SMN affects membrane remodelling and anchoring of the protein synthesis machinery
SMN affects membrane remodelling and anchoring of the protein synthesis machinery
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DOI：
10.1242/jcs.176750
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发表时间：
2016-02-15
影响因子：
4
通讯作者：
Di Certo, Maria Grazia
中科院分区：
文献类型：
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作者：
Gabanella, Francesca;Pisani, Cinzia;Di Certo, Maria Grazia
膜信号和肌动蛋白网络之间的断开可能会产生灾难性的影响，这取决于细胞的大小和极性。存活运动神经元（SMN）蛋白普遍参与剪接体小核核糖核蛋白颗粒的组装。然而，其他SMN功能可能影响细胞活动，驱动不对称的细胞表面扩张。能够减轻SMN缺陷的基因在SMN可以起作用的途径中起作用，例如mRNA翻译，肌动蛋白网络和内吞作用。在这里，我们发现SMN在肌动蛋白丝的动态重排过程中积聚在膜突起处。除了定位数据外，我们还发现SMN与caveolin-1相互作用，介导翻译机械部件的锚定。重要的是，SMN缺乏会耗尽核糖体的质膜，这与成纤维细胞无法延伸膜突起有关。这些发现有力地支持SMN和膜动力学之间的关系。我们提出SMN可以组装与质膜相关并受质膜支配的翻译平台。这种活性在膜重塑和局部蛋白质合成相互依赖加剧的细胞中可能是至关重要的。
Disconnection between membrane signalling and actin networks can have catastrophic effects depending on cell size and polarity. The survival motor neuron (SMN) protein is ubiquitously involved in assembly of spliceosomal small nuclear ribonucleoprotein particles. Other SMN functions could, however, affect cellular activities driving asymmetrical cell surface expansions. Genes able to mitigate SMN deficiency operate within pathways in which SMN can act, such as mRNA translation, actin network and endocytosis. Here, we found that SMN accumulates at membrane protrusions during the dynamic rearrangement of the actin filaments. In addition to localization data, we show that SMN interacts with caveolin-1, which mediates anchoring of translation machinery components. Importantly, SMN deficiency depletes the plasma membrane of ribosomes, and this correlates with the failure of fibroblasts to extend membrane protrusions. These findings strongly support a relationship between SMN and membrane dynamics. We propose that SMN could assembly translational platforms associated with and governed by the plasma membrane. This activity could be crucial in cells that have an exacerbated interdependence of membrane remodelling and local protein synthesis.