在疹病毒核出口期间,CLCC1促进了膜融合
Bing Dai1,2, Lucas Polack1, Adrian Sperl1,2
1Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts, United States of America.
bioRxiv : the preprint server for biology
|October 10, 2024
概括
疹病毒劫持了一个涉及CLCC1的细胞膜融合机制,用于核输出. 这一发现揭示了核外形成和病毒囊体运输所必不可少的古老过程.
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:
- 疹类 (Herpesvirales) 感染了包括人类在内的各种物种.
- 疹病毒通过涉及核膜芽和融合的非正规途径将囊从核转移到细胞质.
- 核出炉核聚变阶段的分子媒介在很大程度上是未知的.
研究的目的:
- 为了确定宿主因子,对于核出口融合阶段的简单疹病毒1感染必不可少.
- 阐明已识别的宿主因子在病毒囊运输和核膜形态发生过程中的作用.
主要方法:
- 使用简单疹病毒1进行全基因组CRISPR选.
- 进行了功能性测试,以评估宿主因子枯竭对病毒核退出和细胞过程的影响.
主要成果:
- 鉴定出CLCC1是疹病毒核出口的融合阶段的关键宿主因素.
- 失去CLCC1导致核出口的缺陷,围核囊泡的积累,并减少病毒标位.
- 此外,CLCC1还参与了核毛孔复合体在未感染细胞中的插入.
- 在感染软体动物和鱼类的古老疹病毒中保存了CLCC1的同类物.
结论:
- 在疹病毒核退出过程中,CLCC1是一个重要的宿主因子,它调解了周核病毒与外核膜的融合.
- 这项研究揭示了一种古老的膜融合机制,对核外形态发生至关重要,疹病毒利用这种机制来有效地运输囊.
- 这些发现表明,CLCC1在病毒感染和基本细胞过程中都起着保留作用.
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