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首页> 外文期刊>Nature >Shiga toxin induces tubular membrane invaginations for its uptake into cells
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Shiga toxin induces tubular membrane invaginations for its uptake into cells

机译：志贺毒素诱导其进入细胞的管状膜内陷

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Clathrin seems to be dispensable for some endocytic processes and, in several instances, no cytosolic coat protein complexes could be detected at sites of membrane invagination. Hence, new principles must in these cases be invoked to account for the mechanical force driving membrane shape changes. Here we show that the Gb3 (glycolipid)-binding B-subunit of bacterial Shiga toxin induces narrow tubular membrane invaginations in human and mouse cells and model membranes. In cells, tubule occurrence increases on energy depletion and inhibition of dynamin or actin functions. Our data thus demonstrate that active cellular processes are needed for tubule scission rather than tubule formation. We conclude that the B-subunit induces lipid reorganization that favours negative membrane curvature, which drives the formation of inward membrane tubules. Our findings support a model in which the lateral growth of B-subunit-Gb3 microdomains is limited by the invagination process, which itself is regulated by membrane tension. The physical principles underlying this basic cargo-induced membrane uptake may also be relevant to other internalization processes, creating a rationale for conceptualizing the perplexing diversity of endocytic routes.
机译：网格蛋白似乎对于某些内吞过程是可有可无的，并且在某些情况下，在膜内陷的位点未检测到胞质外壳蛋白复合物。因此，在这些情况下，必须采用新的原理来说明驱动膜片形状变化的机械力。在这里，我们显示细菌志贺毒素的Gb3（糖脂）结合B亚基诱导人和小鼠细胞和模型膜中的狭窄管状膜内陷。在细胞中，肾小管的出现会增加能量消耗并抑制动力蛋白或肌动蛋白的功能。因此，我们的数据表明，进行小管切开而不是小管形成需要活跃的细胞过程。我们得出的结论是，B亚基诱导脂质重组，有利于负膜曲率，从而驱动内膜小管的形成。我们的发现支持一种模型，其中B亚基Gb3微结构域的侧向生长受到内陷过程的限制，而内陷过程本身受膜张力的调节。这种基本的货物诱导的膜摄取基础的物理原理也可能与其他内在化过程有关，从而为概念化内吞途径的困惑多样性创造了原理。

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