Membrane deformation and scission by the HSV-1 nuclear egress complex.
Membrane deformation and scission by the HSV-1 nuclear egress complex.
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DOI：
10.1038/ncomms5131
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发表时间：
2014-06-11
影响因子：
16.6
通讯作者：
Heldwein, Ekaterina E.
中科院分区：
文献类型：
--
作者：
Bigalke, Janna M.;Heuser, Thomas;Nicastro, Daniela;Heldwein, Ekaterina E.
疱疹病毒如HSV-1的核出口复合物（NEC）对于新生衣壳从细胞核中退出至关重要。NEC驱动细胞中的核膜囊泡形成，但确切的出芽机制和细胞蛋白质的潜在参与尚不清楚。在这里，我们报告说，单纯疱疹病毒-1 NEC是足够的膜出芽在体外，因此代表了一个完整的膜变形和断裂机制。它在出芽囊泡的内表面上形成有序的涂层，这表明它通过支架膜芽和收缩颈部到断裂点来介导断裂。NEC介导的体外出芽的向内拓扑结构类似于HSV-1感染期间衣壳出芽进入内核膜和NEC转染细胞中的核膜囊泡化。我们建议NEC的功能作为最小的病毒编码的膜出芽机器在核出口，并不需要额外的细胞因子。
The nuclear egress complex (NEC) of herpesviruses such as HSV-1 is essential for the exit of nascent capsids from the cell nucleus. The NEC drives nuclear envelope vesiculation in cells, but the precise budding mechanism and the potential involvement of cellular proteins are unclear. Here we report that HSV-1 NEC alone is sufficient for membrane budding in vitro and thus represents a complete membrane deformation and scission machinery. It forms ordered coats on the inner surface of budded vesicles, suggesting that it mediates scission by scaffolding the membrane bud and constricting the neck to the point of scission. The inward topology of NEC-mediated budding in vitro resembles capsid budding into the inner nuclear membrane during HSV-1 infection and nuclear envelope vesiculation in NEC-transfected cells. We propose that the NEC functions as minimal virus-encoded membrane-budding machinery during nuclear egress and does not require additional cellular factors.
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DOI：
10.1073/pnas.0701757104
发表时间：
2007-04-24
影响因子：
11.1
作者：
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通讯作者：
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发表时间：
2012-10-16
影响因子：
11.1
作者：
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通讯作者：
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影响因子：
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作者：
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