。建立统一的微管极性。我们的工作阐明了进化上保守的 Wnt 信号如何通过 Kinesin-13 建立神经元中的微管极性。