Viral genes governing CMV capsid export

控制 CMV 衣壳输出的病毒基因

• 批准号: 14720848
• 负责人: Professor Dr. Ulrich H. Koszinowski
• 金额: --
• 依托单位: Institut für Virologie
• 依托单位国家: 德国
• 项目类别: Priority Programmes
• 财政年份: 2005
• 资助国家: 德国
• 起止时间: 2004-12-31 至 2011-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/14720848?language=en
• 关键词: Viral; genes; governing; CMV; capsid

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.

人们认为疱疹病毒衣壳从细胞核中流出是通过从内核膜（INM）出芽，然后与外核膜（ONM）融合，导致衣壳释放到细胞质中而发生的。正常细胞仅在细胞质中显示出芽现象。尽管有这种不寻常的焦点，但高度冗余的过程，细胞仍可以存活数天，并且没有普遍的核膜破裂。这一过程由两种必需的疱疹病毒蛋白在 INM 上的组装控制，INM 形成核输出复合物 (NEC) 核心并招募更多（很大程度上未知的）蛋白质。在准备工作中，我们研究了 NEC 形成的分子原理。此外，还开发了许多遗传筛选和程序用于致命病毒突变体的条件分析。我们现在希望定义被招募到 NEC 或受 NEC 形成影响以实现衣壳穿透核膜的病毒和细胞伙伴。这应该能够揭示疱疹衣壳出芽和排出的分子细节。