Nirschl Jeffrey J, Magiera Maria M, Lazarus Jacob E, Janke Carsten, Holzbaur Erika L F
Department of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Institut Curie, PSL Research University, CNRS UMR3348, 91405 Orsay, France; Université Paris Sud, Université Paris-Saclay, CNRS UMR3348, 91405 Orsay, France.
Cell Rep. 2016 Mar 22;14(11):2637-52. doi: 10.1016/j.celrep.2016.02.046. Epub 2016 Mar 10.
Motor-cargo recruitment to microtubules is often the rate-limiting step of intracellular transport, and defects in this recruitment can cause neurodegenerative disease. Here, we use in vitro reconstitution assays with single-molecule resolution, live-cell transport assays in primary neurons, computational image analysis, and computer simulations to investigate the factors regulating retrograde transport initiation in the distal axon. We find that phosphorylation of the cytoskeletal-organelle linker protein CLIP-170 and post-translational modifications of the microtubule track combine to precisely control the initiation of retrograde transport. Computer simulations of organelle dynamics in the distal axon indicate that while CLIP-170 primarily regulates the time to microtubule encounter, the tyrosination state of the microtubule lattice regulates the likelihood of binding. These mechanisms interact to control transport initiation in the axon in a manner sensitive to the specialized cytoskeletal architecture of the neuron.
马达蛋白-货物复合体招募到微管通常是细胞内运输的限速步骤,这种招募过程中的缺陷可导致神经退行性疾病。在此,我们使用具有单分子分辨率的体外重建分析、原代神经元中的活细胞运输分析、计算图像分析和计算机模拟,来研究调节轴突远端逆行运输起始的因素。我们发现,细胞骨架-细胞器连接蛋白CLIP-170的磷酸化与微管轨道的翻译后修饰共同精确控制逆行运输的起始。轴突远端细胞器动力学的计算机模拟表明,虽然CLIP-170主要调节与微管相遇的时间,但微管晶格的酪氨酸化状态调节结合的可能性。这些机制相互作用,以一种对神经元特化细胞骨架结构敏感的方式控制轴突中的运输起始。