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首页> 外文期刊>Cell motility and the cytoskeleton >Tau inhibits anterograde axonal transport and perturbs stability in growing axonal neurites in part by displacing kinesin cargo: Neurofilaments attenuate tau-mediated neurite instability.
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Tau inhibits anterograde axonal transport and perturbs stability in growing axonal neurites in part by displacing kinesin cargo: Neurofilaments attenuate tau-mediated neurite instability.

机译：Tau通过置换驱动蛋白货物来抑制生长中的轴突神经突的顺行轴突运输并扰乱稳定性：神经丝可减轻tau介导的轴突的不稳定性。

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Overexpression of tau compromises axonal transport and induces retraction of growing neurites. We tested the hypothesis that increased stability provided by neurofilaments (NFs) may prevent axonal retraction. NB2a/d1 cells were differentiated for 3 days, at which time phosphorylated NFs appear and for 14 days, which induces continued neurite elongation and further phospho-NF accumulation. Cultures were transfected with a construct that expresses full-length, 4-repeat tau. Consistent with prior studies, overexpression of tau induced retraction of day three axonal neurites even following treatment with the microtubule-stabilizing drug taxol. Axonal neurites of day 14 cells were more resistant to tau-mediated retraction. To test whether or not this resistance was derived from their additional NF content, day 3 cultures were co-transfected with constructs expressing tau and NF-M (which increases overall axonal NFs). Overexpression of NF-M attenuated tau-mediated retraction of day 3 axonal neurites. By contrast, co-transfection with constructs expressing tau and vimentin (which increases axonal neurites length) did not attenuate tau-mediated neurite retraction. Co-precipitation experiments indicate that tau is a cargo of kinesin, and that tau overexpression may displace other kinesin-based cargo, including both critical cytoskeletal proteins and organelles. However, cultures simultaneously transfected with constructs expressing NF-M and tau, the level of examined vesicles was maintained. These collectively indicate that NFs stabilize developing axonal neurites and can counteract the destabilizing force resulting from overexpression of tau, and underscore that the development and stabilization of axonal neurites is dependent upon a balance of cytoskeletal elements. Cell Motil. Cytoskeleton 2007. (c) 2007 Wiley-Liss, Inc.
机译：tau蛋白的过度表达会损害轴突运输并诱导生长中的神经突回缩。我们测试了这样的假说，即神经丝（NFs）提供的增加的稳定性可能会阻止轴突缩回。 NB2a / d1细胞分化3天，这时出现磷酸化的NFs，并分化14天，这诱导了持续的神经突伸长和进一步的磷酸化NF积累。用表达全长4-重复tau的构建体转染培养物。与先前的研究一致，tau的过表达即使在用微管稳定药紫杉醇治疗后，也会导致第三天的轴突突缩回。第14天细胞的轴突神经突对tau介导的缩回更具抵抗力。为了测试这种抗性是否源于其额外的NF含量，将第3天的培养物与表达tau和NF-M（会增加总轴突NF）的构建体共转染。 NF-M的过度表达减弱了tau介导的第3天轴突神经突的收缩。相比之下，与表达tau和波形蛋白的构建体共转染（增加轴突神经突长度）不会减弱tau介导的神经突回缩。共沉淀实验表明tau是驱动蛋白的产物，并且tau过表达可能取代其他基于驱动蛋白的产物，包括关键的细胞骨架蛋白和细胞器。然而，用表达NF-M和tau的构建体同时转染的培养物，维持了检查的囊泡水平。这些共同表明，NF稳定了轴突神经突的发育，并可以抵消由tau的过度表达引起的去稳定力，并强调了轴突神经突的发展和稳定取决于细胞骨架元素的平衡。细胞动力。 Cytoskeleton2007。（c）2007 Wiley-Liss，Inc.。

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