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<p>Precise double-strand break (DSB) repair is paramount for genome stability. Homologous recombination (HR) is preferred to repair DSBs when a nearby sister chromatid ensures an error-free template. In <i>Saccharomyces cerevisiae</i>, this preference extends into anaphase and telophase (late mitosis; late-M) despite sister chromatids having been pulled apart. Previously, we identified the nuclear envelope (NE) protein Msc1 as important for late-M DSB repair. Here, we report that Msc1 faces the NE lumen, and its depletion leads to DSB-independent over-compartmentalization of the nucleus and nuclear pore complex (NPC) mislocation. These phenotypes are partly shared by the highly conserved NE healing complex ESCRT-III. Finally, we show that these abnormal NE phenotypes are found throughout the cell cycle and in the DSB-driven G2/M arrest. These findings highlight the essential role of NE homeostasis in DSB repair.</p><p></p>

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Continuous nuclear envelope surveillance is required for DNA double strand break repair

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月2日

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  • Sara Medina-Suárez,
  • Félix Machín

摘要

Precise double-strand break (DSB) repair is paramount for genome stability. Homologous recombination (HR) is preferred to repair DSBs when a nearby sister chromatid ensures an error-free template. In Saccharomyces cerevisiae, this preference extends into anaphase and telophase (late mitosis; late-M) despite sister chromatids having been pulled apart. Previously, we identified the nuclear envelope (NE) protein Msc1 as important for late-M DSB repair. Here, we report that Msc1 faces the NE lumen, and its depletion leads to DSB-independent over-compartmentalization of the nucleus and nuclear pore complex (NPC) mislocation. These phenotypes are partly shared by the highly conserved NE healing complex ESCRT-III. Finally, we show that these abnormal NE phenotypes are found throughout the cell cycle and in the DSB-driven G2/M arrest. These findings highlight the essential role of NE homeostasis in DSB repair.