在疹病毒和宿主过程中,ER蛋白CLCC1促进核膜融合
Bing Dai1,2, Adrian W Sperl1,2, Lucas Polack1,3
1Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, MA, USA.
Nature communications
|November 21, 2025
概括
研究人员发现,ER蛋白CLCC1对于简单疹病毒1核出口至关重要. 这种蛋白质在某些病毒中通过水平基因转移获得,可能促进病毒利用的古老的膜融合机制.
科学领域:
- 病毒学 病毒学
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
背景情况:
- 疹病毒 (Herpesvirales) 是一种古老的病毒,在包括人类在内的各种宿主中引起终身感染.
- 疹病毒利用一种非正规的核出口途径,涉及囊芽和膜融合,以退出核.
研究的目的:
- 为了确定宿主因子,这对于简单疹病毒1 (HSV-1) 的核出口至关重要.
- 调查赫尔佩斯维拉类 (Herpesvirales) 序列中已识别的宿主因子的进化起源和细胞功能.
主要方法:
- 采用全基因组CRISPR屏幕来识别宿主蛋白质,这些蛋白质对HSV-1核退出至关重要.
- 使用比较基因组学和遗传学分析来追踪已识别的基因的进化历史.
- 进行了细胞测试,以评估在未感染细胞中识别的蛋白质的功能.
主要成果:
- 鉴定出细胞内膜网膜蛋白CLCC1对于HSV-1核输出的膜融合阶段至关重要.
- 在感染软体动物和鱼类的Herpesvirales中发现了CLCC1基因,这些基因是通过从宿主基因组的水平基因转移获得的.
- 在未被感染的细胞中,CLCC1的丢失导致了核爆发,这表明它在宿主核出口过程中发挥了作用.
结论:
- CLCC1是一个由HSV-1劫持的关键宿主因子,用于高效的核体出口.
- 这一发现表明,CLCC1介导着病毒利用的古老的细胞膜融合机制.
- 横向基因转移在Herpesvirales的CLCC1利用进化中发挥了作用.
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