Viral genes governing CMV capsid export

疱疹病毒衣壳从细胞核外泄被认为是通过从内核膜(INM)萌发，然后与外核膜(ONM)融合导致衣壳释放到细胞质中发生的。正常细胞只在细胞质中有萌芽现象。尽管有这种不寻常的焦点，但高度冗余的过程，细胞可以保持存活数天，并且没有一般的核膜破裂。这一过程是由两种基本的疱疹病毒蛋白在INM上组装而成的，INM形成了核出口复合体(NEC)核心，并招募了更多的-基本上未知的-蛋白质。在准备工作中，我们研究了NEC形成的分子原理。此外，还开发了一些遗传筛查和程序，用于对致命性病毒突变进行条件分析。我们现在希望定义哪些病毒和细胞伙伴被招募到NEC的形成或受到其影响，以实现衣壳通过核膜的穿透。这应该会揭开疱疹衣壳萌芽和出口的分子细节。

Herpesvirus capsid egress from the cell nucleus is thought to occur through budding from the inner nuclear membrane (INM) followed by fusion with the outer nuclear membrane (ONM) resulting in the release of the capsid into the cytoplasm. Normal cells show budding phenomena only in the cytoplasm. Despite this unusual focal, but highly redundant process the cell can stay alive for days and there is no general nuclear envelope breakdown. This process is governed by the assembly of two essential herpesvirus proteins at the INM that forms the nuclear export complex (NEC) core and recruits further - largely unknown - proteins. In preparatory works we have studied the molecular principles of NEC formation. In addition a number of genetic screens and procedures were develped for conditional analysis of lethal virus mutants. We now wish to define the viral and cellular partners which are recruited to or affected by formation of the NEC to achieve capsid penetration through nuclear membranes. This should unravel the molecular details of herpes capsid budding and egress.