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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Role of actin filaments in the axonal transport of microtubules.
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Role of actin filaments in the axonal transport of microtubules.

机译：肌动蛋白丝在微管的轴突运输中的作用。

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Microtubules originate at the centrosome of the neuron and are then released for transport down the axon, in which they can move both anterogradely and retrogradely during axonal growth. It has been hypothesized that these movements occur by force generation against the actin cytoskeleton. To test this, we analyzed the movement, distribution, and orientation of microtubules in neurons pharmacologically depleted of actin filaments. Actin depletion reduced but did not eliminate the anterograde movements and had no effect on the frequency of retrograde movements. Consistent with the idea that microtubules might also move against neighboring microtubules, actin depletion completely inhibited the outward transport of microtubules under experimental conditions of low microtubule density. Interestingly, visualization of microtubule assembly shows that actin depletion actually enhances the tendency of microtubules to align with one another. Such microtubule-microtubule interactions are sufficient to orient microtubules in their characteristic polarity pattern in axons grown overnight in the absence of actin filaments. In fact, microtubule behaviors were only chaotic after actin depletion in peripheral regions of the neuron in which microtubules are normally sparse and hence lack neighboring microtubules with which they could interact. On the basis of these results, we conclude that microtubules are transported against either actin filaments or neighboring microtubules in the anterograde direction but only against other microtubules in the retrograde direction. Moreover, the transport of microtubules against one another provides a surprisingly effective option for the deployment and orientation of microtubules in the absence of actin filaments.
机译：微管起源于神经元的中心体，然后释放下来沿轴突运输，在微管中，它们可以在轴突生长过程中顺行和逆行移动。已经假设这些运动是通过对肌动蛋白细胞骨架的力产生而发生的。为了测试这一点，我们分析了肌动蛋白丝在药理学上耗竭的神经元中微管的运动，分布和方向。肌动蛋白的消耗减少但没有消除顺行运动，并且对逆行运动的频率没有影响。与微管也可能会移动到邻近的微管的想法一致，肌动蛋白的消耗完全抑制了在低微管密度的实验条件下微管的向外运输。有趣的是，微管组装的可视化显示肌动蛋白的消耗实际上增强了微管彼此对齐的趋势。这样的微管-微管相互作用足以使微管以其特征极性模式在没有肌动蛋白丝的情况下过夜生长的轴突中定向。实际上，微管行为仅在肌动蛋白耗尽后在神经元的外围区域中才是混乱的，在该神经元的外围区域中，微管通常是稀疏的，因此缺少可以与之相互作用的邻近微管。基于这些结果，我们得出结论，微管在顺行方向上针对肌动蛋白丝或邻近的微管运输，而仅在逆行方向上针对其他微管运输。此外，微管彼此之间的运输为在没有肌动蛋白丝的情况下微管的展开和定向提供了令人惊讶的有效选择。

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