Tiam1参与轴突形成的证据。
Evidence for the involvement of Tiam1 in axon formation.
作者信息
Kunda P, Paglini G, Quiroga S, Kosik K, Caceres A
机构信息
Instituto Mercedes y Martin Ferreyra (INIMEC-CONICET), 5000 Cordoba, Argentina.
出版信息
J Neurosci. 2001 Apr 1;21(7):2361-72. doi: 10.1523/JNEUROSCI.21-07-02361.2001.
Abstract
In cultured neurons, axon formation is preceded by the appearance in one of the multiple neurites of a large growth cone containing a labile actin network and abundant dynamic microtubules. The invasion-inducing T-lymphoma and metastasis 1 (Tiam1) protein that functions as a guanosine nucleotide exchange factor for Rac1 localizes to this neurite and its growth cone, where it associates with microtubules. Neurons overexpressing Tiam1 extend several axon-like neurites, whereas suppression of Tiam1 prevents axon formation, with most of the cells failing to undergo changes in growth cone size and in cytoskeletal organization typical of prospective axons. Cytochalasin D reverts this effect leading to multiple axon formation and penetration of microtubules within neuritic tips devoid of actin filaments. Taken together, these results suggest that by regulating growth cone actin organization and allowing microtubule invasion within selected growth cones, Tiam1 promotes axon formation and hence participates in neuronal polarization.
摘要
在培养的神经元中，轴突形成之前，多个神经突中的一个会出现一个大型生长锥，其中含有不稳定的肌动蛋白网络和丰富的动态微管。作为Rac1鸟苷酸交换因子发挥作用的侵袭诱导性T淋巴瘤和转移1（Tiam1）蛋白定位于该神经突及其生长锥，在那里它与微管相关联。过表达Tiam1的神经元会延伸出几条轴突样神经突，而抑制Tiam1则会阻止轴突形成，大多数细胞无法经历生长锥大小和预期轴突典型的细胞骨架组织变化。细胞松弛素D可逆转这种效应，导致多个轴突形成，并使微管穿透缺乏肌动蛋白丝的神经突尖端。综上所述，这些结果表明，通过调节生长锥肌动蛋白组织并允许微管侵入选定的生长锥，Tiam1促进轴突形成，从而参与神经元极化。
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