Listeria monocytogenes exploits ERM protein functions to efficiently spread from cell to cell
Listeria monocytogenes exploits ERM protein functions to efficiently spread from cell to cell
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DOI：
10.1038/sj.emboj.7600595
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发表时间：
2005-03-23
期刊：
影响因子：
11.4
通讯作者：
Herrlich, P
中科院分区：
文献类型：
--
作者：
Pust, S;Morrison, H;Herrlich, P
细胞间传播是单核细胞增多性李斯特菌感染周期中的基本步骤，它严格依赖于细菌诱导突起的形成。由于突起中的李斯特菌肌动蛋白尾巴与质膜密切相关，我们假设膜上的细胞骨架连接物将需要启动和维持它们的形成以及随后的细胞间传播。我们已经发现Ezrin是Ezrin、Radioxin和Moesin(ERM)家族的成员，它是关键的膜-细胞骨架连接子，在李斯特菌的突起处积聚。李斯特菌诱导突起和在相邻细胞之间有效传播的能力取决于ERM蛋白与膜成分如CD44和肌动蛋白细丝的相互作用。干扰这些相互作用或与ERM蛋白的磷酸化不仅减少突起的数量，而且改变它们的形态，导致形成短而塌陷的突起。因此，李斯特菌在细胞间的传播受到严重损害。因此，李斯特菌利用ERM蛋白来逃避宿主的免疫反应，并成功地发展成感染。
Cell-to-cell spread is a fundamental step in the infection cycle of Listeria monocytogenes that strictly depends on the formation of bacteria-induced protrusions. Since Listeria actin tails in the protrusions are tightly associated with the plasma membrane, we hypothesised that membrane cytoskeleton linkers would be required for initiating and sustaining their formation and the subsequent cell-to-cell spread. We have found that ezrin, a member of the ezrin, radixin and moesin (ERM) family that functions as a key membrane - cytoskeleton linker, accumulates at Listeria protrusions. The ability of Listeria to induce protrusions and effectively spread between adjacent cells depends on the interaction of ERM proteins with both a membrane component such as CD44 and actin filaments. Interfering with either of these interactions or with ERM proteins phosphorylation not only reduces the number of protrusions but also alters their morphology, resulting in the formation of short and collapsed protrusions. As a consequence, Listeria cell-to-cell spread is severely impaired. Thus, ERM proteins are exploited by Listeria to escape the host immune response and to succeed in the development of the infection.