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<p><i>Herpesvirales</i> are an ancient viral order that causes lifelong infections in species from mollusks to humans. They export their capsids from the nucleus to the cytoplasm by a noncanonical nuclear egress route that involves capsid budding at the inner nuclear membrane followed by fusion of this temporary envelope with the outer nuclear membrane. Here, using a whole-genome CRISPR screen, we identify ER protein CLCC1 as important for the fusion stage of nuclear egress in&#xa0;herpes simplex virus 1. We also find that the genomes of <i>Herpesvirales</i> that infect mollusks and fish encode <i>CLCC1</i> genes acquired from host genomes by horizontal gene transfer. In uninfected cells, loss of CLCC1 causes a nuclear blebbing defect, suggesting a role in host nuclear export. We hypothesize that CLCC1 facilitates an ancient cellular membrane fusion mechanism that <i>Herpesvirales</i> have hijacked or co-opted for capsid export and propose a mechanistic model.</p>

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ER protein CLCC1 promotes nuclear envelope fusion in herpesviral and host processes

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年11月21日

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  • Bing Dai,
  • Adrian W. Sperl,
  • Lucas Polack,
  • Isabel Mejia,
  • Haley Dame,
  • Tien Huynh,
  • Chloe Deveney,
  • Nathalie Lavoie,
  • Chanyoung Lee,
  • John G. Doench,
  • Matthew D. Daugherty,
  • Ekaterina E. Heldwein

摘要

Herpesvirales are an ancient viral order that causes lifelong infections in species from mollusks to humans. They export their capsids from the nucleus to the cytoplasm by a noncanonical nuclear egress route that involves capsid budding at the inner nuclear membrane followed by fusion of this temporary envelope with the outer nuclear membrane. Here, using a whole-genome CRISPR screen, we identify ER protein CLCC1 as important for the fusion stage of nuclear egress in herpes simplex virus 1. We also find that the genomes of Herpesvirales that infect mollusks and fish encode CLCC1 genes acquired from host genomes by horizontal gene transfer. In uninfected cells, loss of CLCC1 causes a nuclear blebbing defect, suggesting a role in host nuclear export. We hypothesize that CLCC1 facilitates an ancient cellular membrane fusion mechanism that Herpesvirales have hijacked or co-opted for capsid export and propose a mechanistic model.